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Journal of Nutritional Biochemistry
Journal Prestige (SJR): 1.678
Citation Impact (citeScore): 5
Number of Followers: 7  
 
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
ISSN (Print) 0955-2863
Published by Elsevier Homepage  [3162 journals]
  • Long-term follow-up of muscle lipid accumulation, mitochondrial activity
           and oxidative stress and their relationship with impaired glucose
           homeostasis in high fat high fructose diet-fed rats
    • Abstract: Publication date: Available online 14 November 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Yang Wang, Gilles Fouret, Beatrice Bonafos, Agnieszka Blachnio-Zabielska, Thibault Leroy, David Crouzier, Bruno Barea, Sylvie Gaillet, Cedric Moro, Jerome Lecomte, Charles Coudray, Christine Feillet-Coudray Metabolic syndrome components, including obesity, dyslipidemia and impaired glucose homeostasis, become a major public health issue. Muscles play a predominant role in insulin-mediated glucose uptake, and high fat diets may negatively affect muscle function and homeostasis. This work aimed to study the time-course of muscle lipid accumulation, oxidative stress and mitochondrial dysfunction and their association to impaired glucose homeostasis in rats fed an obesogenic diet. Male Wistar rats were fed with a standard or a high fat/high fructose (HFHFr) diet and sacrificed on 4, 8, 12, 16, 20 weeks. Rats fed the HFHFr diet developed mild overweight, increased liver and adipose tissue weights and glucose intolerance. The impaired glucose homeostasis increased gradually with the HFHFr diet to become significant on the 12th and 16th weeks of diet. In parallel, the muscle lipid composition showed an increase in the saturated fatty acids and the monounsaturated fatty acids with a marked decrease in the polyunsaturated fatty acids. The HFHFr diet also increased muscle contents of both diacylglycerols and Ceramides. Surprisingly, HFHFr diet did not induce major muscle mitochondrial dysfunction or oxidative stress. These results indicate that muscle lipid alterations, as well as impaired glucose homeostasis occur as early as the 8th week of HFHFr diet, increase to reach a plateau around the 12th–16th weeks of diet, and then attenuate towards the end of study. At these diet treatment durations, muscle mitochondrial activity and oxidative stress remained unchanged and do not seem to have a major role in the observed impaired glucose homeostasis.
       
  • Heterogeneity in gut microbiota drive polyphenol metabolism that
           influences α-synuclein misfolding and toxicity
    • Abstract: Publication date: Available online 14 November 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Lap Ho, Danyue Zhao, Kenjiro Ono, Kai Ruan, Ilaria Mogno, Mayumi Tsuji, Eileen Carry, Justin Brathwaite, Steven Sims, Tal Frolinger, Susan Westfall, Paolo Mazzola, Qingli Wu, Ke Hao, Thomas E. Lloyd, James E. Simon, Jeremiah Faith, Giulio M. Pasinetti The intestinal microbiota actively converts dietary flavanols into phenolic acids, some of which are bioavailable in vivo and may promote resilience to select neurological disorders by interfering with key pathologic mechanisms. Since every person harbors a unique set of gut bacteria, we investigated the influence of the gut microbiota's interpersonal heterogeneity on the production and bioavailability of flavonoid metabolites that may interfere with the misfolding of alpha (α)-synuclein, a process that plays a central role in Parkinson's disease and other α-synucleinopathies. We generated two experimental groups of humanized gnotobiotic mice with compositionally diverse gut bacteria and orally treated the mice with a flavanol-rich preparation (FRP). The two gnotobiotic mouse groups exhibited distinct differences in the generation and bioavailability of FRP-derived microbial phenolic acid metabolites that have bioactivity towards interfering with α-synuclein misfolding or inflammation. We also demonstrated that these bioactive phenolic acids are effective in modulating the development and progression of motor dysfunction in a Drosophila model of α-synucleinopathy. Lastly, through in vitro bacterial fermentation studies, we identified select bacteria that are capable of supporting the generation of these bioavailable and bioactive phenolic acids. Outcomes from our studies provide a better understanding of how interpersonal heterogeneity in the gut microbiota differentially modulates the efficacy of dietary flavanols to protect against select pathologic mechanisms. Collectively, our findings provide the basis for future developments of probiotic, prebiotic, or synbiotic approaches for modulating the onset and/or progression of α-synucleinopathies and other neurological disorders involving protein misfolding and/or inflammation.
       
  • Purple sweet potato color protects against high-fat diet-induced cognitive
           deficits through AMPK-mediated autophagy in mouse hippocampus
    • Abstract: Publication date: Available online 12 November 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Juan Zhuang, Jun Lu, Xin Wang, Xinfeng Wang, Weicheng Hu, Fashui Hong, Xiang-xiang Zhao, Yuan-lin Zheng Prevention of obesity-induced cognitive decline is an important public health goal. Purple sweet potato color (PSPC), a class of naturally occurring anthocyanins, has beneficial potentials including antioxidant and neuroprotective activity. Evidence shows that anthocyanins can activate AMP-activated protein kinase (AMPK), a critical mediator of autophagy induction. This study investigated whether PSPC could improve cognitive function through regulating AMPK/autophagy signaling in HFD-fed obese mice. Our results showed that PSPC significantly ameliorated obesity, peripheral insulin resistance and memory impairment in HFD-fed mice. Moreover, enhanced autophagy was observed, along with the decreased levels of protein carbonyls, malondialdehyde and reactive oxygen species (ROS) in the hippocampus of HFD-fed mice due to PSPC administration. PSPC also promoted hippocampal brain-derived neurotrophic factor (BDNF) expression and neuron survival in HFD-fed mouse. These improvements were mediated, at least in part, by the activation of AMPK, which was confirmed by metformin treatment. It is concluded that PSPC has great potential to improve cognitive function in HFD-fed mice via AMPK activation that restores autophagy and protects against hippocampal apoptosis.
       
  • Gut microbiota: A potential manipulator for host adipose tissue and energy
           metabolism
    • Abstract: Publication date: Available online 10 November 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Rong Bohan, Xia Tianyu, Zhang Tiantian, Feng Ruonan, Huang Hongtao, Wu Qiong, Sun Chao Normally, the gut microbiota has a mutually beneficial association with host health and maintains its commensal status in mammals. Conversely, it can also negatively influence host physiology under some certain circumstances, including obesity and other disease states. Although numerous gut microbial functions directly affect the gastrointestinal tract, in this paper we focus on the influences of the gut microbiota on host adipose tissue and energy metabolism, particularly lipometabolism. We thoroughly discuss two important microbial products, short chain fat acids (SCFAs) and lipopolysaccharides (LPS), which are linked to several mechanisms involved in obesity and adipose, including differentiation, energy metabolism, and immunity. Furthermore, this review also addresses some potentially beneficial functions of probiotics, which can serve to prevent or alleviate host pathological states, including dysbacteriosis, obesity, low-grade inflammation and metabolic syndrome.
       
  • Effect of omega-3 fatty acids supplementation combined with lifestyle
           intervention on adipokines and biomarkers of endothelial dysfunction in
           obese adolescents with hypertriglyceridemia
    • Abstract: Publication date: Available online 7 November 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Fengyang Huang, Blanca Estela del-Río-Navarro, José Leija-Martinez, Saúl Torres-Alcantara, Eliseo Ruiz-Bedolla, Leticia Hernández Cadena, Albino Barraza Villarreal, Rodrigo Romero-Nava, Fausto Sanchéz-Muñoz, Santiago Villafaña, Laurence A. Marchat, Enrique Hong Obesity in adolescents is considered a major public health problem, combined interventional approaches such as omega-3 supplementation with lifestyle intervention (LI) might exert synergistic effects and exceed the impact of each individual strategy. The purpose of the present study was to evaluate if the supplementation of omega-3 with LI could improve metabolic and endothelial abnormality in obese adolescents with hypertriglyceridemia. The study involved sixty-nine adolescents with normal weight and seventy obese adolescents with hypertriglyceridemia. All obese adolescents were applied to LI and randomly assigned to omega-3 supplementation or placebo group for 12 weeks. The obese adolescents with hypertriglyceridemia presented increased levels of leptin, retinol binding protein 4 (RBP4), selectin E (sE) and asymmetric dimethylarginine (ADMA) and decreased levels of adiponectin compared with control subjects. After 12-week intervention, omega-3 supplementation with LI decreased significantly in triglycerides, HOMA, leptin, RBP4, ADMA and sE. Moreover, omega-3 with LI displayed a significant reduction in triglycerides, ADMA and sE in comparison with LI alone. In subjects with omega-3 combined with LI assessed by multivariate regression model, the reduction in triglycerides was the only independent determinant of the decrease in ADMA. The reductions in triglycerides and HOMA were significantly contributed to the changes in sE. Our data indicated that omega-3 combined with LI in short duration significantly improved dyslipidemia, insulin resistance, abnormality of adipokines, endothelial dysfunction in comparison of LI alone, indicating the combined approach is an effective clinical and applicable strategy to control metabolic abnormality and decrease the risks of cardiovascular diseases in obese adolescents.
       
  • Both low- and regular-fat cheeses mediate improved insulin sensitivity and
           modulate serum phospholipid profiles in insulin resistant rats
    • Abstract: Publication date: Available online 6 November 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Anik RZ Hanning, Xiaofeng Wang, Zohre Hashemi, Sereana Wan, Alexandra England, René L Jacobs, Catherine B Chan Dietary recommendations for cheese usually promote low (LOW)- over regular (REG)-fat versions due to the saturated fat. Conversely, epidemiological evidence shows that cheese consumption associates with reduced risk of type 2 diabetes. To investigate how cheese influences diabetes-related outcomes, a feeding trial comparing LOW and REG cheese was conducted in high fat, lard-based diet (HFD)-fed insulin resistant rats, followed by evaluation of potential mechanisms. After 4 weeks HFD, LOW or REG was added at 7 and 10 g/100 g diet, respectively, for another 8 weeks. Following either an oral glucose or insulin tolerance test to assess glucoregulation, rats were euthanized and serum collected for metabolomic and lipid analyses. Hepatic tissue was used to measure glucoregulatory enzymes and lipid content. Both LOW and REG improved insulin sensitivity without effect on oral glucose tolerance, insulin secretion or body weight. Serum metabolomics identified 33 metabolites of interest, with 21 being phosphatidylcholines (PC) or lysophosphatidylcholines (LPC). HFD rats had significantly reduced LPC C16:1, C17:0, C18:1, C20:3 and C24:0 and these effects were normalized by LOW or REG cheese. Fourteen PC species were lowest in the HFD group and normalized by cheese feeding. Serum choline was elevated 7-fold in HFD but not cheese-fed rats compared with rats fed low-fat diet. Liver triglyceride was elevated by LOW feeding. In conclusion, inclusion of both LOW and REG cheeses in the diet of insulin resistant rats improves in vivo glucoregulation. This is associated with altered phospholipid metabolism, including cheese-mediated normalization of species that are decreased by high fat feeding.
       
  • EGF receptor plays a role in the mechanism of glutamine-mediated
           prevention of alcohol-induced gut barrier dysfunction and liver injury
    • Abstract: Publication date: Available online 6 November 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Avtar S. Meena, Pradeep K. Shukla, Parimal Sheth, RadhaKrishna Rao Recent study indicated that glutamine prevents alcoholic tissue injury in mouse gut and liver. Here we investigated the potential role of Epidermal Growth Factor Receptor (EGFR) in glutamine-mediated prevention of ethanol-induced colonic barrier dysfunction, endotoxemia and liver damage. Wildtype and EGFR*Tg transgenic (expressing dominant negative EGFR) mice were fed 1–6% ethanol in Lieber-DeCarli diet. Gut permeability was measured by vascular-to-luminal flux of FITC-inulin, and junctional integrity assessed by confocal microscopy. Liver injury was evaluated by plasma transaminases, histopathology and triglyceride analyses. Glutamine effect on acetaldehyde-induced tight junction disruption was investigated in Caco-2 cell monolayers. Doxycycline-induced expression of EGFR* blocked glutamine-mediated prevention of ethanol-induced disruption of colonic epithelial tight junction, mucosal permeability and endotoxemia. Ethanol activated cofilin and disrupted actin cytoskeleton, which was blocked by glutamine in an EGFR-dependent mechanism. Ethanol downregulated antioxidant gene expression and upregulated cytokine and chemokine gene expression, which were blocked by glutamine in wildtype mice in the presence or absence of doxycycline, but not in EGFR*Tg mice in the presence of doxycycline. Histopathology, plasma transaminases, triglyceride and expression of chemokine and antioxidant genes indicated ethanol-induced liver damage, which were blocked by glutamine in an EGFR-dependent mechanism. Src kinase activity and extracellular ligand binding domain of EGFR are required for glutamine-mediated protection of barrier function in Caco-2 cell monolayers. Glutamine released metalloproteinases into the medium, and metalloproteinase inhibitors blocked glutamine-mediated protection of barrier function. Results demonstrate that EGFR plays an important role in glutamine-mediated prevention of alcoholic gut permeability, endotoxemia and liver damage.
       
  • Vitamin E δ-tocotrienol inhibits TNF-α-stimulated NF-κB activation by
           up-regulation of anti-inflammatory A20 via modulation of sphingolipid
           including elevation of intracellular dihydroceramides
    • Abstract: Publication date: Available online 3 November 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Chao Yang, Qing Jiang Nuclear factor-κB (NF-κB) regulates inflammation and cell survival, and is considered a potential target for anti-inflammatory and anti-cancer therapy. δ-Tocotrienol (δTE), a vitamin E form, has been shown to inhibit NF-κB, but the mechanism underlying this action is not clear. In the present study, we show that δTE inhibited TNF-α-induced activation of NF-κB and IL-6 in a dose- and time-dependent manner in Raw 264.7 macrophages. δTE potently inhibited TNF-α-induced phosphorylation of transforming growth factor β-activated kinase 1 (TAK1), an upstream kinase essential for the activation of NF-κB. Interestingly, δTE significantly increased the expression of A20 and to a less extent, cylindromatosis (CYLD), both of which are inhibitors of NF-κB. The importance of induction of A20 in δTE's anti-NF-κB effect is validated in A20 knockout cells where δTE's inhibition of NF-κB was largely diminished. In pursuit of the cause for A20 induction, we found that δTE treatment caused rapid and persistent elevation of dihydroceramides, while decreased ceramides initially but increased ceramides during prolonged treatment. These changes of sphingolipids were accompanied by increased cellular stress markers. Importantly, δTE's induction of A20 and inhibition of NF-κB activation were partially counteracted by myriocin, a potent inhibitor of de novo synthesis of sphingolipids, indicating a critical role of sphingolipid modulation in δTE-mediated effects. Since dihydroceramide has been shown to induce A20 and inhibit NF-κB in RAW cells, we conclude that that δTE inhibits NF-κB activation by enhancing its negative regulator A20 as a result of modulating sphingolipids especially elevation of dihydroceramides.
       
  • Bovine milk-derived extracellular vesicles enhance inflammation and
           promote M1 polarization following agricultural dust exposure in mice
    • Abstract: Publication date: Available online 3 November 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Tara M. Nordgren, Art J. Heires, Janos Zempleni, Benjamin J. Swanson, Christopher Wichman, Debra J. Romberger Occupational agricultural dust exposure can cause severe lung injury, including COPD and asthma exacerbations. Cell-derived extracellular vesicles can mediate inflammatory responses and immune activation, but the contribution of diet-derived extracellular vesicles to these processes is poorly understood. We investigated whether bovine milk-derived extracellular vesicles modulate inflammatory responses to agricultural dust exposures in a murine model. C57BL/6 mice were fed either a extracellular vesicle-enriched modification of the AIN-93G diet with lyophilized bovine milk (EV), or a control diet wherein the milk was pre-sonicated, disrupting the milk extracellular vesicles and thereby leading to RNA degradation (DEV). Mice were maintained on the diets for 5–7 weeks and challenged with a single (acute) intranasal instillation of a 12.5% organic dust extract (DE), or with 15 instillations over 3 weeks (repetitive exposure model). Through these investigations, we identified significant interactions between diet and DE when considering numerous inflammatory outcomes, including lavage inflammatory cytokine levels and cellular infiltration into the lung airways. DE-treated peritoneal macrophages also demonstrated altered polarization, with EV-fed mouse macrophages exhibiting an M1 shift compared to an M2 phenotype in DEV-fed mice (IL-6, TNF, IL-12/23 all significantly elevated, and IL-10 and arginase decreased in EV macrophages, ex vivo). In complementary in vitro studies, mouse macrophages treated with purified milk-derived EV were found to express similar polarization phenotypes upon DE stimulation. These results suggest a role for dietary extracellular vesicles in the modulation of lung inflammation in response to organic dust which may involve macrophage phenotype polarization.
       
  • Diallyl disulfide potentiates anti-obesity effect of green tea in
           high-fat/high-sucrose diet-induced obesity
    • Abstract: Publication date: Available online 3 November 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Jaehoon Bae, Motofumi Kumazoe, Yoshinori Fujimura, Hirofumi Tachibana Obesity is a major problem in developed countries and a burden on social health care systems. Several epidemiological studies showed the protective effects of green tea against obesity-related diseases. Cyclic guanosine monophosphate (cGMP) acts as a mediator for the physiological effects of (−)-epigallocatechin-3-O-gallate, the major constituent of green tea. Here, we showed that the level of phosphodiesterase 5, a negative regulator of cGMP, was upregulated in adipose tissues of high-fat/high-sucrose (HF/HS) diet-fed mice and that this upregulation was ameliorated by diallyl disulfide (DADS), the major organosulfur in garlic. A green tea extract (GT) and DADS in combination attenuated HF/HS diet-induced adipose increase and triglyceride accumulation in the liver. In these mechanisms, the combination regimen suppressed the HF/HS diet-induced upregulation of fatty acid synthesis-related enzymes including sterol regulatory element-binding protein-1 (SREBP-1), fatty acid synthase, and stearoyl-CoA desaturase-1. Moreover, this combination diet upregulated thermogenesis-related genes including peroxisome proliferator-activated receptor (PPAR) gamma coactivator 1 alpha and uncoupling proteins in both white and brown adipose tissues. In conclusion, we identified DADS as an enhancer of the anti-obesity effect of GT accompanied by the suppression of SREBP-1 and activation of PPAR axis. The combination diet is a novel and easily applicable approach against obesity-related diseases.
       
  • Secretion of a gastrointestinal hormone, cholecystokinin, by hop-derived
           bitter components activates sympathetic nerves in brown adipose tissue
    • Abstract: Publication date: Available online 30 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Takahiro Yamazaki, Yumie Morimoto-Kobayashi, Kumiko Koizumi, Chika Takahashi, Shiori Nakajima, Sayoko Kitao, Yoshimasa Taniguchi, Mikio Katayama, Yoshihiro Ogawa Matured hop bitter acids (MHBA) are oxidation products from bitter components in hops, which are used widely as food materials to add flavor and bitterness in beer production. Our previous study has shown that MHBA induces thermogenesis in brown adipose tissue (BAT) via sympathetic nerves in rodents and reduces body fat in healthy adults. However, it is unclear how MHBA affects the sympathetic nervous system. In this study, we demonstrate that MHBA treatment of enteroendocrine cells increases Ca2+ levels and induces the secretion of the gastrointestinal hormone, cholecystokinin (CCK), in a dose dependent manner. These effects were eliminated by Ca2+ depletion from the medium or blockers of L-type voltage-sensitive Ca2+ channels during pre-treatment. Induction of CCK secretion by MHBA was also confirmed using isolated rat small intestines. Elevation of the sympathetic nerve activity innervating BAT (BAT-SNA) and BAT temperature by MHBA administration in rats was blocked by pre-treatment with a CCK receptor 1 (CCK1R) antagonist. Moreover, the intraperitoneal injection of CCK fragment elevated BAT-SNA and this increase was blocked by subdiaphragmatic vagotomy. These results demonstrate that MHBA induces CCK secretion in the gastrointestinal tracts and elevates BAT-SNA via CCK1R and vagal afferent nerves. In addition, MHBA increases BAT temperature via CCK1R. Our findings reveal a novel mechanism of the beneficial metabolic effects of food ingredients.
       
  • A peroxidized omega-3-enriched polyunsaturated diet leads to adipose and
           metabolic dysfunction
    • Abstract: Publication date: Available online 26 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): James L. Miller, Magdalena Blaszkiewicz, Cordell Beaton, Cory P. Johnson, Stephen Waible, Amanda L. Dubois, Amanda Klemmer, Michael Kiebish, Kristy L. Townsend Consumption of diets that differ in fat type and amount, and sequestration of various fatty acids to tissues and organs, likely have effects on overall physiology and metabolic health. However, the contributions of dietary lipids to brain-adipose communication and adipose tissue function are poorly understood. We designed 6 custom diets that differed only in amount and type of dietary fat, with high or low levels of saturated fatty acids (SFA), omega-6 polyunsaturated fatty acids (n-6 PUFA), or omega-3 (n-3) PUFA. Mice fed the n-3 PUFA diet for 16 weeks displayed a striking reduction in weight gain, accompanied by smaller adipose depots and improved glucose sensitivity. Reduced body weight occurred despite lowered energy expenditure and no difference in food intake. Despite the apparent beneficial effects to whole body physiology, we have demonstrated for the first time that a peroxidized n-3 enriched diet led to lipotoxicity of white adipose tissue, as evidenced by increased fibrosis, lipofuscin, reduced anti-inflammatory markers, and loss of proper nerve supply. While healthful, n-3 fats are prone to peroxidation, and we observed peroxidated lipid metabolites in the adipose tissue of mice on these diets. Furthermore, using a lipidomics approach we have observed that brain, white adipose tissue, and brown adipose tissue accumulate lipid metabolites differently. The brain remained mostly shielded from changes in dietary fat type and amount, but differences in adipose lipid metabolites across these six diets may have affected metabolic function and brain-adipose communication, as observed in this study.
       
  • B cell activation and proliferation increase intracellular zinc levels
    • Abstract: Publication date: Available online 26 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Johanna Ollig, Veronika Kloubert, Kathryn M. Taylor, Lothar Rink Zinc ions serve as second messengers in major cellular pathways, including the regulation pathways of proliferation and their proper regulation is necessary for homeostasis and a healthy organism. Accordingly, expression of zinc transporters can be altered in various cancer cell lines and is often involved in producing elevated intracellular zinc levels. In this study, human B cells were infected with Epstein–Barr virus (EBV) to generate immortalized cells, which revealed traits of tumor cells, such as high proliferation rates and an extended lifespan. These cells showed differentially altered zinc transporter expression with ZIP7 RNA and protein expression being especially increased as well as a corresponding increased phosphorylation of ZIP7 in EBV-transformed B cells. Accordingly, free zinc levels were elevated within these cells. To prove whether the observed changes resulted from immortalization or rather high proliferation, free zinc levels in in vitro activated B cells and in freshly isolated B cells expressing the activation marker CD69 were determined. Here, comparatively increased zinc levels were found, suggesting that activation and proliferation, but not immortalization, act as crucial factors for the elevation of intracellular free zinc.Graphical abstractB cell activation and proliferation increase intracellular zinc levels.Neoplastic transformation of B cells by Epstein–Barr-Virus transformation increased the intracellular free zinc. However, this is not a part of neoplastic transformation, but a physiological response to B cell activation, since B cells activated by CD40 ligand in vitro, as well as in vivo activated B cells from peripheral blood, indicated by CD69 expression, increased intracellular free zinc. This seems to be mediated by phosphorylation of zinc transporter Zip7.Unlabelled Image
       
  • (+)-Sesamin attenuates chronic unpredictable mild stress-induced
           depressive-like behaviors and memory deficits via suppression of
           neuroinflammation
    • Abstract: Publication date: Available online 25 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Yihang Zhao, Qianxu Wang, Mengzhen Jia, Shangchen Fu, Junru Pan, Chuanqi Chu, Xiaoning Liu, Xuebo Liu, Zhigang Liu Depression is a mood disorder that is related to neuroinflammation and cognition loss. This study is aimed to determine the potential antidepressant effects of (+)-sesamin, a lignan component of sesame, in a mild stress-induced depression mouse model. CD-1 mice were treated with chronic unpredictable mild stress (CUMS) process and orally administrated with sesamin (50 mg/kg/d) for 6 weeks. Behavioral tests including forced swimming test, tail suspension test, open field test, and elevated plus maze test demonstrated that sesamin treatment inhibited CUMS-induced mice depressant-like behaviors and anxiety, without changing immobility. It was found that sesamin prevented stress-induced decease levels of 5-HT and NE in striatum and serum. Cognitive deficits were assessed using Y-maze and Morris water maze test. Sesamin treatment also prevented stressed-induced memory impairments and neuronal damages. Consistently, sesamin also enhanced synapse ultrastructure and improved expressions of PSD-95 in stressed mice hippocampus with improving neurotrophic factors expression including BDNF and NT3. Moreover, sesamin treatment significantly prevented CUMS-induced neuroinflammation by inhibiting over-activation of microglia and expressions of inflammatory mediators including iNOS, COX-2, TNF-α and IL-1β in stressed mice hippocampus and cortex. These results illustrated that sesamin markedly improved CUMS-induced depression and memory loss via inhibiting neuroinflammation, which indicate that as food component, sesamin might be also a novel potential therapeutic for depression.Graphical abstractSupplementation of sesamin, a lignan from sesame seed, improved chronic unpredictable mild stress (CUMS)-induced anxiety, depressive-like behaviors and memeory deficits. Sesamin treatment also enhanced levels of monoamine neurotransmitter and neurotrophic factor BDNF in hippocampus. The ultrastructure of synapses was rescued by sesamin with the enhancement of PSD expressions in depressed mice. Moreover, sesamin suppressed stress-induced neuroinflammation by decreasing overexpression of IBA-1 and inhibiting COX-2, iNOS, TNF-α, and IL-1β levels in mice brain.Unlabelled Image
       
  • Fucoxanthin potentiates anoikis in colon mucosa and prevents
           carcinogenesis in AOM/DSS model mice
    • Abstract: Publication date: Available online 25 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Masaru Terasaki, Tatsuya Iida, Fubuki Kikuchi, Kanae Tamura, Tetsuya Endo, Yasuhiro Kuramitsu, Takuji Tanaka, Hayato Maeda, Kazuo Miyashita, Michihiro Mutoh Fucoxanthin (Fx) and its biotransformed fucoxanthinol (FxOH) present strong anti-cancer effects in vitro and in vivo, however, the underlying mechanisms are not well known. We recently demonstrated that FxOH could induce anoikis-like cells in human colorectal cancer (CRC) cells. Thus, we developed molecular hallmarks for anoikis in vitro, and to confirm induction of such molecular hallmarks in an azoxymethane/ dextran sodium sulfate carcinogenic model by Fx ingestion. During the process of anoikis by FxOH (2.5 μmol/l) in DLD-1 cells, the cells show the characteristics of integrin β1low/−, p-FAK(Tyr397)low/− or p-Paxillin(Tyr31)low/− cells with cleaved caspase-3high, which may be useful as molecular hallmarks. Fx administration (30 mg/kg body weight) significantly suppressed the number and size of polyps compared with untreated control mice. In addition, the incidence and multiplicity of colonic lesions tended to reduce. Moreover, cells showing integrin β1low/−, p-FAK(Tyr397)low/− and p-Paxillin(Tyr31)low/− with cleaved caspase-3high in colonic crypts were significantly increased 2.2-, 4.8- and 5.2-fold by Fx administration compared with untreated control mice, respectively. Our results suggest that Fx showed a chemopreventive effect in the carcinogenic models through anoikis-like cells induction.
       
  • Dietary saturated fatty acid type impacts obesity-induced metabolic
           dysfunction and plasma Lipidomic signatures in mice
    • Abstract: Publication date: Available online 21 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Petr Žáček, Michael Bukowski, Aaron Mehus, LuAnn Johnson, Huawei Zeng, Susan Raatz, Joseph P. Idso, Matthew Picklo Saturated fatty acid (SFA) intake is associated with obesity, insulin resistance, and hepatic steatosis, but scant work examines the impact of SFA type upon these outcomes. We tested the hypothesis that an obesogenic diet prepared with medium chain SFA (MCSFA), mostly as lauric acid-derived from coconut oil, reduces obesity-induced outcomes compared to obesogenic diets prepared with increasing amounts long chain SFA (LCSFA), primarily palmitic acid. Mice were fed (16 weeks) a control, low fat diet or obesogenic diets prepared with differing content of MCSFA or LCSFA in which polyunsaturated and monounsaturated fatty acids (PUFA; MUFA) were kept constant. Inclusion of MCSFA in an obesogenic diet prevented hepatic lipid accumulation and lowered indices of insulin resistance. Obesogenic diets reduced hepatic levels of de novo lipogenesis proteins (SCD1 and FASN) but elevated the adipose levels of mRNA for the pro-inflammatory markers Mcp-1 and Tnfα. Lipidomic analysis of plasma indicated that MCSFA intake resulted in a different lipidomic signature than LCSFA intake, prevented elevation of pro-inflammatory ceramides, but elevated concentrations of some lipids associated with elevated cardiovascular disease risk. Intake of the obesogenic diets in an SFA-type dependent manner elevated plasma concentrations of several phosphatidylcholine (PC) lipids having the long chain PUFA (LCPUFA) arachidonic acid (ARA) and docosahexaenoic acid (DHA), altered phospholipid ethers, and changed the triacylglyceryl environments of these LCPUFA. Our data indicate that (1) MCSFA reduce the severity of some obesogenic co-morbidities, (2) SFA-type modulates lipidomic signatures associated with cardiovascular disease and diabetes, and (3) dietary SFA type impacts LCPUFA metabolism.
       
  • Dairy milk, regardless of fat content, protects against postprandial
           hyperglycemia-mediated impairments in vascular endothelial function in
           adults with prediabetes by limiting oxidative stress responses that reduce
           nitric oxide bioavailability
    • Abstract: Publication date: Available online 16 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Joshua D. McDonald, Eunice Mah, Priyankar Dey, Bryan D. Olmstead, Geoffrey Y. Sasaki, Frederick A. Villamena, Richard S. Bruno Postprandial hyperglycemia (PPH) transiently impairs vascular endothelial function (VEF) in an oxidative-stress-dependent manner by decreasing nitric oxide (NO•) bioavailability. Dairy milk, regardless of fat content, attenuates PPH, but whether this improves VEF by limiting oxidative stress responses that otherwise decrease NO• bioavailability is not known. We hypothesized that nonfat and full-fat dairy milk would similarly improve VEF by attenuating PPH-induced oxidative stress that otherwise decreases NO• biosynthesis and bioavailability. A randomized, crossover trial was conducted in adults with prediabetes (n=22) who ingested glucose (75 g) dissolved in 473 ml of water (GLU), or glucose with an equal volume of nonfat dairy milk (NFM) or full-fat dairy milk (FFM). Prior to and at 30-min intervals for 180 min postprandially, we assessed brachial artery flow-mediated dilation (FMD) and measured circulating biomarkers of glycemic control, oxidative stress and NO• homeostasis. AUC0–180 min for FMD and NO• metabolites was lowest in GLU but relatively greater in NFM and FFM. Compared with GLU, AUCs for glucose, malondialdehyde, F2-isoprostanes and endothelin-1 were similarly lower in dairy trials. Milk-mediated vasoprotection was accompanied by greater levels of plasma arginine and lower levels of asymmetric dimethylarginine and symmetric dimethylarginine. Postprandial insulin, lipids and tetrahydrobiopterin redox status did not differ among trials. Thus, dairy milk, regardless of its fat content, attenuates PPH-mediated impairments in VEF by limiting oxidative stress. This improves NO• bioavailability to the vascular endothelium by increasing arginine availability and limiting competitive inhibition on NO• biosynthesis by asymmetric dimethylarginine.Graphical Unlabelled Image
       
  • Quercetin inhibits proliferation of endometriosis regulating cyclin D1 and
           its target MicroRNAs In Vitro and In Vivo
    • Abstract: Publication date: Available online 16 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Sunwoo Park, Whasun Lim, Fuller W. Bazer, Kwang-Youn Whang, Gwonhwa Song Quercetin (3,3′,4′,5,7-pentahydroxyflavone) is a major dietary flavonol found in diverse fruits and vegetables such as onions, cauliflower, apple skin, lettuce, and chili peppers. In recent studies, quercetin is reported as a functional compound and shows a wide range of biological effects such as anti-oxidant, anti-inflammatory, and anti-angiogenic properties in obesity, diabetes, cardiovascular diseases, and various cancers. However, to date, the therapeutic effect of quercetin on the progression of endometriosis, which is a common gynecological disease in reproductive aged women and brings chronic pelvic pain and infertility, has not been examined in depth. Results of this study demonstrated that quercetin inhibited the proliferation and induced the cell cycle arrest in VK2/E6E7 and End1/E6E7 cells. Furthermore, it induced cell apoptosis with DNA fragmentation, loss of mitochondrial membrane potential (MMP), and reactive oxygen species (ROS) production. The effects accompanied down-regulation of ERK1/2, P38 MAPK, and AKT signaling molecules. Additionally, the administration of quercetin indicated anti-proliferative and anti-inflammatory effects on endometriosis auto-implanted mouse models. The mRNA expression of Ccnd1 significantly decreased in response to quercetin i.p. injection when compared to that in vehicle-treated mice. The knockdown of CCND1 mRNA attenuated the proliferation with sub-G0/G1 cell cycle arrest and increased the apoptosis of VK2/E6E7 and End1/E6E7 cells. Furthermore, the treatment of quercetin induced miR-503-5p, miR-1283, miR-3714, and miR-6867-5p related to CCND1 in both cell lines and also stimulated miR-503-5p and miR-546 expression in the mouse model. Hence, quercetin may potentially act as a natural therapeutic to reduce and treat human endometriosis.
       
  • Fisher discriminant analysis for classification of autism Spectrum
           disorders based on folate-related metabolism markers
    • Abstract: Publication date: Available online 13 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Mingyang Zou, Caihong Sun, Shuang Liang, Yi Sun, Dexin Li, Ling Li, Lili Fan, Lijie Wu, Wei Xia Autism spectrum disorders (ASD) are an increasing prevalence of neurodevelopmental disorders, but lack reliable biomarkers for early diagnosis. The present study investigated 13 serological metabolites and two genetic variants related to folate metabolism in a total of 89 ASD cases and 89 matched controls. Fisher discriminant analysis was used to establish the classification model to recognize ASD cases and controls. Ten metabolites were significantly different between the groups, of which six metabolites were used as predictors to determine the discriminant prediction model: vitamin B12, 5-methylene-tetrahydrofolate, methonine, the ratio of S-adenosylmethionine/S-adenosylhomocysteine, methionine synthase and transcobalamin II. The model had statistical significance (lambda=0.520, χ2=113.103, df=6, P
       
  • Dietary polyphenols and their roles in fat browning
    • Abstract: Publication date: Available online 13 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Allwin Jennifa Silvester, Kanikkai Raja Aseer, Jong Won Yun Discovery of the presence of brown adipose tissue (BAT) in new-born babies and adult humans, especially constitutively active brown fat or inducible beige fat, has led to investigation of strategies employing BAT aimed at the development of novel therapeutic avenues for combating obesity and diabetes. Such anti-obesity therapeutic tools include pharmaceutical and nutraceutical dietary polyphenols. Although there have been emerging notable advances in knowledge of and an increased amount of research related to brown and beige adipocyte developmental lineages and transcriptional regulators, current knowledge regarding whether and how food factors and environmental modifiers of BAT influence thermogenesis have not been extensively investigated. Therefore, in this review, we summarized recent updates on the exploration of dietary polyphenols while paying attention to activation of BAT and thermogenesis. Specifically, we summarized findings pertaining to BAT metabolism, white adipose tissue (WAT) browning and thermogenic function of polyphenols (e.g., flavan-3-ols, green tea catechins, resveratrol, capsaicin/capsinoids, curcumin, thymol, chrysin, quercetin, and berberine) that may foster a relatively safe and effective therapeutic option to improve metabolic health. We also deciphered the underlying proposed mechanisms through which these dietary polyphenols facilitate BAT activity and WAT browning. Characterization of thermogenic dietary factors may offer novel insight enabling revision of nutritional intervention strategies aimed at obesity and diabetes prevention and management. Moreover, identification of polyphenolic dietary factors among plant-derived natural compounds may provide information that facilitates nutritional intervention strategies against obesity, diabetes and metabolic syndrome.
       
  • Epigenetic regulation of hepatic Dpp4 expression in response to
           dietary protein
    • Abstract: Publication date: Available online 13 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Sophie Saussenthaler, Meriem Ouni, Christian Baumeier, Kristin Schwerbel, Pascal Gottmann, Sabrina Christmann, Thomas Laeger, Annette Schürmann Dipeptidyl peptidase 4 (DPP4) is known to be elevated in metabolic disturbances such as obesity, type 2 diabetes and fatty liver disease. Lowering DPP4 concentration by pharmacological inhibition improves glucose homeostasis and exhibits beneficial effects to reduce hepatic fat content. As factors regulating the endogenous expression of Dpp4 are unknown, the aim of this study was to examine whether the Dpp4 expression is epigenetically regulated in response to dietary components. Primary hepatocytes were treated with different macronutrients and Dpp4 mRNA levels and DPP4 activity were evaluated. Moreover, dietary low protein intervention was conducted in New Zealand Obese (NZO) mice and subsequently effects on Dpp4 expression, methylation as well as plasma concentration and activity were determined. Our results indicate that Dpp4 mRNA expression is mediated by DNA methylation in several tissues. We therefore consider the Dpp4 southern shore as tissue differentially methylated region (tDMR). Amino acids increased Dpp4 expression in primary hepatocytes, whereas glucose and fatty acids were without effect. Dietary protein restriction in NZO mice increased Dpp4 DNA methylation in liver leading to diminished Dpp4 expression and consequently to lowered plasma DPP4 activity. We conclude that protein restriction in the adolescent and adult states is a sufficient strategy to reduce DPP4 which in turn contributes to improve glucose homeostasis.
       
  • Comparative effects of dietary n-3 docosapentaenoic acid (DPA), DHA and
           EPA on plasma lipid parameters, oxidative status and fatty acid tissue
           composition
    • Abstract: Publication date: Available online 12 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Gaetan Drouin, Daniel Catheline, Etienne Guillocheau, Pierre Gueret, Charlotte Baudry, Pascale Le Ruyet, Vincent Rioux, Philippe Legrand The specific and shared physiologic and metabolic effects of eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) and even more of n-3 docosapentaenoic acid (DPA) are poorly known. We investigated the physiological effects and the overall fatty acid tissue composition of a nutritional supplementation of DPA, compared both to EPA and DHA in healthy adult rats. Rats (n=32) were fed with semi-synthetic diets supplemented or not with 1% of total lipids as EPA, DPA or DHA in ethyl esters form from weaning for 6 weeks. Fatty acid tissue composition was determined by GCMS and blood assays were performed. The DPA supplementation was the only one that led to a decrease in plasma triglycerides, total cholesterol, non-HDL-cholesterol, cholesterol esters and total cholesterol/HDL-cholesterol ratio compared to the non-supplemented control group. The three supplemented groups had increased plasma total antioxidant status and superoxide dismutase activity. In all supplemented groups, the n-3 PUFA level increased in all studied tissues (liver, heart, lung, spleen, kidney, red blood cells, splenocytes, peripheral mononucleated cells), except in the brain. We showed that the DPA supplementation affected the overall fatty acid composition and increased DPA, EPA and DHA tissue contents in a similar way than with EPA. However, liver and heart DHA contents increased in DPA-fed rats at the same levels than in DHA-fed rats. Moreover, a large part of DPA seemed to be retroconverted into EPA in the liver (38.5%) and in the kidney (68.6%). In addition, the digestibility of DPA was lower than that of DHA and EPA.Graphical Unlabelled Image
       
  • Ferulic acid reverses P-glycoprotein mediated multidrug resistance via
           inhibition of PI3K/Akt/NF-κB signaling pathway
    • Abstract: Publication date: Available online 12 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Ganesan Muthusamy, Srithar Gunaseelan, Nagarajan Rajendra Prasad In this study, the modulatory effect of ferulic acid on P-glycoprotein (P-gp) mediated multidrug resistance (MDR) was examined in KB ChR8–5 resistant cells and drug resistant tumor xenografts. We observed that ferulic acid enhanced the cytotoxicity of doxorubicin and vincristine in the P-gp overexpressing KB ChR8–5 cells. Further, ferulic acid enhances the doxorubicin induced γH2AX foci formation and synergistically augment doxorubicin-induced apoptotic signaling in the drug resistant cells. It has also been noticed that NF-κB nuclear translocation was suppressed by ferulic acid and this response might be associated with the modulation of phosphatidyinositol 3-kinase (PI3K)/Akt/signaling pathway. We also found that ferulic acid and doxorubicin combination reduced the size of KB ChR8–5 tumor xenograft by three fold as compared to doxorubicin alone treated group. Thus, ferulic acid contributes to the reversal of the MDR through suppression of P-gp expression via the inhibition of PI3K/Akt/ NF-κB signaling pathway.
       
  • A higher flavonoid intake is associated with less likelihood of
           non-alcoholic fatty liver disease: Results from a multi-ethnics study
    • Abstract: Publication date: Available online 11 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Mohsen Mazidi, Niki Katsiki, Maciej Banach Limited information exists on the impact of flavonoid intake on non-alcoholic fatty liver disease (NAFLD). We evaluated the link between flavonoid intake, liver tests and risk of NAFLD in a randomly selected sample of US adults (from the National Health and Nutrition Examination Survey, NHANES, 2005–2010). Of the 17,685 participants, 46.9% were men and 45.4% had NAFLD. NAFLD patients had a significantly lower mean flavonoid intake than healthy individuals (111.3±3.6 vs 201.3±2.3 mg/d, respectively; P
       
  • A comprehensive evaluation of OMEGA-3 fatty acid supplementation in cystic
           fibrosis patients using LIPIDOMICS
    • Abstract: Publication date: Available online 11 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Óscar Pastor, Paula Guzmán-Lafuente, Jorge Serna, Marta Muñoz-Hernández, Alejandro López-Neyra, Patricia García-Rozas, David García-Seisdedos, Alberto Alcázar, Miguel A. Lasunción, Rebeca Busto, Adelaida Lamas The evaluation of the benefits of omega-3 fatty acid supplementation in humans requires the identification and characterization of suitable biomarkers of its incorporation in the body. The reference method for the evaluation of omega-3, gas chromatography, is difficult to apply in clinical practice because of its low throughput and does not provide information about the incorporation of specific fatty acids in lipid species and the potential effects of supplementation on lipid classes. We used a quantitative lipidomic approach to follow the incorporation of omega-3 fatty acids into plasma lipids in cystic fibrosis patients (n=50) from a randomized controlled clinical trial after the supplementation of seaweed oil enriched with docosahexaenoic acid (DHA). Lipidomic analysis accurately determined the distribution of fatty acids in different lipid classes after omega-3 supplementation and the performance in determining the compliance to supplementation was similar to that of gas chromatography coupled to mass spectrometry. Twelve-months after fatty-acid supplementation, DHA was predominantly incorporated into highly unsaturated cholesteryl esters (110.9±16.2 vs. 278.6±32.6 μM, mean ± SEM), phosphatidylcholine (142.4±11.9 vs. 272.9±21.4 μM) and to a lesser extent into phosphatidylethanolamine (9.4±0.8 vs. 15.5±1.5 μM) and triglycerides (0.4±0.04 vs. 1.1±0.12 μM). In addition, a technique was developed for the fast measurement of the DHA/AA ratio to simplify the follow-up of nutritional intervention with DHA-enriched foods. We conclude that lipidomics is a suitable approach for monitoring the incorporation of omega-3 fatty acids in nutritional studies.
       
  • Curcumin, but not curcumin-glucuronide, inhibits Smad-signaling in
           TGFβ-dependent bone metastatic breast cancer cells and is enriched in
           bone compared to other tissues
    • Abstract: Publication date: Available online 11 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Andrew G Kunihiro, Julia A Brickey, Jennifer B Frye, Paula B Luis, Claus Schneider, Janet L Funk Breast cancer (BCa) bone metastases (BMETs) drive osteolysis via a feed-forward loop involving tumoral secretion of osteolytic factors (e.g., PTHrP) induced by bone matrix-derived growth factors (e.g., TGFβ). In prior experiments, turmeric-derived curcumin inhibited in vivo BMET progression and in vitro TGFβ/Smad-signaling in a TGFβ-stimulated PTHrP-dependent human xenograft BCa BMET model (MDA-SA cells). However, it is unclear whether curcumin or curcumin-glucuronide mediates in vivo protection since curcumin-glucuronide is the primary circulating metabolite in rodents and in humans. Thus, effects of curcumin vs. curcumin-glucuronide on Smad-dependent TGFβ signaling were compared in a series of BCa cell lines forming TGFβ-dependent BMET in murine models, and tissue-specific metabolism of curcumin in mice was examined by LC–MS. While curcumin inhibited TGFβ-receptor-mediated Smad2/3 phosphorylation in all BCa cells studied (human MDA-SA, MDA-1833, MDA-2287, and murine 4 T1 cells), curcumin-glucuronide did not. Similarly, curcumin, but not curcumin-glucuronide, blocked TGFβ-stimulated secretion of PTHrP from MDA-SA and 4 T1 cells. Because the predominant serum metabolite, curcumin-glucuronide, lacked bioactivity, we examined tissue-specific metabolism of curcumin in mice. Compared to serum and other organs, free curcumin (both absolute and percentage of total) was significantly increased in bone, which was also a rich source of enzymatic deglucuronidation activity. Thus, curcumin, and not curcumin-glucuronide, appears to inhibit bone-tropic BCa cell TGFβ-signaling and undergo site specific activation (deconjugation) within the bone microenvironment. These findings suggest that circulating curcumin-glucuronide may act as a pro-drug that preferentially targets bone, a process that may contribute to the bone-protective effects of curcumin and other highly glucuronidated dietary polyphenols.
       
  • A low-protein diet eliminates the circadian rhythm of serum insulin and
           hepatic lipid metabolism in mice
    • Abstract: Publication date: Available online 11 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Shin-Ichi Yokota, Kaai Nakamura, Midori Ando, Atsushi Haraguchi, Kanako Omori, Shigenobu Shibata Insulin is a key molecule that synchronizes peripheral clocks, such as that in the liver. Although we previously reported that mice fed a low-protein diet showed altered expression of lipid-related genes in the liver and induction of hepatic steatosis, it is unknown whether a low-protein diet impairs insulin secretion and modifies the hepatic circadian rhythm. Therefore, we investigated the effects of the intake of a low-protein diet on the circadian rhythm of insulin secretion and hepatic lipid metabolism in mice. Under 12-h light/12-h dark cycle, mice fed a low-protein diet for 7 days displayed enhanced food intake at the end of the light phase, although central and peripheral PER2 expression rhythm was maintained. Serum insulin levels in mice fed a low-protein diet remained low during the day and the insulin secretion in OGTT was also markedly lower than in normal mice. In low-protein diet fed mice, hepatic TG accumulation was observed during the nighttime, with relatively high levels of ACC1 mRNA and total ACC proteins. Although there were no differences in the activity rhythm of hepatic mTOR between mice fed a normal or low-protein diet, hepatic IRS-2 expression in mice fed a low-protein diet remained low during the day, with no increase at the beginning of the light period. These results suggested that the low-protein diet eliminated the circadian rhythm of serum insulin and hepatic lipid metabolism in mice, providing insights into our understanding of the mechanisms of hepatic disorders of lipid metabolism.
       
  • Gut microbiome and type 2 diabetes: Where we are and where to go'
    • Abstract: Publication date: Available online 11 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Sapna Sharma, Prabhanshu Tripathi Type 2 diabetes mellitus (T2D) is a highly prevalent metabolic disorder characterized by an imbalance in blood glucose level, altered lipid profile and high blood pressure. Genetic constituents, high fat and high-energy dietary habits and a sedentary lifestyle are three major factors that contribute to high risk of T2D. Several studies have reported gut microbiome dysbiosis as a factor in rapid progression of insulin resistance in T2D that accounts about 90% of all diabetes cases worldwide. The gut microbiome dysbiosis may reshape intestinal barrier functions and host metabolic and signaling pathways, which are directly or indirectly related to the insulin resistance in T2D. Thousands of the metabolites derived from microbes interact with the epithelial, hepatic and cardiac cell receptors that modulate host physiology. Xenobiotics including dietary components, antibiotics and non-steroidal anti-inflammatory drugs (NSAIDS) strongly affect the gut microbial composition and can promote dysbiosis. Any change in the gut microbiota can shift the host metabolism towards increased energy harvest during diabetes and obesity. However, the exact mechanisms behind the dynamics of gut microbes and their impact on host metabolism at the molecular level are yet to be deciphered. We reviewed the published literature for better understanding of the dynamics of gut microbiota, factors that potentially induce gut microbiome dysbiosis and their relation to the progression of T2D. Special emphasis was also given to understand the gut microbiome induced breaching of intestinal barriers and/or tight junctions and their relation to insulin resistance.
       
  • Omega-3 polyunsaturated fatty acids attenuate inflammatory activation and
           alter differentiation in human adipocytes
    • Abstract: Publication date: Available online 11 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Jane F Ferguson, Kailey Roberts, Cristina Borcea, Holly M Smith, Yasmeen Midgette, Rachana Shah BackgroundOmega-3 polyunsaturated fatty acids, specifically the fish oil derived eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have been proposed as inflammation resolving agents via their effects on adipose tissue.ObjectiveWe proposed to determine the effects of EPA and DHA on human adipocyte differentiation and inflammatory activation in vitro.MethodsPrimary human subcutaneous adipocytes from lean and obese subjects were treated with 100 μM EPA and/or DHA throughout differentiation (differentiation studies) or for 72 h post-differentiation (inflammatory studies). THP-1 monocytes were added to adipocyte wells for co-culture experiments. Subcutaneous and visceral adipose explants from obese subjects were treated for 72 h with EPA and DHA. Oil-Red-O staining was performed on live cells. Cells were collected for mRNA analysis by qPCR and media collected for protein quantification by ELISA.ResultsIncubation with EPA and/or DHA attenuated inflammatory response to LPS and monocyte co-culture with reduction in post-LPS mRNA expression and protein levels of IL6, CCL2, and CX3CL1. Expression of inflammatory genes was also reduced in the endogenous inflammatory response in obese adipose. Both DHA and EPA reduced lipid droplet formation and lipogenic gene expression without alteration in expression of adipogenic genes or adiponectin secretion.ConclusionsEPA and DHA attenuate inflammatory activation of in vitro human adipocytes and reduce lipogenesis.Graphical abstractUnlabelled Image
       
  • Folic acid inhibits colorectal cancer cell migration
    • Abstract: Publication date: Available online 6 October 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Pei-Ching Ting, Woan-Ruoh Lee, Yen-Nien Huo, Sung-Po Hsu, Wen-Sen Lee We recently showed that folic acid (FA) could decrease the proliferation rate of colorectal cancer cells in vitro and reduce the volume of COLO-205 tumor in vivo. Since cancer cell proliferation and migration are two major events during cancer development, we further examined whether FA could also affect the migration of colorectal cancer cells. Transwell invasion assays demonstrated that FA reduced the invasion ability of colorectal cancer cell lines, COLO-205, LoVo and HT-29. Using COLO-205 as a cell model, we further delineated the molecular mechanism underlying FA-inhibited colorectal cancer cell invasion. Western blot analyses showed that FA (10 μM) activated cSrc, ERK1/2, NFκB, and p27 at serine 10 (Ser10), and up-regulated p53, p27, and KIS protein. Subcellular fractionation illustrated that FA treatment increased cytosolic translocation of p27, formation of the p27-RhoA complex, and RhoA degradation. The FA-induced migration inhibition in COLO-205 was abolished by blockade of the cSrc or ERK1/2 activity, knockdown of p27 or KIS using the siRNA technique, or over-expression of a constitutive active RhoA cDNA. Our results suggest that FA up-regulated p27 through increasing the cSrc/ERK1/2/NFκB/p53-mediated pathway. In the nucleus, FA up-regulated KIS, which in turn increased p27 phosphorylation at serine 10 (Ser10), subsequently resulting in cytosolic translocation of p27 and forming the p27-RhoA complex, thereby causing RhoA degradation, and eventually inhibited COLO-205 cell migration. Together with our previous findings suggest that FA reduced colorectal cancer development through inhibiting colorectal cancer cell proliferation and migration.Graphical abstractUnlabelled Image
       
  • Anti-inflammatory effects of preserved egg white
    • Abstract: Publication date: Available online 27 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Mengya Zhang, Yan Zhao, Yao Yao, Mingsheng Xu, Huaying Du, Na Wu, Yonggang Tu Simulated gastrointestinal digestion of preserved egg white (SGD-PEW) exerts anti-inflammatory effects on Caco-2 cells and a mouse model of DSS-induced colitis. Here, we aimed to separate peptides derived from SGD-PEW and evaluate their anti-inflammatory effects using an in vitro inflammatory model. Six peptides were isolated and identified. DEDTQAMPFR (DR-10), DEDTQAMPF (DF-9), MLGATSL (ML-7) and MSYSAGF (MF-7) significantly inhibited IL-8 secretion and markedly decreased gene expression, including TNF-α, IL-8, IL-6, IL-1β and IL-12 and promoted IL-10 gene expression in Caco-2 cells. DR-10, DF-9, ML-7 and MF-7 significantly inhibited the phosphorylation of JNK. In the meantime, DR-10 and DF-9 significantly reduced the phosphorylation of IκB and p38. These results indicated that ML-7 and MF-7 exerted their anti-inflammatory activity through the MAPK signaling pathway in TNF-α-induced Caco-2 cells. Whereas, DR-10 and DF-9 inhibited the NF-κB and MAPK signaling pathways. The results suggested that DR-10, DF-9, ML -7 and MF-7 derived from SGD-PEW may be a new type of prophylactic food for the treatment of inflammation.
       
  • Association of serum bilirubin in newborns affected by jaundice with gut
           microbiota dysbiosis
    • Abstract: Publication date: Available online 26 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Shaoming Zhou, Zhangxing Wang, Fusheng He, Huixian Qiu, Yan Wang, Huihui Wang, Jianli Zhou, Jiaxiu Zhou, Guoqiang Cheng, Wenhao Zhou, Ruihuan Xu, Mingbang Wang Background & aimsBreast milk jaundice (BMJ) is common and benign, but neonatal cholestasis (NC) is rare and not benign, so early differentiation between NC and non-NC jaundice is important and may facilitate diagnosis and treatment. Gut microbiota plays an important role in enterohepatic circulation, which in turn plays an important role in the secretion of bilirubin. We aimed to determine the composition of gut microbiota in patients with NC and BMJ, and to identify the gut microbiota composition associated with NC and BMJ.MethodsData on age, gender, delivery, feeding mode, serum total bilirubin, direct bilirubin, and liver function were collected for NC patients, BMJ patients and healthy controls,respectively. Shotgun metagenomic sequencing and metagenome-wide association were performed.ResultsForty NC patients, 16 patients affected by BMJ, and 14 healthy controls (CON) without jaundice were enrolled. A significant increase in species richness, especially Bacteroides, was found in NC patients. The abundances of potentially pathogenic species and KEGG orthologies (KOs) of virulence factor genes were positively correlated with serum bilirubin level. The abundances of nine species of Bifidobacterium and three KOs of galactose metabolism were significantly decreased in the jaundice group (NC and BMJ) and were negatively correlated with serum bilirubin level.ConclusionsThe gut microbiota in NC patients is characterized by a significant increase in species richness, possibly due to the proliferation of potentially pathogenic species.Additionally, the gut microbiota in jaundice patients is characterized by a decreased abundance of Bifidobacterium. Decreased Bifidobacterium has been associated with elevated bilirubin and abnormal gut microbiota galactose metabolic pathway. Further, ten bacteria species were identified as potential biomarker of jaundice.Key pointsQuestion Is there any alteration of gut microbiotain neonatal cholestasis patients' Does gut microbiota have any involvement in the occurrence of neonatal cholestasis or breast milk jaundice'Findings The alteration of gut microbiota in neonatal cholestasis patients mainly manifested as a significant increase in species richness and an increased abundance of potentially pathogenic species, while the main manifestation in jaundice patients was a significant decrease in Bifidobacterium which may be involved in the metabolism of bilirubin through the galactose metabolic pathway.Meaning The results suggest that an imbalance of gut microbiota exist in neonatal cholestasis and breast milk jaundice patients, primarily in the form of a substantial reduction in the abundance of Bifidobacterium, suggesting the possibility of intervention treatment for neonatal cholestasis and breast milk jaundice by supplementing probiotics.
       
  • Dietary EPA and DHA prevent changes in white adipose tissue omega-3 PUFA
           and oxylipin content associated with a Fads2 deficiency
    • Abstract: Publication date: Available online 26 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Ousseynou Sarr, George W. Payne, Barbora Hucik, Salma Abdelmagid, Manabu T Nakamura, David WL Ma, David M. Mutch Fatty acid desaturase 2 (Fads2) encodes the delta-6 desaturase (D6D) enzyme, which is rate-limiting for the endogenous production of omega-3 long-chain polyunsaturated fatty acids (LC-PUFA). Numerous studies have reported the cardiometabolic health benefits of omega-3 LC-PUFA. Humans carrying genetic variants in the FADS2 gene have reduced levels of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), as well as their derived oxylipins, in blood, erythrocytes and white adipose tissue (WAT). Similar findings have been reported in whole-body Fads2−/− mice fed a diet deficient in omega-3 LC-PUFA. The objective of this study was to determine if a diet containing EPA and DHA would prevent the deficiencies in WAT lipid profiles seen in Fads2−/− mice fed a diet containing only ALA. Male C57BL/6 J Fads2−/− and wild type (WT) mice were fed a low fat (7% w/w) diet for 9 weeks containing either flaxseed oil + ARASCO (FD, containing~53% ALA) or menhaden oil (MD, containing~14% EPA and 10% DHA). Fads2−/− mice fed an ALA-enriched diet had reduced body weight, little-to-no omega-3 LC-PUFA and a near complete loss of all omega-3 derived oxylipins in both epididymal and inguinal WAT (P
       
  • Dairy Milk proteins attenuate hyperglycemia-induced impairments in
           vascular endothelial function in adults with Prediabetes by limiting
           increases in Glycemia and oxidative stress that reduce nitric oxide
           bioavailability
    • Abstract: Publication date: Available online 25 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Joshua D. McDonald, Eunice Mah, Chureeporn Chitchumroonchokchai, Priyankar Dey, Allison N. Labyk, Frederick A. Villamena, Jeff S. Volek, Richard S. Bruno Postprandial hyperglycemia (PPH) transiently impairs vascular endothelial function (VEF) in an oxidative stress-dependent manner by decreasing nitric oxide (NO•) bioavailability. Dairy milk and its proteins attenuate PPH, but whether this improves VEF is unknown. We hypothesized that dairy milk, mediated by its whey and/or casein proteins, improves VEF by attenuating PPH-induced oxidative stress that otherwise decreases NO• bioavailability. A randomized, cross-over trial was conducted in adults with prediabetes (n=23) who ingested glucose (75 g, GLU) alone or with 473 mL of non-fat dairy milk (MILK) or isonitrogenous (16.5 g) amounts of whey (WHEY) or casein (CASEIN) in 473 mL of water. Prior to and at 30 min intervals for 180 min postprandially, we assessed brachial artery flow-mediated dilation (FMD) and measured biomarkers of glycemic control, oxidative stress, and NO• homeostasis. FMDAUC decreased to the greatest extent during GLU, which was similarly improved in dairy trials. Compared with GLU, AUCs for glucose, malondialdehyde, F2-isoprostanes, methylglyoxal, and endothelin-1 were similarly lower in dairy trials. Plasma arginine and NO• metabolites were greater but methylated arginine metabolites were lower in dairy trials compared with GLU. Postprandial insulin, lipids, and tetrahydrobiopterin redox status did not differ among trials. Thus, dairy milk, mediated by its whey and casein proteins, attenuates PPH-mediated impairments in VEF by limiting oxidative stress. This improves NO• bioavailability to the vascular endothelium by increasing arginine availability and limiting competitive inhibition on NO• biosynthesis by asymmetric dimethylarginine. These findings support observational studies that dairy milk lowers cardiovascular disease risk.
       
  • Allicin induces beige-like adipocytes via KLF15 signal cascade
    • Abstract: Publication date: Available online 23 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Chung Gi Lee, Dong Kwon Rhee, Byung Oh Kim, Sung Hee Um, Suhkneung Pyo Under specific conditions, white adipose tissue (WAT) depots are readily converted to a brown-like state, which is associated with weight loss. However, whether diet-derived factors directly induce browning of white adipocytes has yet to be established. Thus, we investigated the effects of allicin, one of the major components of garlic, on brown-like adipocyte formation in inguinal WAT (iWAT), and prevention of obesity and related complications in animal models. Allicin significantly increased mRNA and/or protein expression of brown adipocyte markers including uncoupling protein 1 (UCP1) in differentiated mouse embryonic fibroblast cell line 3 T3-L1 and differentiated iWAT stromal vascular cells (SVC), suggesting that allicin induced brown-like adipocyte formation in vitro. Concomitantly, allicin markedly enhanced the protein expression of KLF-15 and its interaction with UCP-1 promoter region. Such changes were absent in cells lacking KLF-15, suggesting the critical role of KLF15 in allicin action. Allicin also induced brown-like adipogenesis in vivo along with the appearance of multilocular adipocytes, increased UCP1 expression and increased lipid oxidation. In summary, our data suggest that allicin potentially prevents obesity and associated metabolic disorders such as type 2 diabetes mellitus by enhancing the expression of brown adipocyte-specific genes, including UCP-1, through KLF15 signal cascade.
       
  • Reduction of high-fat diet-induced liver pro-inflammatory state by
           eicosapentaenoic acid plus hydroxytyrosol supplementation: Involvement of
           resolvins RvE1/2 and RvD1/2
    • Abstract: Publication date: Available online 21 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): F. Echeverría, R. Valenzuela, A. Espinosa, A. Bustamante, D. Álvarez, D. Gonzalez-Mañan, M. Ortiz, S.A. Soto-Alarcon, L.A. Videla High-fat diet (HFD) fed mice show obesity with development of liver steatosis and a pro-inflammatory state without establishing an inflammatory reaction. The aim of this work was to assess the hypothesis that eicosapentaenoic acid (EPA) plus hydroxytyrosol (HT) supplementation prevents the inflammatory reaction through enhancement in the hepatic resolvin content in HFD-fed mice. Male C57BL/6 J mice were fed a HFD or a control diet and supplemented with EPA (50 mg/kg/day) and HT (5 mg/kg/day) or their respective vehicles for 12 weeks. Measurements include liver levels of EPA, DHA and palmitate (gas chromatography), liver resolvins and triglyceride (TG) and serum aspartate transaminase (AST) (specific kits) and hepatic and serum inflammatory markers (qPCR and ELISA). Compared to CD, HFD induced body weight gain, liver steatosis and TG accumulation, with upregulation of pro-inflammatory markers in the absence of histological inflammation or serum AST changes; these results were accompanied by higher hepatic levels of resolvins RvE1, RvE2, RvD1 and RvD2, with decreases in EPA and DHA contents. EPA + HT supplementation in HFD feeding synergistically reduced the steatosis score over individual treatments, increased the hepatic levels of EPA, DHA and resolvins, with attenuation of pro-inflammatory markers. Lack of progression of HFD-induced pro-inflammatory state into overt inflammation is associated with resolvin upregulation, which is further increased by EPA + HT supplementation eliciting steatosis attenuation. These findings point to the importance of combined protocols in hepatoprotection due to the involvement of crosstalk mechanisms, which increase effectiveness and diminish dosages avoiding undesirable effects.Graphical abstractUnlabelled Image
       
  • Retroconversion of dietary trans-vaccenic (trans-C18:1 n-7) acid to
           trans-palmitoleic acid (trans-C16:1 n-7): Proof of concept and
           quantification in both cultured rat hepatocytes and pregnant rats
    • Abstract: Publication date: Available online 21 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Etienne Guillocheau, Cyrielle Garcia, Gaëtan Drouin, Léo Richard, Daniel Catheline, Philippe Legrand, Vincent Rioux Trans-palmitoleic acid (trans-C16:1 n-7, or trans Δ9-C16:1, TPA) is believed to improve several metabolic parameters according to epidemiological data. TPA may mainly come from direct intakes: however, data is inconsistent due to its very low amount in foods. Instead, TPA might arise from dietary trans-vaccenic acid (trans-C18:1 n-7, TVA), which is more abundant in foods. TVA chain-shortening would be involved, but formal proof of concept is still lacking to our knowledge. Therefore, the present study aimed at providing in vitro and in vivo evidence of TVA retroconversion to TPA. First, fresh rat hepatocytes cultured with growing doses of TVA were able to synthesise growing amounts of TPA, according to a 10%-conversion rate. In addition, TPA was found in secreted triacylglycerols (TAG). Inhibiting peroxisomal β-oxidation significantly reduced TPA synthesis, whereas no effect was observed when mitochondrial β-oxidation was blocked. Second, pregnant female rats fed a TVA-supplemented diet free of TPA did metabolise dietary TVA, leading to detectable amounts of TPA in the liver. Apart from the brain, TPA was also found in all analysed tissues, including the mammary gland. Hepatic peroxisomal β-oxidation of dietary TVA, combined with exportation of TPA under VLDL-TAG may explain amounts of TPA in other tissues. In conclusion, dietary TVA undergoes peroxisomal β-oxydation and yields TPA. Thus, not only TPA circulating levels in humans can be explained by dietary TPA itself, but dietary TVA is also of importance.Graphical abstractUnlabelled Image
       
  • Broccoli consumption affects the human gastrointestinal microbiota
    • Abstract: Publication date: Available online 21 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Jennifer L. Kaczmarek, Xiaoji Liu, Craig S. Charron, Janet A. Novotny, Elizabeth H. Jeffery, Harold E. Seifried, Sharon A. Ross, Michael J. Miller, Kelly S. Swanson, Hannah D. Holscher The human gastrointestinal microbiota is increasingly linked to health outcomes; however, our understanding of how specific foods alter the microbiota is limited. Cruciferous vegetables such as broccoli are a good source of dietary fiber and phytonutrients, including glucosinolates, which can be metabolized by gastrointestinal microbes. This study aimed to determine the impact of broccoli consumption on the gastrointestinal microbiota of healthy adults. A controlled feeding, randomized, crossover study consisting of two 18-day treatment periods separated by a 24-day washout was conducted in healthy adults (n=18). Participants were fed at weight maintenance with the intervention period diet including 200 g of cooked broccoli and 20 g of raw daikon radish per day. Fecal samples were collected at baseline and at the end of each treatment period for microbial analysis. Beta diversity analysis indicated that bacterial communities were impacted by treatment (P=.03). Broccoli consumption decreased the relative abundance of Firmicutes by 9% compared to controls (P=.05), increased the relative abundance of Bacteroidetes by 10% compared to controls (P=.03), and increased Bacteroides by 8% relative to controls (P=.02). Furthermore, the effects were strongest among participants with BMI
       
  • Cherry consumption out of season alters lipid and glucose homeostasis in
           normoweight and cafeteria-fed obese Fischer 344 rats
    • Abstract: Publication date: Available online 21 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Roger Mariné-Casadó, Cristina Domenech-Coca, Josep Maria del Bas, Cinta Bladé, Antoni Caimari, Lluís Arola The xenohormesis theory postulates that animals, through the consumption of chemical cues, mainly polyphenols, synthetized by plants, are able to favorably adapt to changing environmental conditions. We hypothesized that the intake of fruits with a seasonally distinctive phenotype (in terms of bioactive compounds) produced a metabolic response that depends on mammals' circannual rhythms and that fruit intake out of season can lead to a disruption in characteristic seasonal metabolism. Fischer 344 rats were chronically exposed to short (L6, 6 h light/day) and long (L18, 18 h light/day) photoperiods in order to simulate autumn and spring seasons, respectively, and were fed either a standard diet (STD) or an obesogenic cafeteria diet (CAF) and orally treated with either vehicle or 100 mg.kg-1.day-1 of lyophilized sweet cherry (Prunus avium L.), a fruit consumed during long-day seasons. Cherry consumption exerted a marked photoperiod-dependent effect, inducing more changes when it was consumed out of season, which was apparent in the following observations: 1) in L6 STD-fed rats, a downregulation of the phosphorylated (p) levels of the downstream postreceptor target of insulin Akt2 in the soleus muscle and an enhancement of fatty acid transport and β-oxidation-related pathways, which was evidenced by increased Had gene expression (soleus) and pAMPK levels (soleus and gastrocnemius); 2) an increase in whole-body fat oxidation and circulating levels of glucose and insulin in L6-CAF-fed obese rats. Although the pathophysiological significance of these results requires further research, our findings could contribute to highlighting the importance of the consumption of seasonal fruits to maintain optimal health.
       
  • Zinc deficiency drives Th17 polarization and promotes loss of Treg
           cell-function
    • Abstract: Publication date: Available online 21 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Leonie Kulik, Martina Maywald, Veronika Kloubert, Inga Wessels, Lothar Rink A high number of illnesses and disorders are connected to zinc deficiency. Equally, T cell polarization and a balance between different T helper (Th) cell subsets is essential. Therefore, in this study the influence of zinc deficiency on T cell polarization and on respective signaling pathways was investigated. We uncovered a significantly increased number of regulatory T cells (Treg) and Th17 cells in expanded T cells during zinc deficiency after three days of combined treatment with IL-2 and TGF-β1 (Treg) or IL-6 and TGF-β1 (Th17). No difference in Th1 and Th2 cell polarization between zinc deficient and zinc adequate status was prominent. On the molecular level, Smad signaling was significantly enhanced by stimulation with TGF-β1/IL-6 during zinc deficiency compared to adequate zinc condition. This represents an explanation for the elevated Th17 cell numbers associated with autoimmune disease especially during zinc deficiency.Moreover, Treg cell numbers are increased during zinc deficiency as well. However, those cells might be non-functional, since a lower expression of miR-146a was uncovered compared to normal zinc concentrations.In summary, an adequate zinc homeostasis is fundamental to slow down or propably stop the progression of autoimmune diseases and infections. Therefore, supplementing zinc might be a therapeutic approach to dampen autoimmune diseases connected to Th17 cells.Graphical abstractUnlabelled Image
       
  • Plant microRNAs in human sera are likely contaminants
    • Abstract: Publication date: Available online 5 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Bastian Fromm, Wenjing Kang, Carlos Rovira, Alfonso Cayota, Kenneth Witwer, Marc R. Friedländer, Juan Pablo Tosar
       
  • Reply to Fromm et al.
    • Abstract: Publication date: Available online 5 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Dongxia Hou, Zhen Zhou, Xi Chen, Xiaohong Jiang, Ke Zen, Chen-Yu Zhang
       
  • Alterations to the microbiota-colon-brain axis in high-fat diet-induced
           obese mice compared to diet-resistant mice
    • Abstract: Publication date: Available online 1 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Peng Zhang, Yinghua Yu, Yanfang Qin, Yuan Zhou, Renxian Tang, Qingling Wang, Xiangyang Li, Hongqin Wang, Katrina Weston-Green, Xu-Feng Huang, Kuiyang Zheng Obesity is underpinned by both genetic and environmental factors, including a high saturated fat diet. Some mice develop diet-induced obesity (DIO) but others remain diet-resistant (DR), despite intake of the same high-saturated fat diet; a phenomenon that mimics characteristics of the human obese phenotype. Microbiota-colon-brain axis regulation is important for energy metabolism and cognition. Using DIO and DR mouse models, this study aimed to examine gut microbiota, colonic inflammation and cognitive function to elucidate the role of microbiota-gut-brain regulation in diet-induced obesity. C57Bl6/J mice fed a chronic saturated palmitic acid diet for 22 weeks showed significant body weight gain differences, with the top one third gaining 48% heavier body weight than the lower one third. There was significant reduction in gut microbiota richness and diversity in DIO mice, but not in DR mice. At the phylum level, DIO mice had increased abundance of Firmicutes and Antinobacteria, and decreased abundance of Bacterioides and Proteobacteria in gut microbiota. DIO mice exhibited reduced tight junction proteins, increased plasma endotoxin lipopolysaccharide (LPS) and increased inflammation in the colon and liver. Recognition memory and spatial memory were impaired in DIO mice, associated with decreased Bacteroidetes. Further examination showed that hippocampal brain-derived neurotrophic factor (BDNF) was significantly decreased in DIO mice (vs DR). Conversely, DR mice showed no changes in the above parameters measured. Therefore, gut microbiota, colon inflammation and circulating LPS may play a major role in the development of the obese phenotype and cognitive decline associated with a chronic high saturated palmitic acid diet.Graphical abstractUnlabelled Image
       
  • Virgin coconut oil is effective to treat metabolic and inflammatory
           dysfunction induced by high refined carbohydrate-containing-diet in mice
    • Abstract: Publication date: Available online 1 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Marina Campos Zicker, Ana Letícia Malheiros Silveira, Débora Romualdo Lacerda, Débora Fernandes Rodrigues, Cíntia Tarabal Oliveira, Letícia Maria de Souza Cordeiro, Leandro Ceotto Freitas Lima, Sérgio Henrique Sousa Santos, Mauro Martins Teixeira, Adaliene Versiani Matos Ferreira The global rise in obesity rates is alarming since this condition is associated with chronic low-grade inflammation and secondary comorbidities as glucose intolerance, cardiovascular disease and liver damage. Therefore, a lot of dietary approaches are proposed to prevent and to treat obesity and its associated disorders. Virgin coconut oil (VCO) is well known as a functional food due to its significant amounts of medium-chain triglycerides. This study aimed to evaluate the effect of VCO on adiposity, metabolic and inflammatory dysfunctions induced by a high-refined carbohydrate-containing (HC) diet in mice. Male BALB/c mice were divided into two groups and fed with control (C) or HC diet to induce obesity for eight weeks. At the 9th week mice fed with HC diet were randomly regrouped into four groups, and were kept this way until the 12th week, as following: (i) HC diet alone or HC diet supplemented with three different VCO doses (ii) 1000 mg/Kg, (iii) 3000 mg/Kg and (iv) 9000 mg/Kg. Regardless of the concentration used, VCO supplementation promoted lower adiposity and also improvement in glucose tolerance, lower serum glucose and lipid levels and decreased hepatic steatosis. Moreover, VCO intake induced a lower inflammatory response due to decreased number of leukocytes and TNF-α and IL-6 concentrations in adipose tissue, as well as reduced counts of total leukocytes, mononuclear and polymorphonuclear circulating cells. Our data showed that VCO can be considered as an interesting potential dietary approach to attenuate obesity and its metabolic and inflammatory alterations.
       
  • Blueberry polyphenols extract as a potential prebiotic with anti-obesity
           effects on C57BL/6 J mice by modulating the gut microbiota
    • Abstract: Publication date: Available online 11 August 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Xinyao Jiao, Yuehua Wang, Yang Lin, Yuxi Lang, Enhui Li, Xiuyan Zhang, Qi Zhang, Ying Feng, Xianjun Meng, Bin Li Polyphenols are known for their various health benefits. Blueberries are dietary sources of polyphenols with reported health benefits. However, the role of blueberry polyphenols in alleviating obesity is not completely understood. This study investigated the potential positive effect of blueberry polyphenol extract (PPE) on high-fat diet (HFD)-induced obesity in C57BL/6 J mice by modulation of the gut microbiota. Four-week-old C57BL/6 J mice were fed a normal-fat diet or HFD with or without PPE or Orlistat for 12 weeks. Mice fed HFD exhibited increased body weight and adipose tissue weight and disordered lipid metabolism. In contrast, PPE inhibited body weight gain and returned lipid metabolism to normal. Furthermore, 16S rRNA gene sequencing of the fecal microbiota suggested that PPE changed the composition of the gut microbiota in C57BL/6 J mice and modulated specific bacteria such as Proteobacteria, Deferribacteres, Actinobacteria, Bifidobacterium, Desulfovibrio, Adlercreutzia, Helicobacter, Flexispira, and Prevotella. Orlistat also improved obesity and metabolic alterations of HFD mice and modulated the composition of the gut microbiota. Our findings suggest that PPE, as a potential prebiotic agent, influences the gut microbiota to positively affect HFD-induced obesity in C57BL/6 J mice.Graphical abstractUnlabelled Image
       
  • Dietary modulation of mitochondrial DNA damage: Implications in ageing and
           associated diseases
    • Abstract: Publication date: Available online 7 July 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Juwela Lam, Maureen McKeague Mammalian mitochondria contain small genomes (mtDNA), which encode several of the proteins that are crucial for respiration. As such, maintaining the integrity of mtDNA is essential for healthy life. Nutrition and strategies such as “Dietary Restriction” may play an important role in regulating mtDNA integrity and prolonging lifespan. In this review, we compare mitochondrial DNA with nuclear DNA damage and discuss how the resulting cell fates relate to human health. We provide a description of the mechanisms behind Dietary Restriction as an approach to induce mitochondrial processes contributing to a longer lifespan. We make connections between the current repertoire of studies to propose how nutrition may mitigate mitochondrial dysfunction and potentially reducing DNA damage. Finally, we describe nutritional-based approaches to prevent mitochondrial dysfunction with a focus on mimetics of dietary and calorie restriction.
       
 
 
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