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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  [3161 journals]
  • Sulforaphane triggers a functional elongation of microglial process
           via the Akt signal
    • Abstract: Publication date: Available online 13 February 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Yue Wu, Minhui Gao, Jingjing Wu, Peili Hu, Xing Xu, Yaru Zhang, Dan Wang, Zhuo Chen, Chao Huang Microglia are a kind of innate immune cells in the nervous system. The amoeboid morphology in microglia indicates a pro-inflammatory status, while their ramified morphologies are associated with anti-neuroinflammation. Recently, we and others have reported that drugs that trigger microglial process elongation may be beneficial for neuroinflammation inhibition. In this study, we found that sulforaphane (SFN), a compound extracted from broccoli sprouts, promotes primary cultured microglial process elongation in both normal and pro-inflammatory conditions in a reversible manner. This pro-elongation effect of SFN was also observed in the prefrontal cortex in vivo and accompanied with an attenuation of pro-inflammatory response as well as an enhancement of anti-inflammatory response in primary cultured microglia. Mechanistic studies revealed that the SFN treatment increased Akt phosphorylation levels in primary cultured microglia and Akt inhibition blocked the effect of SFN on microglial process elongation, suggesting that the regulation of microglial process by SFN is mediated by Akt activation. Functional studies showed that Akt inhibition reversed the effect of SFN on both pro- and anti-inflammatory responses in lipopolysaccharide (LPS)-stimulated microglia. In a inflammation model in vivo, SFN pretreatment not only prevented LPS-induced retractions of microglial process in the prefrontal cortex, but improved LPS-induced behavioral abnormalities in mice, including the increase in immobility time in the tail suspension test and forced swim test as well as the decrease in sucrose preference. These results indicate that the SFN inhibits microglial activation and neuroinflammation-triggered behavioral abnormalities likely through triggering Akt-mediated microglial process elongation.
       
  • Maternal high-fructose intake increases circulating corticosterone levels
           via decreased adrenal corticosterone clearance in adult offspring
    • Abstract: Publication date: Available online 12 February 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Eiji Munetsuna, Hiroya Yamada, Mirai Yamazaki, Yoshitaka Ando, Genki Mizuno, Yuji Hattori, Nao Sadamoto, Hiroaki Ishikawa, Yoshiji Ohta, Ryosuke Fujii, Koji Suzuki, Shuji Hashimoto, Koji Ohashi Global fructose consumption is on the rise; however, maternal high-fructose intake may have adverse effects on offspring. We previously demonstrated that excessive fructose intake by rat dams altered steroidogenic gene transcription in the hippocampus of offspring. Herein, we examined how maternal high-fructose intake influences the regulation of adrenal glucocorticoid levels in offspring. Rat dams received 20% fructose solution during gestation and lactation. After weaning, the offspring were provided normal water. Maternal high-fructose intake did not alter mRNA expression levels of adrenal corticosterone-synthesizing and corticosterone-inactivating proteins nor the circulating adrenocorticotropic hormone levels of offspring at postnatal day (PD) 21; however, it increased circulating corticosterone levels and decreased mRNA and protein levels of adrenal 5α-reductase type 1 and 11β-hydroxysteroid dehydrogenase type 2 in offspring at PD160. Furthermore, maternal high-fructose intake enhanced DNA methylation of the adrenal 5α-reductase 1 promoter region in PD160 offspring. Thus, maternal high-fructose intake was found to affect adrenal steroid hormone clearance in adult offspring—at least in part—through epigenetic mechanisms.
       
  • Profiling of Alzheimer´s disease related genes in mild to moderate
           vitamin D hypovitaminosis
    • Abstract: Publication date: Available online 11 February 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Marcus O.W. Grimm, Anna A. Lauer, Sven Grösgen, Andrea Thiel, Johannes Lehmann, Jakob Winkler, Daniel Janitschke, Christian Herr, Christoph Beisswenger, Robert Bals, Heike S. Grimm, Tobias Hartmann A vast majority of the elder population shows a mild to moderate vitamin D deficiency. Besides the well-known function of vitamin D, vitamin D-receptor is also expressed in brain and is discussed to regulate several genes. However very little is known whether genes are regulated, associated with Alzheimer´s disease (AD). Here we investigate 117 genes, known to be affected in AD, in mouse brain samples with a mild vitamin D hypovitaminosis comparable to the vitamin D status of the elderly population (20-30% deficiency). The 117 genes include two positive controls, Nep and Park7, already known to be affected both by AD and vitamin D hypovitaminosis. The 25 most promising candidates were verified in a second independent mouse-cohort resulting in eleven genes further evaluated against three additional housekeeping genes. Three of the remaining eight significantly altered genes are involved in APP-homeostasis (Snca, Nep, Psmb5), and each one gene in oxidative stress (Park7), inflammation (Casp4), lipid metabolism (Abca1), signal transduction (Gnb5) and in neurogenesis (Plat). Our results tighten the link of vitamin D and AD and underline that vitamin D influences several genes also in brain, highlighting that not only a strong link to AD but also to other neurodegenerative diseases might exist.Graphical abstractUnlabelled Image
       
  • Tissue-dependent effects of cis-9,trans-11- and trans-10,cis-12-CLA
           isomers on glucose and lipid metabolism in adult male mice
    • Abstract: Publication date: Available online 10 February 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Jose Cordoba-Chacon, Sugasini Dhavamani, CR Yalagala Poorna, Apoorva Tummala, Zachary C. White, Toshihiro Nagao, Rhonda D. Kineman, Papasani V. Subbaiah Mixtures of the two major conjugated linoleic acid (CLA) isomers trans-10,cis-12-CLA and cis-9,trans-11-CLA are used as over the counter supplements for weight loss. Because of the reported adverse effects of CLA on insulin sensitivity in some mouse studies, we sought to compare the impact of dietary t10c12-CLA and c9t11-CLA on liver, adipose tissue, and systemic metabolism of adult lean mice. We fed 8 week-old C57Bl/6J male mice with low fat diets (10.5% Kcal from fat) containing 0.8% t10c12-CLA or c9t11-CLA for 9 or 38 days. Diets containing c9t11-CLA had minimal impact on the endpoints studied. However, 7 days after starting the t10c12-CLA diet, we observed a dramatic reduction in fat mass measured by NMR spectroscopy, which interestingly rebounded by 38 days. This rebound was apparently due to a massive accumulation of lipids in the liver, because adipose tissue depots were visually undetectable. Hepatic steatosis and the disappearance of adipose tissue after t10c12-CLA feeding was associated with elevated plasma insulin levels and insulin resistance, compared to mice fed a control diet or c9t11-CLA diet. Unexpectedly, despite being insulin resistant, mice fed t10c12-CLA had normal levels of blood glucose, without signs of impaired glucose clearance. Hepatic gene expression and fatty acid composition suggested enhanced hepatic de novo lipogenesis without an increase in expression of gluconeogenic genes. These data indicate that dietary t10c12-CLA may alter hepatic glucose and lipid metabolism indirectly, in response to the loss of adipose tissue in mice fed a low fat diet.Graphical abstractUnlabelled Image
       
  • Resveratrol improves endothelial dysfunction and attenuates atherogenesis
           in apolipoprotein E-deficient mice
    • Abstract: Publication date: Available online 10 February 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Jinghua Li, Zhenwei Zhong, Jiru Yuan, Xiaohang Chen, Ziyang Huang, Zeyu Wu Endothelial dysfunction is an early and central feature of atherosclerosis. Dietary resveratrol (RSV), a class of flavonoid compounds, have been demonstrated to exert several beneficial effects on human body. In this study, we investigated the protective effects of RSV on high fat diet-induced endothelial dysfunction. Human aortic endothelial cells (HAECs) were treated with RSV to evaluate the gene expression of the endothelial nitric oxide synthase (eNOS). Apolipoprotein E (apoE−/−) mice were fed a high-fat, high-cholesterol diet (HCD) or HCD supplemented with RSV for 8 weeks. Treatment of cultured HAECs with RSV dose-dependently upregulated the eNOS expression as assessed by quantitative RT-PCR and Western blot, respectively. In addition, RSV increased the promoter activity of the human eNOS gene, as determined by luciferase assays of the eNOS promoter gene. The cAMP-response element binding protein (CREB) was identified as the target transcription factor involved in the RSV mediated upregulation of eNOS expression. RSV increased phosphorylation of CREB through protein kinase A (PKA) activation, which induced a CREB-mediated upregulation of eNOS transcription. Consequently, RSV treatment significantly reversed the deleterious effects of oxidized LDL (oxLDL)-induced oxidative stress in HAECs. In vivo, treatment with RSV improves endothelial dysfunction and attenuates atherosclerotic plaque formation in apoE−/− mice through PKA-CREB-dependent pathway. Our findings demonstrate that RSV has an effect of activating eNOS expression, contributing to the prevention of dyslipidemia-induced endothelial dysfunction and atherosclerosis.
       
  • Grape seed proanthocyanidin inhibits monocrotaline-induced pulmonary
           arterial hypertension via attenuating inflammation: In vivo and in vitro
           studies
    • Abstract: Publication date: Available online 10 February 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Fangzheng Chen, Heng Wang, Jie Zhao, Junjie Yan, Hanyan Meng, Huilu Zhan, Luowei Chen, Linbo Yuan Inflammation in pulmonary arterioles initiates and maintains pathological processes in pulmonary arterial hypertension (PAH) and inhibition of it attenuates PAH development. Grape seed proanthocyanidin (GSP) is believed to be effective in protecting vascular system via inhibiting inflammation while its effect on pulmonary circulation remains inconclusive. In this study, we made observations in monocrotaline (MCT)-induced PAH rats, and found decreases in mPAP, PVR, RVHI, WT%, WA% and lung W/D ratio after GSP administration in vivo. At the cellular and molecular levels, we also found several effects of GSP on MCT-induced PAH: (1) eNOS expression in lung tissue and plasma NO level were increased; (2) Ca2+ level in pulmonary arterial smooth muscle cell (PASMC) was decreased; (3)Transcription of inflammatory factors such as MPO, IL-1β, IL-6, TNF-α was down-regulated in lung tissue; (4) NF-κB pathway was inhibited as IκBα was less phosphorylated; (5) TNFα-induced PASMC over-proliferation could be inhibited. These results indicated a possible mechanism of GSP reversing pulmonary vascular remodeling and vascular contraction by inhibiting inflammation, and it may be useful for preventing PAH development.
       
  • Hypothalamic insulin receptor expression and DNA promoter methylation are
           sex-specifically altered in adult offspring of high-fat diet (HFD)-overfed
           mother rats
    • Abstract: Publication date: Available online 10 February 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Karen Schellong, Kerstin Melchior, Thomas Ziska, Raffael Ott, Wolfgang Henrich, Rebecca C. Rancourt, Andreas Plagemann Maternal overnutrition around reproduction has been shown to increase the offspring's risk for ‘diabesity’, mediated by altered hypothalamic neuropeptide expression. In this report, a possible contribution of altered hypothalamic sensing capacity for the peripheral satiety signals glucose, insulin and leptin will be addressed, taking into account potential sex-differences. Specifically, we evaluated the effects a maternal high-fat diet (HFD)-overfeeding has in rats pre- and during pregnancy and lactation on the hypothalamic gene expression patterns of insulin and leptin receptors (InsR, ObRb) and glucose transporter 3 (Glut3) as well as DNA methylation in the offspring at adult age (day 200 of life). Maternal HFD-consumption resulted in a metabolic syndrome phenotype, i.e., obesity, hyperleptinemia, hyperinsulinemia, impaired glucose tolerance and increased HOMA-IR. Interestingly, in turn insulin resistance was more pronounced in male offspring, accompanied by decreased hypothalamic InsR-mRNA. This was linked with hypermethylation of an activating transcription factor-binding site within the hypothalamic InsR promoter. The degree of methylation correlated inversely with respective InsR expression, while InsR expression itself was inversely related to phenotypic ‘diabesity’. Expression of ObRb- and Glut3-mRNA were not significantly changed. In conclusion, sex-specific alterations of hypothalamic InsR expression and DNA promoter methylation in adult offspring of HFD-overfed dams may lead to hypothalamic insulin resistance and ‘diabesity’, with males predisposed to this epigenetic malprogramming.
       
  • Effect of annatto-extracted tocotrienols and green tea polyphenols on
           glucose homeostasis and skeletal muscle metabolism in obese male mice
    • Abstract: Publication date: Available online 10 February 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Eunhee Chung, Salvatore N. Campise, Hayli E. Joiner, Michael D. Tomison, Gurvinder Kaur, Jannette M. Dufour, Lillian Cole, Latha Ramalingam, Naima Moustaid-Moussa, Chwan-Li Shen Skeletal muscle is the major site for glucose uptake and thus plays an important role in initiating insulin resistance in type 2 diabetes mellitus. This study evaluated the effects of tocotrienols (TT) and green tea polyphenols (GTP) individually or in combination on glucose homeostasis and skeletal muscle metabolism in obese mice with insulin resistance and elevation of blood glucose. Forty-eight male mice were fed a high fat diet and assigned to 4 groups in a 2 (no TT vs. 400 mg TT/kg diet) × 2 (no GTP vs. 0.5% vol/wt GTP in water) for 14 weeks. Both GTP and TT improved area under curve of insulin intolerance; while GTP increased serum insulin levels in obese mice, probably due to the addition of sweetener in drinking water. An interaction (TTxGTP) was observed in glucose tolerance test, total pancreas insulin concentration, and citrate synthase activity of soleus in mice. Neither TT nor GTP affected insulin and glucagon protein expression in pancreas based on immunohistochemistry. Both TT and GTP individually increased soleus muscle weight of mice; while only GTP increased gastrocnemius muscle weight of mice. The TT + GTP group had the greatest gastrocnemius muscle cross sectional area than other groups. GTP, not TT, induced cytochrome c oxidase activity and reduced thiobarbituric acid reactive substances levels in soleus muscle. Our results suggest that TT and GTP, individually or synergistically have the potential to improve skeletal muscle metabolism in obese mice by improving glucose homeostasis, reducing lipid peroxidation, and increasing rate limiting enzymes of oxidative phosphorylation.
       
  • Pea polyphenolics and hydrolysis processing alter microbial community
           structure and early pathogen colonization in mice
    • Abstract: Publication date: Available online 8 February 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Andrew J. Forgie, Yanhua Gao, Tingting Ju, Deanna M. Pepin, Kaiyuan Yang, Michael G. Gänzle, Jocelyn A. Ozga, Catherine B. Chan, Benjamin P. Willing Health benefits associated with pea consumption have been attributed to the fiber and polyphenolic content concentrated within the pea seed coat. However, the amount of pea polyphenols can vary between cultivars, and it has yet to be studied whether pea polyphenols impact the intestinal microbiota. We hypothesized that pea polyphenols promote a healthy microbiome that supports intestinal integrity and pathogen colonization resistance. To investigate the effects of pea polyphenols, pea cultivars rich and poor in proanthocyanidins were supplemented in raw or acid hydrolyzed form to an isocaloric diet in mice. Acid hydrolysis increases the absorption of pea polyphenols by cleaving polymeric proanthocyanidins to their readily absorbable anthocyanidin monomers. After three weeks of diet, mice were challenged with Citrobacter rodentium and pathogen colonization and inflammation were assessed. Counter to our hypothesis, pea seed coat fraction supplementation, especially the non-hydrolyzed proanthocyanidin-rich fraction diet adversely increased C. rodentium pathogen load and inflammation. Ileal, cecal and colon microbial communities were notably distinct between pea seed cultivar and hydrolysis processing. The consumption of intact proanthocyanidins decreased microbial diversity indicating that proanthocyanidins have antimicrobial properties. Together our results indicate supplementation of raw pea seed coat rich in proanthocyanidins adversely affect intestinal integrity. However, acid hydrolysis processing restored community structure and colonization resistance, and the anthocyanidin-rich fractions reduced weight gain on a high fat diet. Establishing a clear understanding of the effects of pea fiber and polyphenolic form on health will help to develop research-based pea products and dietary recommendations.
       
  • reen+tea+extract+prevents+obesity+in+male+mice+by+alleviating+gut+dysbiosis+in+association+with+improved+intestinal+barrier+function+that+limits+endotoxin+translocation+and+adipose+inflammation&rft.title=Journal+of+Nutritional+Biochemistry&rft.issn=0955-2863&rft.date=&rft.volume=">Green tea extract prevents obesity in male mice by alleviating gut
           dysbiosis in association with improved intestinal barrier function that
           limits endotoxin translocation and adipose inflammation
    • Abstract: Publication date: Available online 8 February 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Priyankar Dey, Geoffrey Y. Sasaki, Ping Wei, Jinhui Li, Lingling Wang, Jiangjiang Zhu, Dana McTigue, Zhongtang Yu, Richard S. Bruno Gut-derived endotoxin translocation provokes obesity by inducing TLR4/NFκB inflammation. We hypothesized that catechin-rich green tea extract (GTE) would protect against obesity-associated TLR4/NFκB inflammation by alleviating gut dysbiosis and limiting endotoxin translocation. Male C57BL/6J mice were fed a low-fat (LF) or high-fat (HF) diet containing 0% or 2% GTE for 8-wk. At wk 7, fluorescein isothiocyanate (FITC)-dextran was administered by oral gavage before assessing its serum concentrations as a gut permeability marker. HF-feeding increased (P
       
  • Resveratrol attenuates doxorubicin-induced cardiotoxicity in rats by
           up-regulation of vascular endothelial growth factor B
    • Abstract: Publication date: Available online 8 February 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Wencong Tian, Lei Yang, Yuansheng Liu, Jianxiang He, Liang Yang, Qiong Zhang, Fei Liu, Jing Li, Jie Liu, Shoichiro Sumi, Yanna Shen, Zhi Qi
       
  • Prebiotics from acorn and sago prevent high-fat diet-induced insulin
           resistance via microbiome-gut-brain axis modulation
    • Abstract: Publication date: Available online 30 January 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Shokouh Ahmadi, Ravinder Nagpal, Shaohua Wang, Jason Gagliano, Dalane W Kitzman, Sabihe Soleimanian-Zad, Mahmoud Sheikh-Zeinoddin, Russel Read, Hariom YadavABSTRACTRole of gut microbiome in obesity and type 2 diabetes (T2D) became apparent from several independent studies, indicating that gut microbiome modulators like prebiotics may improve microbiome perturbations (dysbiosis) to ameliorate metabolic derangements. We herein isolate water soluble, non-digestible polysaccharides from five plant based foods (acorn, quinoa, sunflower, pumpkin and sago seeds) and assess their impact on human fecal microbiome and amelioration of high fat diet (HFD)-induced obesity/T2D in mice. During polysaccharide isolation, purification, biochemical and digestion resistance characterization, and fermentation pattern by human fecal microbiome, we select acorn- and sago- derived prebiotics (on the basis of relatively higher purity and yield and lower protein contamination) and examine their effects in comparison to inulin. Prebiotics treatments in human fecal microbiome culture system not only preserve microbial diversity but also appear to foster beneficial bacteria and short-chain fatty acids (SCFAs). Feeding of acorn- and sago-derived prebiotics ameliorates HFD-induced glucose intolerance and insulin resistance in mice, with effects comparatively superior to those seen in inulin-fed mice. Feeding of both of novel prebiotics as well as inulin increases SCFAs levels in the mouse gut. Interestingly, gut hyperpermeability and mucosal inflammatory markers were significantly reduced upon prebiotics feeding in HFD-fed mice. Hypothalamic energy signaling in terms of increased expression of pro-opiomelanocortin, was also modulated by prebiotics administration. Results demonstrate that these (and/or such) novel prebiotics can ameliorate HFD-induced defects in glucose metabolism via positive modulation of gut-microbiome-brain axis and hence could be useful in preventing/treating diet-induced obesity/T2D.Graphical abstractUnlabelled Image
       
  • A decrease in iron availability to human gut microbiome reduces the growth
           of potentially pathogenic gut bacteria; an in vitro colonic fermentation
           study
    • Abstract: Publication date: Available online 27 January 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Bhavika A Parmanand, Lee Kellingray, Gwenaelle Le Gall, Abdul W Basit, Susan Fairweather-Tait, Arjan Narbad Iron-supplements are widely consumed; however most of the iron is not absorbed and enters the colon where potentially pathogenic bacteria can utilise it for growth. This study investigated the effect of iron availability on human gut microbial composition and function using an in vitro colonic fermentation model inoculated with faecal microbiota from healthy adult donors, as well as examining the effect of iron on the growth of individual gut bacteria. Batch fermenters were seeded with fresh faecal material and supplemented with the iron chelator, bathophenanthroline disulphonic acid (BPDS). Samples were analysed at regular intervals to assess impact on the gut bacterial communities. The growth of Escherichia coli and Salmonella Typhimurium was significantly impaired when cultured independently in iron-deficient media. In contrast, depletion of iron did not affect the growth of the beneficial species, Lactobacillus rhamnosus, when cultured independently. Analysis of the microbiome composition via 16S-based metataxonomics indicated that under conditions of iron chelation, the relative abundance decreased for several taxa, including a 10% decrease in Escherichia and a 15% decrease in Bifidobacterium. Metabolomics analysis using 1 H-NMR indicated that the production of SCFAs was reduced under iron-limited conditions. These results support previous studies demonstrating the essentiality of iron for microbial growth and metabolism, but, in addition, they indicate that iron chelation changes the gut microbiota profile and influences human gut microbial homeostasis through both compositional and functional changes.Graphical Unlabelled Image
       
  • Subacute oral administration of folic acid elicits anti-inflammatory
           response in a mouse model of allergic dermatitis
    • Abstract: Publication date: Available online 26 January 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Emi Makino, Tomoki Fukuyama, Yuko Watanabe, Risako Tajiki-Nishino, Hitoshi Tajima, Aya Ohnuma-Koyama, Naofumi Takahashi, Ryoichi Otsuka, Yoshimasa Okazaki Folic acid (FA) deficiency is associated with several health problems, including megaloblastic anemia and fetal neural tube defects. Therefore, supplementation with FA is strongly recommended by governments worldwide. Recent published reports indicate that FA functions in immune system maintenance. The main objective of this study is to examine possible anti-inflammatory and anti-pruritic effects of FA using a mouse model of allergic dermatitis. The mouse model was developed by repetitive sensitization to the Th2-type hapten toluene-2,4-diisocyanate (TDI). During the development of allergic dermatitis, FA was orally administered to the mice at doses of 8, 160, 1000, or 10,000 μg/day for 5 weeks. The ear swelling response and scratching behavior were monitored after the TDI challenge. Serum, ear tissue, and auricular lymph node samples were isolated for further analysis 24 h after the TDI challenge. The ear swelling response was reduced in a dose-dependent manner by FA administration, and a significant change was observed at a concentration of 10,000 μg/day group. Comparable results were obtained through histological evaluation and cytokine level measurement in the ear tissue samples. Oral administration of FA exhibited the inhibitory effect on T cell infiltration and T cell related cytokine production in auricular lymph nodes. Scratching behavior was not altered by FA administration. The in vivo evidence was corroborated by in vitro results, which showed that FA treatment significantly interfered with T cell proliferation in a dose-dependent manner. Our findings imply that subacute oral administration of FA elicits an anti-inflammatory response, mainly through inhibition of T cell proliferation.
       
  • Journal of nutritional biochemistry special issue: Nutritional modulation
           of the gut microbiome in gastrointestinal and metabolic disease
    • Abstract: Publication date: Available online 23 January 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Joseph F. Pierre, Vanessa Leone, Kristina Martinez-Guryn
       
  • Characterization of the mouse white adipose tissue redox environment and
           associations with perinatal environmental exposures to bisphenol-a and
           high fat diets
    • Abstract: Publication date: Available online 18 January 2019Source: The Journal of Nutritional BiochemistryAuthor(s): K. Neier, E.M. Marchlewicz, L.D. Bedrosian, D.C. Dolinoy, C. Harris White adipose tissue (WAT) plays an important role in obesity pathophysiology. Redox signaling underlies several aspects of WAT physiology; however, the thiol redox environment of WAT has not yet been fully characterized. Dietary and endocrine disrupting chemical (EDC) exposures during development can transiently impact the cellular redox environment, but it is unknown whether these exposures can reprogram the WAT thiol redox environment. To characterize the WAT thiol redox environment, we took a descriptive approach and measured thiol redox parameters using HPLC in mouse mesenteric (mWAT), gonadal (gWAT), and subinguinal (sWAT) depots. Cysteine (CYSS:CYS) and glutathione (GSSG:GSH) redox potentials (Eh) were more oxidizing in gWAT and sWAT than mWAT. Increased body weight, relative WAT weight, and age were associated with oxidizing GSSG:GSH Eh in mWAT in a sex-specific manner. Body weight and relative WAT weight were also positively associated with GSSG:GSH Eh in sWAT. We carried out a second mouse study with perinatal exposures to bisphenol-A (BPA) and Mediterranean and Western high fat diets (HFDs) to determine whether early-life chemical and dietary factors have long-lasting impacts on mWAT redox parameters. Mice exposed to Mediterranean HFD or BPA had more oxidizing GSSG:GSH mWAT Eh than controls, with more pronounced differences in females. These findings suggest an important role for the thiol redox environment in WAT physiology. Observed sex-specific and depot-specific differences in thiol redox parameters are consistent with known WAT physiology. Lastly, mWAT GSSG:GSH Eh may be reprogrammed by developmental exposure to HFDs and EDCs, which may have implications for obesity risk.Graphical abstractUnlabelled Image
       
  • Effects of exercise and dietary protein sources on adiposity and insulin
           sensitivity in obese mice
    • Abstract: Publication date: Available online 18 January 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Even Fjære, Lene Secher Myrmel, Ditte Olsen Lützhøft, Hanne Andersen, Jacob Bak Holm, Pia Kiilerich, Rita Hannisdal, Bjørn Liaset, Karsten Kristiansen, Lise Madsen Low-fat diets and exercise are generally assumed to ameliorate obesity related metabolic dysfunctions, but the importance of exercise versus dietary changes is debated. Male C57BL/6J mice were fed a high fat/high sucrose (HF/HS) diet to induce obesity and then either maintained on the HF/HS or shifted to low-fat (LF) diets containing either salmon or entrecote. For each diet, half of the animals exercised voluntarily for 8 weeks. We determined body composition, glucose tolerance, insulin sensitivity and hepatic triacylglycerol levels. The microbiota composition in cecal and fecal samples was analyzed using 16S ribosomal RNA gene amplicon sequencing. Voluntary exercise improved insulin sensitivity, but did not improve glucose tolerance. Voluntary exercise did not reduce adiposity in mice maintained on a HF/HS diet, but enhanced LF-induced reduction in adiposity. Hepatic triacylglycerol (TAG) levels were reduced by voluntary exercise in LF, but not HF/HS fed mice. Voluntary exercise induced shifts in the cecal and fecal microbiota composition and functional potential in mice fed LF or HF/HS diets. Whereas voluntary exercise improved insulin sensitivity, a switch to a LF diet was the most important factor related to body weight and fat mass reduction.
       
  • Bifidobacterium with the role of 5-hydroxytryptophan synthesis regulation
           alleviate the symptom of depression and related microbiota dysbiosis
    • Abstract: Publication date: Available online 18 January 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Peijun Tian, Gang Wang, Jianxin Zhao, Hao Zhang, Wei Chen Depression disorder is rapidly advancing worldwide and therapeutic strategy through gut-brain axis has been proven to be effective in the treatment. Here we studied the effect of lactic acid bacteria (LAB) treatment on depression. C57BL/6J mice were administered with LAB during a five-week chronic unpredictable mild stress. Bifidobacterium longum subsp. infantis E41 and Bifidobacterium breve M2CF22M7, which improved the expression of Tph1 and secretion of 5-hydroxytryptophan (5-HTP) in RIN14B cells, significantly reduced depressive behaviors of mice in the forced swim test, sucrose preference test, and step down test, as well as increased the level of 5-hydroxytryptamine and brain derived neurotrophic factor concentration in brain. Besides, M2CF22M7 reduced the serum corticosterone level. E41 increased cecal butyrate level, which significantly and positively correlated with some depression related indexes. Using 16S rRNA-amplicon sequencing of faces, E41 and M2CF22M7 were found to improve the chronic stress induced microbial dysbiosis. They also normalized the host's pathways involving metabolism and gene information processing. These results indicate that Bifidobacterium E41 and M2CF22M7 have an antidepressant effect in mice partly in a 5-HTP dependent and microbiota-regulating manner. Nurturing the gut microbiota with these strains may become an emerging therapeutic way for mood disorder.Graphical abstractUnlabelled Image
       
  • Long-term treatment with kefir probiotics ameliorates cardiac function in
           spontaneously hypertensive rats
    • Abstract: Publication date: Available online 18 January 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Mirian A Silva-Cutini, Simone A Almeida, Andrews M Nascimento, Gláucia R Abreu, Nazaré S Bissoli, Dominik Lenz, Denise C Endringer, Girlandia A Brasil, Ewelyne M Lima, Vinicia C Biancardi, Tadeu U Andrade This work evaluated the effects of long-term kefir treatment in cardiac function (cardiac contractility and calcium-handling proteins) and the central nervous system (CNS) control of the sympathetic signaling in spontaneously hypertensive rats (SHR). Male normotensive rats (WKYs) and SHRs were divided into three groups: WKYs and SHRs treated with vehicle, and SHRs treated with milk fermented by the grains of kefir (5%; SHR-Kefir; oral gavage, 0.3 mL/100 g daily/9 weeks). At the end of treatment, mean arterial pressure (MAP) and heart rate (HR) were measured by direct arterial catheterization. Hemodynamic parameters (left ventricular systolic pressure, left ventricular isovolumetric relaxation time constant, maximal and minimal pressure decay) were acquired through a left ventricular catheter implantation. Left ventricle protein expressions of phospholamban (PLB), its phosphorylated form (p-PLB) and sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) were determined by Western blot. Tyrosine hydroxylase (TH) protein expression was evaluated via immunofluorescence within the paraventricular nucleus (PVN) of the hypothalamus and the rostral ventrolateral medulla (RVLM). SHR-Kefir group presented lower MAP and HR compared to SHRs. Kefir treatment ameliorated cardiac hypertrophy and promoted reduced expression of PLB, p-PLB, and SERCA2a contractile proteins. Within the PVN and RVML, TH protein overexpression observed in SHRs was reduced by probiotic treatment. In addition, kefir improved cardiac hemodynamic parameters in SHR-treated animals. Altogether, the data show that long-term kefir treatment reduced blood pressure by mechanisms involving reduction of cardiac hypertrophy, improvement of cardiac contractility and calcium-handling proteins, and reduction in the CNS regulation of the sympathetic activity.
       
  • Dietary supplementation with strawberry induces marked changes in the
           composition and functional potential of the gut microbiome in diabetic
           mice
    • Abstract: Publication date: Available online 18 January 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Chrissa Petersen, Umesh D. Wankhade, Divya Bharat, Kiana Wong, Jennifer Ellen Mueller, Sree V. Chintapalli, Brian D. Piccolo, Thunder Jalili, Zhenquan Jia, J. David Symons, Kartik Shankar, Pon Velayutham Anandh Babu Gut microbiota contribute to the biological activities of berry anthocyanins by transforming them into bioactive metabolites and anthocyanins support the growth of specific bacteria indicating a two-way relationship between anthocyanins and microbiota. In the present study, we tested the hypothesis that strawberry supplementation alters gut microbial ecology in diabetic db/db mice. Control (db/+) and diabetic (db/db) mice (7-wk) consumed standard diet or diet supplemented with 2.35% freeze-dried strawberry (db/db + SB) for 10 weeks. Colon contents were used to isolate bacterial DNA. V4 variable region of 16S rRNA gene was amplified. Data analyses were performed using standardized pipelines (QIIME 1.9 and R packages). Differences in predictive metagenomics function was identified by PICRUSt. Principle coordinate analyses confirmed that the microbial composition was significantly influenced by both host genotype and strawberry consumption. Further, α-diversity indices and β-diversity were different at the phylum and genus levels, and genus and OTU levels, respectively (P
       
  • CSRP3 mediates polyphenols-induced Cardioprotection in hypertension
    • Abstract: Publication date: Available online 8 January 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Carole Oudot, Andreia Gomes, Valérie Nicolas, Morgane Le Gall, Philippe Chaffey, Cédric Broussard, Giuseppe Calamita, Maria Mastrodonato, Patrizia Gena, Jean-Luc Perfettini, Jocelyne Hamelin, Antoinette Lemoine, Rodolphe Fischmeister, Helena L.A. Vieira, Claudia N. Santos, Catherine Brenner Berries contain bioactive polyphenols, whose capacity to prevent cardiovascular diseases have been established recently in animal models as well in human clinical trials. However, cellular processes and molecular targets of berries polyphenols remain to be identified. The capacity of a polyphenol-enriched diet (i.e. blueberries, blackberries, raspberries, strawberry tree fruits and Portuguese crowberries berries mixture) to promote animal survival and protect cardiovascular function from salt-induced hypertension was evaluated in a chronic salt sensitive Dahl rat model. The daily consumption of berries improved survival of Dahl/Salt Sensitive rats submitted to high salt diet and normalized their body weight, renal function and blood pressure. In addition, a prophylactic effect was observed at the level of cardiac hypertrophy and dysfunction, tissue cohesion and cardiomyocyte hypertrophy. Berries also protected the aorta from fibrosis and modulated the expression of Aquaporin-1, a channel involved in endothelial water and nitric oxide (NO) permeability. Left ventricle proteomics analysis led to the identification of berries and salt metabolites targets, including Cystein and glycin-rich protein 3 (CSRP3), a protein involved in myocyte cytoarchitecture. In neonatal rat ventricular cardiomyocytes, CSRP3 was validated as a target of a berries derived polyphenol metabolite, 4-methylcatechol sulfate, at micromolar concentrations, mimicking physiological conditions of human plasma circulation. Accordingly, siRNA silencing of CSRP3 and 4-methylcatechol sulfate pretreatment reversed cardiomyocyte hypertrophy and CSRP3 overexpression induced by phenylephrine. Our systemic study clearly supports that the modulation of CSRP3 by a polyphenol-rich berries diet as an efficient cardioprotective strategy in hypertension-induced heart failure.
       
  • Lycopene protects against pressure overload-induced cardiac hypertrophy by
           attenuating oxidative stress
    • Abstract: Publication date: Available online 7 January 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Junyi Zeng, Jingjing Zhao, Bin Dong, Xingming Cai, Jingzhou Jiang, Ruicong Xue, Fengjuan Yao, Yugang Dong, Chen Liu Oxidative stress is considered an important pathogenic process of cardiac hypertrophy. Lycopene is a kind of carotenoid antioxidant that protects the cardiovascular system, so we hypothesized that lycopene might inhibit cardiac hypertrophy by attenuating oxidative stress. Phenylephrine and pressure overload were used to set up the hypertrophic models in vitro and in vivo respectively. Our data revealed that treatment with lycopene can significantly block pressure overload-induced cardiac hypertrophy in in vitro and in vivo studies. Further studies demonstrated that lycopene can reverse the increase in reactive oxygen species (ROS) generation during the process of hypertrophy and can retard the activation of ROS-dependent pro-hypertrophic MAPK and Akt signaling pathways. In addition, protective effects of lycopene on the permeability transition pore opening in neonatal cardiomyocytes were observed. Moreover, we demonstrated that lycopene restored impaired antioxidant response element (ARE) activity and activated ARE-driven expression of antioxidant genes. Consequently, our findings indicated that lycopene inhibited cardiac hypertrophy by suppressing ROS-dependent mechanisms.
       
  • Lycopene mitigates pulmonary emphysema induced by cigarette smoke in a
           murine model
    • Abstract: Publication date: Available online 21 December 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Keila Karine Duarte Campos, Camila de Oliveira Ramos, Thais Lourenço Martins, Guilherme de Paula Costa, André Talvani, Camila Carrião Machado Garcia, Laser Antônio Machado Oliveira, Sílvia Dantas Cangussú, Daniela Caldeira Costa, Frank Silva Bezerra Chronic obstructive pulmonary disease (COPD) is an inflammatory lung disease characterized by a non-fully reversible airflow limitation comprising chronic bronchitis and pulmonary emphysema both being induced by cigarette smoke (CS) exposure. Lycopene has shown antioxidant and anti-inflammatory properties that can prevent acute lung inflammation and emphysema. We hypothesized that administration with lycopene would repair lung damage in emphysema caused by CS exposure. Mice were administered with two different doses of lycopene (25 or 50 mg/kg/day, diluted in sunflower oil by orogastric gavage) and then exposed to 60 days of CS or not (CG). Lycopene promoted a reduction in the number of total leukocytes and it improved pulmonary emphysema. Lycopene was able to minimize redox processes by decreasing lipid peroxidation and DNA damage, and by having an increase in the activities of SOD, CAT and GSH content. Furthermore, it decreased levels of TNF-α, IFN-γ and IL-10. In addition, it was able to decrease MPO activity and nitrite content. In conclusion, our data elucidated the role of lycopene as an antioxidant and anti-inflammatory agent in mice exposed to CS.
       
  • Dietary pomegranate supplement alleviates murine pancreatitis by
           modulating Nrf2-p21 interaction and controlling apoptosis to survival
           switch
    • Abstract: Publication date: Available online 21 December 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Payal Gupta, Sreetama Choudhury, Sayan Ghosh, Sudeshna Mukherjee, Olivia Chowdhury, Arindam Sain, Sreya Chattopadhyay Dietary supplementation of polyphenol rich pomegranate extract (POMx) has been shown to have anti-oxidant and anti-inflammatory activities. Here, we evaluate the efficacy of POMx in mitigating pancreatitis in mice and provide a mechanistic outline of the process. Age-matched male Swiss albino mice were injected with Lipopolysaccharide (LPS) and given POMx supplement alone or in combination with LPS. After 4 weeks of treatment histological scoring for pancreatic edema and vacuolization was performed. Serum insulin levels were estimated and glucose tolerance test (IPGTT) data revealed that POMx reduced inflammation induced hyperglycemia in mice. Analysis of TLR4, IκB expression and NF-κB nuclear translocation, and concentrations of IL-6 and TNFα showed that POMx is able to modulate the molecular instigators of inflammatory responses. Annexin V assay indicated that POMx protects again inflammation-mediated apoptosis in the pancreas. Expression profile of SAPK/JNK pathway, p53, Bax, Bcl-2 and Caspase-3 validate an apoptotic to survival shift in POMx treatment group. Co-immunoprecipitation studies show that POMx stabilizes p21 and Nrf2 interaction and increases its nuclear translocation. The study also proves that nuclear fraction of Nrf2 is able to bind to the Bcl-2 promoter and activate an anti-apoptotic program. The findings of our study underlines an anti-inflammatory, anti-oxidative and anti-apoptotic role of POMx and provides a mechanistic idea of how POMx confers protection during pancreatitis.
       
  • Acute effects of milk polar lipids on intestinal tight junction
           expression: Towards an impact of sphingomyelin through the regulation of
           IL-8 secretion'
    • Abstract: Publication date: Available online 21 December 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Marine Milard, Armelle Penhoat, Annie Durand, Charline Buisson, Emmanuelle Loizon, Emmanuelle Meugnier, Karène Bertrand, Florent Joffre, David Cheillan, Lorna Garnier, Sébastien Viel, Fabienne Laugerette, Marie-Caroline Michalski Milk polar lipids (MPL) are specifically rich in milk sphingomyelin (MSM) which represents 24% of MPL. Beneficial effects of MPL or MSM have been reported on lipid metabolism, but information on gut physiology is scarce. Here we assessed whether MPL and MSM can impact tight junction expression. Human epithelial intestinal Caco-2/TC7 cells were incubated with mixed lipid micelles devoid of MSM (Control) or with 0.2 or 0.4 mM of MSM via pure MSM or via total MPL. C57Bl/6 mice received 5 or 10 mg of MSM via MSM or via MPL (oral gavage); small intestinal segments were collected after 4 h. Impacts on tight junction and cytokine expressions were assessed by qPCR; IL-8 and IL-8 murine homologs (Cxcl1, Cxcl2) were analyzed. In vitro, MSM increased tight junction expression (Occludin, ZO-1) vs Control, unlike MPL. However, no differences were observed in permeability assays (FITC-dextran, Lucifer yellow). MSM increased the secretion and gene expression of IL-8 but not of other inflammatory cytokines. Moreover, cell incubation with IL-8 induced an overexpression of tight junction proteins. In mice, mRNA level of Cxcl1 and Cxcl2 in the ileum were increased after gavage with MSM vs NaCl but not with MPL. Altogether, these results suggest a specific action of MSM on intestinal tight junction expression, possibly mediated by IL-8. Our study provides clues to shed light on the beneficial effects of MPL on intestinal functions and supports the need for further mechanistic exploration of the direct vs indirect effects of MSM and IL-8 on the gut barrier.Graphical abstractUnlabelled Image
       
  • Puerariae Lobatae Radix with chuanxiong Rhizoma for treatment of cerebral
           ischemic stroke by remodeling gut microbiota to regulate the brain–gut
           barriers
    • Abstract: Publication date: Available online 21 December 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Runzhi Chen, Peng Wu, Zheng Cai, Yingying Fang, Hao Zhou, Yi Lasanajak, Lan Tang, Ling Ye, Chuqi Hou, Jie Zhao The combination of Puerariae Lobatae Radix (PLR) and Chuanxiong Rhizoma (CXR) is commonly used to treat cerebrovascular diseases. This work aimed to clarify the mechanisms of their action in treating cerebral ischemic stroke from the perspective of gut microecology. The PLR and CXR combination effectively improved the neurological function, reduced the cerebral infarction, and relieved the complications of cerebral ischemic stroke, including dyslipidemia, increased blood viscosity, and thrombotic risk. Cerebral ischemic stroke triggered gut microbial disturbances by enriching pathogens and opportunistic microorganisms, including Bacteroides, Escherichia_Shigella, Haemophilus, Eubacterium_nodatum_group, Collinsella, Enterococcus, Proteus, Alistipes, Klebsiella, Shuttleworthia, and Faecalibacterium. Cerebral ischemic stroke also increased the intestinal permeability, disrupted the gut barrier, and caused intestinal microbial translocation. Occludin, claudin-5, and ZO-1 levels in the brain–gut barriers showed a high positive correlation. However, the combination remodeled the gut microecology by modulating endogenous bacteria whose effects may mitigate cerebral damage, such as Alloprevotella, Ruminococcaceae, Oscillospira, Lachnospiraceae_NK4B4_group, Akkermansia, and Megasphaera, protected the brain–gut barriers by increasing claudin-5 and ZO-1 levels; and weakened the gut microbiota translocation by decreasing diamine oxidase, lipopolysaccharide, and d-lactate. Although nimodipine effectively reduced the cerebral infarction, it did not relieve the gut microbiota dysbiosis and instead aggravated the gut barrier disruption and microbiota translocation. In conclusion, cerebral ischemic stroke caused gut microbiota dysbiosis, increased intestinal permeability, disrupted the gut barrier, and triggered gut microbiota translocation. The PLR and CXR combination was an effective treatment for cerebral ischemic stroke that relieved the gut microbiota dysbiosis and brain–gut barriers disruption.Graphical abstractUnlabelled Image
       
  • Tryptophan restriction partially recapitulates the age-dependent effects
           of total amino acid restriction on energy balance in diet-induced obese
           rats
    • Abstract: Publication date: Available online 21 December 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Rizaldy C. Zapata, Arashdeep Singh, Adel Pezeshki, Prasanth K. Chelikani Moderate dietary protein restriction promotes hyperphagia and thermogenesis; however, little is known of whether these responses are due to restriction of the essential amino acids tryptophan and histidine. Here, we determined whether restriction of tryptophan and histidine alone recapitulate the effects of total amino acid restriction on energy balance, and whether the metabolic responses are age-dependent. We fed young (12 weeks old) and older (29 weeks old) diet-induced obese rats with one of four high fat diets: control (CON, 100% amino acid requirement), total amino acid restriction (TAA, 67% amino acid restriction), tryptophan restriction (TRP, 67% tryptophan restriction) or histidine restriction (HIS, 67% histidine restriction) for 21 days. Energy balance, hormones, and key markers of hepatic nutrient sensing and brown adipose thermogenesis were measured. We found that TAA increased food intake in both young and older rats, with TRP, but not HIS, transiently simulating the hyperphagia. TAA promoted sympathetically mediated increase in energy expenditure in young rats partly through increased β2-adrenergic and FGF21 signaling in brown fat; TRP partially emulated these responses. TRP and HIS transiently increased fat mass in young rats, and TAA promoted adiposity in older rats. TAA, TRP and HIS increased postprandial FGF21 concentrations in older rats. TAA induced age-dependent differential changes in markers of hepatic amino acid sensing; TRP and HIS partially mimicked these responses. Collectively, restriction of tryptophan, but not histidine, partially recapitulated the age-dependent metabolic effects of total amino acid restriction, in concert with distinct changes in hepatic amino acid sensing and signaling mechanisms.
       
  • Macrophage plasticity, polarization, and function in response to curcumin,
           a diet-derived polyphenol, as an immunomodulatory agent
    • Abstract: Publication date: Available online 21 December 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Asadollah Mohammadi, Christopher N. Blesso, George E. Barreto, Maciej Banach, Muhammed Majeed, Amirhossein Sahebkar Monocytes and macrophages are important cells of the innate immune system that have diverse functions, including defense against invading pathogens, removal of dead cells by phagocytosis, antigen presentation in the context of MHC class I and class II molecules, and production of various pro-inflammatory cytokines and chemokines such as IL-1β, IL-6, TNF-α and MCP-1. In addition, pro-inflammatory (M1) and anti-inflammatory (M2) macrophages clearly play important roles in the progression of several inflammatory diseases. Therefore, therapies that target macrophage polarization and function by either blocking their trafficking to sites of inflammation, or skewing M1 to M2 phenotype polarization may hold clinical promise in several inflammatory diseases. Dietary-derived polyphenols have potent natural anti-oxidative properties. Within this group of polyphenols, curcumin has been shown to suppress macrophage inflammatory responses. Curcumin significantly reduces co-stimulatory molecules and also inhibits MAPK activation and the translocation of NF-κB p65. Curcumin can also polarize/repolarize macrophages toward the M2 phenotype. Curcumin-treated macrophages have been shown to be highly efficient at antigen capture and endocytosis via the mannose receptor. These novel findings provide new perspectives for the understanding of the immunopharmacological role of curcumin, as well as its therapeutic potential for impacting macrophage polarization and function in the context of inflammation-related disease. However, the precise effects of curcumin on the migration, differentiation, polarization, and immunostimulatory functions of macrophages remain unknown. Therefore, in this review, we summarized whether curcumin can influence macrophage polarization, surface molecule expression, cytokine and chemokine production, and their underlying pathways in the prevention of inflammatory diseases.Graphical abstractUnlabelled Image
       
  • Unsaturated Fatty Acids from Flaxseed oil and exercise modulate GPR120 but
           not GPR40 in the liver of Obese Mice: A new anti-inflammatory approach
    • Abstract: Publication date: Available online 12 December 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Rafael Calais Gaspar, Camilla Bertuzzo Veiga, Mariana Pereira Bessi, Marcella Neves Dátilo, Marcella Ramos Sant'Ana, Patrícia Brito Rodrigues, Leandro Pereira de Moura, Adelino Sanchez Ramos da Silva, Gustavo Aparecido Santos, Rodrigo Ramos Catharino, Eduardo Rochete Ropelle, José Rodrigo Pauli, Dennys Esper Cintra GPR120 and GPR40 were recently reported as omega-3 (ω3) receptors with anti-inflammatory properties. Physical exercise could increase the expression of these receptors in the liver, improving hepatic metabolism in obesity and type 2 diabetes. Our aim was to investigate GPR120/40 in the liver of lean and obese mice after acute or chronic physical exercise, with or without the supplementation of ω3 rich flaxseed oil (FS), as well as assess the impact of exercise and FS on insulin signaling and inflammation. Mice were fed a high-fat diet (HF) for 4 weeks to induce obesity and subsequently subjected to exercise with or without FS, or FS alone. Insulin signaling, inflammatory markers and GPR120/40 and related cascades were measured. Chronic, but not acute, exercise and FS increased GPR120, but not GPR40, activating β-arrestin-2, and decreasing the inflammatory response, as well as reducing fat depots in liver and adipose tissue. Exercise or a source of ω3 led to a higher tolerance to fatigue, and an increased running distance and speed. The combination of physical exercise and ω3 food sources could provide a new strategy against obesity through the modulation of hepatic GPR120 and an increase in exercise performance.Graphical abstract(A) Pro-inflammatory cascades are induced by saturated fatty acids (SFA) or TNFα, through the receptors TLR4 and TNF-R, respectively. (B) The insulin signaling cascade is blocked by cytokines. (C) Exercise increases GPR120 gene expression and subsequent protein levels, and upon their activation by alpha-linolenic fatty acids (C18:3) inflammatory signaling is disrupted via βarrestin2 (β-arr2). IR-Insulin receptor. Y-Tyrosine. IRS1/2-Insulin receptor substrate 1 or 2. PI3K-Phosphatidyl inositol 3 kinase. Akt-Protein kinase B. DD-death domain. TNFα-Tumoral Necrosis Factor alpha. Tradd-death domain associated to TNF receptor. RIP-Receptor-interacting protein. TRAF2-Factor 2 associated to TNFα receptor. TLR4-Toll like receptor. Myd88- Myeloid differentiation primary response 88. TAK1-TGFβ activated kinase1. JNK-cJun N-terminal Kinase. IκK-Inhibitor kappa kinase. IκBα-NF-κB Inhibitor alpha. P50/P65-Protein 50/65. UB-Ubiquitin. NF-κB-Nuclear Factor kappa B.Unlabelled Image
       
  • A mix of dietary fermentable fibers improves lipids handling by the liver
           of overfed minipigs
    • Abstract: Publication date: Available online 8 December 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Ahmed Ben Mohamed, Didier Rémond, Christophe Chambon, Thierry Sayd, Michel Hebraud, Frédéric Capel, Benoit Cohade, Noureddine Hafnaoui, Daniel Béchet, Cécile Coudy-Gandilhon, Carole Migné, Jeremie David, Dominique Dardevet, Joel Doré, Sergio Polakof, Isabelle Savary-Auzeloux Obesity induced by overfeeding ultimately can lead to non-alcoholic fatty liver disease whereas dietary fiber consumption is known to have a beneficial effect. We aimed to determine if a supplementation of a mix of fibers (inulin, resistant starch and pectin) could limit or alleviate overfeeding-induced metabolic perturbations. Twenty female mini-pigs were fed with a control diet (C) or an enriched fat/sucrose diet supplemented (O + F) or not (O) with fibers. Between 0 and 56 days of overfeeding, insulin (+88%), HOMA (+102%), cholesterol (+45%) and lactate (+63%) were increased, without any beneficial effect of fibers supplementation. However, fibers supplementation limited body weight gain (vs O, −15% at D56) and the accumulation of hepatic lipids droplets induced by overfeeding. This could be explained by a decreased lipids transport potential (−50% FABP1 mRNA, O + F vs O) inducing a down regulation of regulatory elements of lipids metabolism / lipogenesis (−36% SREBP1c mRNA, O + F vs O) but not to an increased oxidation (O + F not different from O and C for proteins and mRNA measured). Glucose metabolism was also differentially regulated by fibers supplementation with an increased net hepatic release of glucose in the fasted state (diet x time effect, P
       
  • MicroRNA-103a regulates sodium-dependent vitamin C transporter-1
           expression in intestinal epithelial cells
    • Abstract: Publication date: Available online 7 December 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Veedamali S. Subramanian, Subrata Sabui, Jonathan S. Marchant, Hamid M. Said Intestinal absorption of ascorbic acid (AA) occurs via a Na+-dependent carrier-mediated process facilitated through the human sodium-dependent vitamin C transporters-1 &-2 (hSVCT1 and hSVCT2). Many studies have shown that hSVCT1 (product of the SLC23A1 gene) is expressed on the apical membrane of polarized enterocytes where it mediates AA absorption. hSVCT1 expression levels are therefore an important determinant of physiological vitamin C homeostasis. However, little is known about posttranscriptional mechanisms that regulate hSVCT1 expression in intestinal epithelia. In this study, we investigated regulation of hSVCT1 by microRNA (miRNA). A pmirGLO-SLC23A1–3’-UTR construct transfected into human intestinal cell lines (Caco-2 and NCM460 cells) showed markedly reduced luciferase activity. Bioinformatic analysis of the SLC23A1–3’-UTR predicted five miRNA binding sites (miR-103a, miR-107, miR-328, miR-384, and miR-499-5p) in the 3’-UTR. Expression of mature miR-103a was markedly higher compared to the other four putative miRNA regulators in both intestinal cell lines and mouse jejunal mucosa. Addition of a miR-103a mimic, but not a miR-103a mutant construct, markedly reduced the luminescence of the pmirGLO-SLC23A1–3’-UTR reporter. Reciprocally, addition of a miR-103a inhibitor significantly increased luciferase reporter activity. Addition of the miR-103a mimic led to a significant inhibition in AA uptake, associated with decreased hSVCT1 mRNA and protein expression in Caco-2 cells. In contrast, the miR-103a inhibitor increased AA uptake, associated with increased levels of hSVCT1 mRNA and protein. These findings provide the first evidence for posttranscriptional regulation of hSVCT1 by miRNA in intestinal epithelial cells.
       
  • Novel metabolic disturbances in marginal vitamin B6-deficient
           rat heart
    • Abstract: Publication date: Available online 4 December 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Thanutchaporn Kumrungsee, Dwi Eva Nirmagustina, Takeshi Arima, Kai Onishi, Kanako Sato, Norihisa Kato, Noriyuki Yanaka Vitamin B6 deficiency is associated with cardiovascular disease (CVD). Although plasma biomarkers have been proposed, no studies have yet directly profiled heart tissue and the mechanisms have to be fully defined. Thus, in order to provide better insight into vitamin B6-deficient effects on cardiac functions, we sought to identify the metabolic profile in heart tissue consequent to change in dietary vitamin B6 levels by applying metabolomics. Heart tissues of rats fed a basal diet containing a marginal vitamin B6-deficient, vitamin B6-recommended, or vitamin B6-supplemented level were analyzed by metabolomics analysis. Among over 500 detected metabolites, imidazole metabolites including carnosine, anserine, homocarnosine, and histamine exhibited the highest decrease upon vitamin B6 deficiency (>− 45%, P
       
  • Perinatal phthalate and high-fat diet exposure induce sex-specific changes
           in adipocyte size and DNA methylation
    • Abstract: Publication date: Available online 4 December 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Laura Moody, Daniel Kougias, Paul M. Jung, Isabel Digan, Aaron Hong, Aleksandra Gorski, Hong Chen, Janice Juraska, Yuan-Xiang Pan Environmental factors such as diet and endocrine-disrupting chemicals have individually been shown to mediate metabolic function. However, the underlying mechanism by which the combination disrupts adipocyte morphology and fat storage remains unknown. The current study evaluated early-life programming by diet and phthalate exposure. During gestation and lactation, pregnant Long-Evans hooded rat dams were fed either a control (C) or high fat (HF) diet and were orally administered one of three phthalate dosages (0, 200, or 1000 μg/kg/day), yielding 6 groups of offspring: C-0, C-200, C-1000, HF-0, HF-200, and HF-1000. On postnatal day (PND) 90, gonadal fat pads were collected and analyzed for histology, gene expression, and DNA methylation. Differences in body weight were observed only in males. H&E staining revealed larger adipocyte size in HF-0 versus C-0 females. Exposure to 200 or 1000 μg/kg/day phthalates modulated diet-induced changes in adipose morphology. Compared to C-0 females, HF-0 females also had higher expression of the adipogenesis gene Wnt receptor, frizzled 1 (Fzd1), and the triglyceride cleaving enzyme, lipoprotein lipase (Lpl). These increases in gene expression were accompanied by lower DNA methylation surrounding the transcription start sites of the two genes. Diet-driven effects were observed in unexposed females, but not in phthalate-treated rats. Results suggest a sex-specific association between perinatal HF diet and body weight, adipocyte size, and DNA methylation. Perinatal phthalate exposure appears to produce a phenotype that more closely resembles HF-fed animals.
       
  • Natural flavonoid galangin alleviates microglia-trigged blood-retinal
           barrier dysfunction during the development of diabetic retinopathy
    • Abstract: Publication date: Available online 4 December 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Tianyu Zhang, Xiyu Mei, Hao Ouyang, Bin Lu, Zengyang Yu, Zhengtao Wang, Lili Ji Hyperglycemia-induced blood-retinal barrier (BRB) breakdown is an early and typical event of diabetic retinopathy (DR). Although chronic inflammation plays an important role in DR development, the concrete mechanism remains unclear. This study aims to investigate the role of microglia cells-triggered inflammatory response in hyperglycemia-induced BRB breakdown and the amelioration of galangin, a natural flavonoid. Galangin alleviated BRB breakdown in streptozotocin (STZ)-induced diabetic mice. D-glucose (25 mM)-stimulated microglia BV2 cells induced BRB damage in vitro, but galangin reversed this injury. Galangin decreased the activation of microglia cells, ROS formation, the phosphorylation of extracellular regulated protein kinase (ERK)1/2, the transcriptional activation of nuclear factor κB (NFκB) and early growth response protein (Egr1), and the elevated expression of tumor necrosis factor (TNF)-α both in vitro and in vivo. ERK1/2 inhibitor U0126 reduced ROS formation, the activation of NFκB and Egr1, and the elevated TNFα expression in D-glucose-stimulated BV2 cells. N-acetyle-cysteine (NAC), a well-known antioxidant, abrogated D-glucose-induced NFκB and Egr1 activation in BV2 cells. Galangin also reversed the decreased expression of claudin1 and occludin, and the increased BRB injury and ROS formation in TNFα-treated human retinal endothelial cells (HRECs) and ARPE19 cells. Galangin induced the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) in both HRECs and ARPE19 cells. Moreover, the galangin-provided attenuation on BRB breakdown was diminished in Nrf2 knock-out diabetic mice. In conclusion, galangin alleviated DR by attenuating BRB damage via inhibiting microglia-triggered inflammation and further reversing TNFα-induced BRB dysfunction by abrogating oxidative stress injury via activating Nrf2.
       
  • Vitamin D produces a perilipin 2-dependent increase in mitochondrial
           function in C2C12 myotubes
    • Abstract: Publication date: Available online 22 November 2018Source: The Journal of Nutritional BiochemistryAuthor(s): David M. Schnell, R. Grace Walton, Hemendra J. Vekaria, Patrick G. Sullivan, Lance M. Bollinger, Charlotte A. Peterson, D. Travis Thomas Vitamin D has been connected with increased intramyocellular lipid (IMCL) and has also been shown to increase mitochondrial function and insulin sensitivity. Evidence suggests that perilipin 2 (PLIN2), a perilipin protein upregulated with calcitriol treatment, may be integral to managing increased IMCL capacity and lipid oxidation in skeletal muscle. Therefore, we hypothesized that PLIN2 is required for vitamin D induced IMCL accumulation and increased mitochondrial oxidative function. To address this hypothesis, we treated C2C12 myotubes with 100 nM calcitriol (the active form of vitamin D) and/or PLIN2 siRNA in a four group design and analyzed markers of IMCL accumulation and metabolism using qRT-PCR, cytochemistry, and oxygen consumption assay. Expression of PLIN2, but not PLIN3 or PLIN5 mRNA was increased with calcitriol, and PLIN2 induction was prevented with siRNA knockdown without compensation by other perilipins. PLIN2 knockdown did not appear to prevent lipid accumulation. Calcitriol treatment increased mRNA expression of triglyceride synthesizing genes DGAT1 and DGAT2 and also lipolytic genes ATGL and CGI-58. PLIN2 knockdown decreased the expression of CGI-58 and CPT1, and was required for calcitriol-induced upregulation of DGAT2. Calcitriol increased oxygen consumption rate while PLIN2 knockdown decreased oxygen consumption rate. PLIN2 was required for a calcitriol-induced increase in oxygen consumption driven by mitochondrial complex II. We conclude that calcitriol increases mitochondrial function in myotubes and that this increase is at least in part mediated by PLIN2.
       
  • 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.
       
  • 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
       
  • 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
       
 
 
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