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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  [3185 journals]
  • Apigenin ameliorates HFD-induced NAFLD through regulation of the XO/NLRP3
           pathways
    • Abstract: Publication date: Available online 14 June 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Yanan Lv, Xiaona Gao, Wentao Fan, Tongtong Shen, Chenchen Ding, Ming Yao, Suquan Song, Liping Yan Non-alcoholic fatty liver disease (NAFLD) is the most common cause of liver-related morbidity and mortality disease in the world. However, no effective pharmacological treatment for NAFLD has been found. In this study, we used a high fat diet (HFD)-induced NAFLD model to investigate hepatoprotective effect of apigenin (API) against NAFLD and further explored its potential mechanism. Our results demonstrated that gavage administration of API could mitigate HFD-induced liver injury, enhance insulin sensitivity and markedly reduce lipid accumulation in HFD-fed mice livers. In addition, histological analysis showed that hepatic steatosis and macrophages recruitment in the API treatment group were recovered compared with mice fed with HFD alone. Importantly, API could reverse the HFD-induced activation of the NLRP3 inflammasome, further reduced inflammatory cytokines IL-1β and IL-18 release, accompanied with the inhibition of xanthine oxidase (XO) activity and the reduction of uric acid and reactive oxygen species (ROS) production. The pharmacological role of API was further confirmed using free fatty acid (FFA) induced cell NAFLD model. Taking together, our results demonstrated that API could protect against HFD-induced NAFLD by ameliorating hepatic lipid accumulation and inflammation. These protective effects may be partially attributed to the regulation of XO by API, which further modulated NLRP3 inflammasome activation and inflammatory cytokines IL-1β and IL-18 release. Therefore API is a potential therapeutic agent for the prevention of NAFLD.Graphical abstractUnlabelled Image
       
  • Association between duration of obesity and severity of ovarian
           dysfunction in rat-cafeteria diet approach
    • Abstract: Publication date: Available online 10 June 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Saranya Kannan, Divya Srinivasan, Prasanth Balan Raghupathy, Ravi Sankar Bhaskaran Consumption of unhealthy, energy-dense palatable food during early age leads to obesity in children and the onset of obesity during childhood has a profound effect on the reproductive health of women. In this study, the mechanism underlying diet-induced obesity on ovarian dysfunction was studied by exposing rats to cafeteria diet (CAFD) for two different durations. For that purpose, 21-day-old female Sprague Dawley rats were fed ad libitum with a standard diet (control group) and a cafeteria diet (CAFD group) for a period of 20 weeks (20 W) and 32 weeks (32 W). We observed obesity, hyperglycemia, hyperlipidemia, hyperleptinemia and hypoadiponectinemia in CAFD fed groups. Hyperinsulinemia, hypergonadotrophism, hypertestosteronemia and hyperprogesteronemia were observed in the 20 W-CAFD group. Conversely, in the 32 W-CAFD group hypersecretion declined to hyposecretion. The levels of estradiol remained low during both time periods. The duration of estrous cycle was extended in the CAFD fed rats. The ovary weight was higher in the 20 W-CAFD fed rats but it was drastically reduced over a longer duration cafeteria diet feeding. In the 20 W-CAFD fed rats, the protein levels of LHR, StAR, CYP11A1, 3β-HSD and 17β-HSD were increased but FSHR and CYP19A1 levels were decreased in the ovary. On the other hand, gonadotropin receptor and the protein levels of steroidogenic enzymes were decreased in the ovary of 32 W-CAFD fed rats. We conclude that the duration of energy-dense diet consumption has differential regulatory mechanism in altering the ovarian steroid production. In 20 W-CAFD fed rats, hypergonadotropic condition was observed whereas, 32 W-CAFD consumption induced hypogonadotropic hypogonadism.
       
  • Fructose-induced AGEs-RAGE signaling in skeletal muscle contributes to
           impairment of glucose homeostasis
    • Abstract: Publication date: Available online 8 June 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Amit K. Rai, Natasha Jaiswal, Chandan K. Maurya, Aditya Sharma, Ishbal Ahmad, Shadab Ahmad, Anand P. Gupta, Jiaur R. Gayen, Akhilesh K. Tamrakar Increased fructose intake has been linked to the development of dyslipidemia, obesity and impaired glucose tolerance. Due to its specific metabolic fate, fructose impairs normal lipid and carbohydrate metabolism and facilitates the non-enzymatic glycation reaction leading to enhanced accumulation of advanced glycation end products (AGEs). However, the formation of fructose-AGEs under in vivo setup and its tissue specific accumulation is less explored. Here, we investigated the impact of high fructose on AGEs accumulation in skeletal muscle and its causal role in impaired glucose homeostasis. In L6 rat skeletal muscle cells, chronic exposure to fructose induced AGEs accumulation and the cellular level of the receptor for AGEs (RAGE) and the effect was prevented by pharmacological inhibition of glycation. Under in vivo settings, Sprague Dawley rats exposed to 20% fructose in drinking water for 16 weeks, displayed increased fasting glycemia, impaired glucose tolerance, decreased skeletal muscle Akt (Ser-473) phosphorylation, and enhanced triglyceride levels in serum, liver and gastrocnemius muscle. We also observed a high level of AGEs in serum and gastrocnemius muscle of fructose-supplemented animals, associated with methylglyoxal accumulation and up regulated expression of RAGE in gastrocnemius muscle. Treatment with aminoguanidine inhibited fructose-induced AGEs accumulation and normalized the expression of RAGE and Dolichyl-Diphosphooligosaccharide-Protein Glycosyltransferase (DDOST) in gastrocnemius muscle. Inhibition of AGEs-RAGE axis counteracted fructose-mediated glucose intolerance without affecting energy metabolism. These data reveal diet-derived AGEs accumulation in skeletal muscle and the implication of tissue specific AGEs in metabolic derangement, that may opens new perspectives in pathogenic mechanisms and management of metabolic diseases.
       
  • Fructose increases the activity of sodium hydrogen exchanger in renal
           proximal tubules that is dependent on Ketohexokinase
    • Abstract: Publication date: Available online 8 June 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Takahiro Hayasaki, Takuji Ishimoto, Tomohito Doke, Akiyoshi Hirayama, Tomoyoshi Soga, Kazuhiro Furuhashi, Noritoshi Kato, Tomoki Kosugi, Naotake Tsuboi, Miguel A. Lanaspa, Richard J. Johnson, Shoichi Maruyama, Kenji Kadomatsu High fructose intake has been known to induce metabolic syndrome in laboratory animals and humans. Although fructose intake enhances sodium reabsorption and elevates blood pressure, role of fructose metabolism in this process has not been studied. Here we show that by ketohexokinase—the primary enzyme of fructose—is involved in regulation of renal sodium reabsorption and blood pressure via activation of the sodium hydrogen exchanger in renal proximal tubular cells. First, wild-type and ketohexokinase knockout mice (Male, C57BL/6) were fed fructose water or tap water with or without a high salt diet. Only wild type mice fed the combination of fructose water and high salt diet displayed increased systolic blood pressure and decreased urinary sodium excretion. In contrast, ketohexokinase knockout mice were protected. Second, urinary sodium excretion after intraperitoneal saline administration was reduced with the decreased phosphorylation of sodium hydrogen exchanger 3 in fructose-fed WT; these changes were not observed in the ketohexokinase knockout mice, however. Third, knockdown of ketohexokinase attenuated fructose-mediated increases of NHE activity with decreased cAMP levels in porcine renal proximal tubular cells (LLC-PK1). In conclusion, fructose metabolism by ketohexokinase increases sodium hydrogen exchanger activity in renal proximal tubular cells via decreased intracellular cAMP level, resulting in increased renal sodium reabsorption and blood pressure in mice.
       
  • 1-Deoxynojirimycin improves high fat diet-induced nonalcoholic
           steatohepatitis by restoring gut dysbiosis
    • Abstract: Publication date: Available online 8 June 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Junping Zheng, Lin Zhu, Baifei Hu, Xiaojuan Zou, Haiming Hu, Zhigang Zhang, Nan Jiang, Jun Ma, Huabing Yang, Hongtao Liu Non-alcoholic steatohepatitis (NASH) is associated with chronic inflammation and gut bacterial dysbiosis. Studies show that 1-deoxynojirimycin (DNJ) may improve NASH, yet the role of gut microbiota in protective effect of DNJ on NASH remains to be known. In present study, we aimed to examine how DNJ ameliorated high-fat diet (HFD)-induced mouse NASH through the regulation of gut microbiota dysbiosis. C57BL/6 J mice fed with HFD were treated with DNJ (0.1 mg/mL, in drinking water) for four months. The results by using histochemical staining and qPCR confirmed that DNJ remarkably modulated glucose intolerance and hyperlipidemia, attenuated hepatic steatosis and systemic chronic inflammation in HFD-induced mice. Moreover, DNJ greatly reshaped the structure of disbalanced intestinal flora, as indicated by the enhanced bacterial richness and diversity, the decreased Firmicutes-to-Bacteroidetess ratio and the increased Akkermansia level. The prediction algorithm suggests that DNJ may extensively dampen the bacterial motility and bacterial energy metabolism. Consistently, the altered gut microbiota was closely correlated with metabolic biomarkers of mice with NASH. Based on our studies, DNJ could alleviate the progress of HFD-induced NASH by rebuilding the gut microbial community structure, suggesting that DNJ may serve as a functional food to prevent or treat NASH clinically.Graphical abstractUnlabelled Image
       
  • Impact of maternal overweight on the sexual maturity of male offspring in
           rats
    • Abstract: Publication date: Available online 7 June 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Rocío Alejandra Galarza, Eric Alejandro Rhon-Calderón, Marianne Bizzozero, María Agustina Meneghini, Analía Elisabeth Cortez, Victoria Adela Lux-Lantos, Alicia Graciela Faletti
       
  • Gamma-glutamyl carboxylated Gas6 mediates the beneficial effect of vitamin
           K on lowering hyperlipidemia via regulating the AMPK/SREBP1/PPARĪ±
           signaling cascade of lipid metabolism
    • Abstract: Publication date: Available online 25 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Jijnasa Bordoloi, Dibyajyoti Ozah, Thaneswar Bora, Jatin Kalita, Prasenjit Manna The present study for the first time aims to examine the hypothesis that circulating gamma-glutamyl carboxylated growth arrest specific protein 6 (Gla-Gas6) deficiency may be associated with hyperlipidemia and vitamin K (VK) supplementation may ameliorate the impaired lipid homeostasis via activating Gas6 protein. Subjects with hyperlipidemia (n=22) and age-matched healthy controls (n=19) were included in this study. Results showed that plasma levels of Gla-Gas6 protein and VK were significantly lower in hyperlipidemic subjects compared to control. Moreover, Gla-Gas6 levels were significantly and positively correlated with VK (P=.034, r=0.452) and negatively with triglyceride (P=.022, r=−0.485) and total cholesterol (P=.043, r=−0.435) in hyperlipidemic subjects, which suggests that VK supplementation may have a positive effect in activating Gas6 protein and thereby reducing the aberrant plasma lipid levels. Further studies with high fat diet (HFD)-fed animal model of hyperlipidemia demonstrated that VK supplementation (5 μg/kg BW, 8 wks) reduced the plasma lipid levels, stimulated both the plasma levels and the hepatic protein expression of Gla-Gas6 protein, and regulated the AMPK/SREBP1/PPARα signaling pathways of hepatic lipid metabolism in HFD-fed mice. Moreover, by using palmitic acid (PA, 0.75 mM)-treated both control and GGCX knockdown hepatocytes, this study dissected the direct role of Gla-Gas6 in mediating the positive effect of VK on preventing the PA-induced impaired hepatic lipid metabolism via regulating AMPK/SREBP1/PPARα pathways. Combining all, the present study demonstrated the beneficial effect of VK supplementation in preventing the impaired lipid homeostasis via activating VK-dependent Gas6 protein.
       
  • Maternal folic acid supplementation modulates the growth performance,
           muscle development and immunity of Hu sheep offspring of different litter
           size
    • Abstract: Publication date: Available online 25 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Bo Wang, Heqiong Li, Zhen Li, Luyang Jian, Yuefeng Gao, Yanghua Qu, Ce Liu, Chenchen Xu, Yuxia Li, Zhicheng Diao, Wei Lu, Ying Yu, Zoltan Machaty, Hailing Luo It is generally accepted that the phenotype and gene expression pattern of the offspring can be altered by maternal folic acid (FA) supplementation during the gestation period. The aims of this study were to investigate the effects of maternal FA supplementation on the growth performance, muscle development and immunity of newborn lambs of different litter size. According to litter size (twins, TW; triplets, TR) and maternal dietary FA supplementation levels (control, C; 16 or 32 mg·kg−1 FA supplementation, F16 and F32), neonatal lambs were randomly divided into six groups (TW-C, TW-F16, TW-F32, TR-C, TR-F16 and TR-F32). After farrowing, the birth weight in TW was higher than TR group, and increased with FA supplementation of their mothers (P
       
  • Browning is activated in the subcutaneous white adipose tissue of mice
           metabolically challenged with a high-fructose diet submitted to
           high-intensity interval training
    • Abstract: Publication date: Available online 25 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Victor F. Motta, Thereza L. Bargut, Vanessa Souza-Mello, Marcia B. Aguila, Carlos A. Mandarim-de-Lacerda Fructose may induce an endocrine dysfunction in adipose tissue in rodents. Browning is identified by deposits of beige adipocytes in subcutaneous white adipose tissue (sWAT). We study the effects of the high-intensity interval training (HIIT) on the formation of beige adipocytes in the sWAT of mice fed a high-fructose diet. Sixty male mice, three months old (C57BL/6) were fed two diets for 18 weeks (n=30 each): control diet (C), or high-fructose diet (F). At the 10th week, for an additional eight-week period the groups were (n=15 each): non-trained (NT) or trained (HIIT): C-NT, C-HIIT, F-NT, and F-HIIT. We evaluated body mass (BM), energy expenditure (EE), and molecular analyses for browning and thermogenic markers in sWAT. The HIIT groups showed significantly lower BM and increased EE. The consumption of fructose was linked with an increased sWAT mass. However, HIIT caused a reduction of sWAT mass compared to the NT-groups. Energy intake was parallel in the groups, regardless of the diet type and HIIT. Fructose was related to higher glucose and insulin levels and hypertrophied sWAT adipocytes, but HIIT decreased both glucose and insulin levels and led to the appearance of brown fat-like adipocytes dispersed in sWAT with higher expression of browning markers. Also, fructose reduced the sWAT markers of mitochondrial biogenesis and beta-oxidation, which were enhanced by HIIT. In conclusion, HIIT might stimulate the sWAT browning in mice fed a high-fructose diet associated with beneficial changes in mitochondrial biogenesis and beta-oxidation markers, contributing to a whole-body metabolic improvement.
       
  • VD3 mitigates breast cancer aggressiveness by targeting
           V-H+-ATPase
    • Abstract: Publication date: Available online 25 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Julianna M. Santos, Fazle Hussain Low Vitamin D levels increase the risk of developing several cancer types including breast cancer. Breast cancer is the most incident cancer among women worldwide and in the US. Our previous study showed that Vitamin D (VD3) decreases breast cancer aggressiveness by inhibiting mammalian target of rapamycin (mTOR). However, the full mechanism underlying VD3 effects in breast cancer, including some activators of mTORC1, is yet to be explored. Metastatic cancer cells overexpress the V-H+-ATPase proton pump at the plasma membrane to maintain the optimal pH to sustain cancer growth promoting their own invasion and metastasis by acidifying the extracellular environment. Among its other roles, V-H+-ATPase overexpression and activity are associated with high glycolytic flux, mTORC1 activation, and hypoxia. V-H+-ATPase's role in mTORC1 activation and glycolytic metabolism supports our hypothesis that VD3, a non-toxic and widely used compound, inhibits the proton pump resulting in a significant decrease in cancer aggressiveness. VD3 and the specific inhibitor Bafilomycin A1 (positive control) profoundly inhibit V-H+-ATPase function and expression. Highly metastatic MB231 has more pronounced effects (high extracellular pH, low migration speed, and changes in cell mechanics) than lowly metastatic MCF-7 due to the higher expression of V-H+-ATPase, that drives the more aggressive phenotype. Our data show, for the first time, that VD3 strongly inhibited V-H+-ATPase function and expression in breast cancer cells – thereby suggesting its use as a possible therapeutic agent.
       
  • Oral L-glutamine pre-treatment attenuates skeletal muscle atrophy induced
           by 24h-fasting in mice
    • Abstract: Publication date: Available online 25 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Diogo Antonio Alves de Vasconcelos, Pieter Giesbertz, Diego Ribeiro de Souza, Kaio Fernando Vitzel, Phablo Sávio Abreu, Gabriel Nasri Marzuca-Nassr, Marco Aurélio Salomão Fortes, Gilson Masahiro Murata, Sandro Massao Hirabara, Rui Curi, Hannelore Daniel, Tania Cristina Pithon-Curi L-Glutamine (L-Gln) supplementation has been pointed out as an anticatabolic intervention but its effects on protein synthesis and degradation signaling in skeketal muscle are still poorly known. The effects of L-Gln pre-treatment (1 g.kg-1.day-1 body weight for ten days) on muscle fiber cross-sectional area (CSA), amino acid composition (measured by LC-MS/MS) and protein synthesis (Akt-mTOR) and degradation (ubiquitin ligases) signaling in soleus and Extensor Digitorum Longus (EDL) muscles in 24-h fasted mice were investigated. The fiber CSA of EDL muscle was not different between the L-Gln fasted and L-Gln fed groups. This finding was associated with reduced contents of L-Leu and L-Iso and activation of protein synthesis signaling (p-RPS6Ser240/244 and Akt-mTOR). The spectrum of soleus muscle fiber CSA distribution was larger in L-Gln fasted as compared with placebo fasted mice. This effect of L-Gln pre-treatment was associated with changes in red fibers L-Gln metabolism as indicated by increased intracellular L-glutamine/L-glutamate ratio, L-aspartate, and GABA levels. L-Gln supplementation reduced fasting-induced mass loss in tibialis anterior and gastrocnemius muscles. Evidence is presented that pre-treatment with L-glutamine attenuates skeletal muscle atrophy induced by 24 h fasting through mechanisms that vary with the muscle fiber type.
       
  • Piperine attenuates cognitive impairment in an experimental mouse model of
           sporadic Alzheimer's disease
    • Abstract: Publication date: Available online 24 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Che Wang, Zhengxu Cai, Wei Wang, Min Wei, Daqing Kou, Tianbai Li, Zhaofei Yang, Huishu Guo, Weidong Le, Song Li Piperine, the major alkaloid constituent of black pepper, has been reported to possess a wide range of pharmacological effects on the central nervous system, including antidepressant, anticonvulsant and anti-ischemic activities. In the present study, we aimed to investigate the therapeutic potential and neuroprotective mechanisms of piperine in an experimental mouse model of sporadic Alzheimer's disease (sAD) induced by intracerebroventricular (ICV) infusion of streptozotocin (STZ). STZ was infused bilaterally at a dose of 1.5 mg/kg/day on day 1 and day 3. From day 8, piperine (2.5–10 mg/kg body weight) was administered intraperitoneally once daily for 15 consecutive days. The locomotor activity and cognitive performance of mice were evaluated using open field test and Morris water maze test, respectively. On day 23, all animals were sacrificed and the hippocampus was used for biochemical, neurochemical, and neuroinflammatory determinations. Our data revealed that the ICV-STZ-infused sAD mouse showed an increased oxidative-nitrosative stress, an altered neurotransmission, and an elevated neuroinflammation in hippocampus, as well as significant cognitive deficits. All these alterations can be ameliorated by piperine in a dose-dependent manner. In summary, our findings predict a therapeutic potential of piperine against cognitive deficits in sAD mouse. This effect might be due to its abilities to ameliorate oxidative-nitrosative stress, restore neurotransmission, and reduce neuroinflammation.
       
  • Dietary polyunsaturated fatty acids modulates adipose Secretome and is
           associated with changes in mammary epithelial stem cell self-renewal
    • Abstract: Publication date: Available online 24 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Evan M. Hill, Raymond M. Esper, Ananda Sen, Becky R. Simon, Muhammad N. Aslam, Yan Jiang, Michael K. Dame, Shannon D. McClintock, Justin A. Colacino, Zora Djuric, Max S. Wicha, William L. Smith, Dean E. Brenner Chronic low-grade adipose inflammation, characterized by aberrant adipokine production and pro-inflammatory macrophage activation/polarization is associated with increased risk of breast cancer. Adipocyte fatty acid composition is influenced by dietary availability and may regulate adipokine secretion and adipose inflammation. After feeding F344 rats for 20 weeks with a western diet or a fish oil supplemented diet, we cultured primary rat adipose tissue in a 3-dimensional explant culture and collected the conditioned medium. The rat adipose tissue secretome was assayed using the Proteome Profiler Cytokine XL Array and adipose tissue macrophage polarization (M1/M2 ratio) was assessed using the iNOS/ARG1 ratio. We then assessed the adipokine's effects upon stem cell self-renewal using primary human mammospheres from normal breast mammoplasty tissue. Adipose from rats fed the fish oil diet had an ω-3:ω-6 fatty acid ratio of 0.28 compared to 0.04 in western diet rats. The adipokine profile from the fish oil-fed rats was shifted towards adipokines associated with reduced inflammation compared to the rats fed the western diet. The M1/M2 macrophage ratio decreased by 50% in adipose of fish oil fed rats compared to that from rats fed the Western diet. Conditioned media from rats fed the high ω-6 western diet increased stem cell self-renewal by 62±9% (X¯% ± SD) above baseline compared to only an 11±11% increase with the fish oil rat adipose. Modulating the adipokine secretome with dietary interventions therefore may alter stromal-epithelial signaling that plays a role in controlling mammary stem cell self-renewal.
       
  • Cyp2b-null male mice are susceptible to diet-induced obesity and
           perturbations in lipid homeostasis
    • Abstract: Publication date: Available online 21 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Melissa M Heintz, Ramiya Kumar, Meredith M Rutledge, William S. Baldwin Obesity is an endemic problem in the United States and elsewhere, and data indicate that in addition to overconsumption, exposure to specific chemicals enhances obesity. CYP2B metabolizes multiple endo- and xenobiotics, and recent data suggests that repression of Cyp2b activity increases dyslipidemia and age-onset obesity, especially in males. To investigate the role played by Cyp2b in lipid homeostasis and obesity, we treated wildtype and Cyp2b-null mice with a normal (ND) or 60% high-fat diet (HFD) for 10 weeks and determined metabolic and molecular changes. Male HFD-fed Cyp2b-null mice weigh 15% more than HFD-fed wildtype mice, primarily due to an increase in white adipose tissue (WAT); however, Cyp2b-null female mice did not demonstrate greater body mass or WAT. Serum parameters indicate increased ketosis, leptin and cholesterol in HFD-fed Cyp2b-null male mice compared to HFD-fed wildtype mice. Liver triglycerides and liver:serum triglyceride ratios were higher than their similarly treated wildtype counterparts in Cyp2b-null male mice, indicating a role for Cyp2b in fatty acid metabolism regardless of diet. Furthermore, RNAseq demonstrates that hepatic gene expression in ND-fed Cyp2b-null male mice is similar to HFD-fed WT male mice, suggestive of fatty liver disease progression and a role for Cyp2b in lipid homeostasis. Females did not show as demonstrative changes in liver health, and significantly fewer changes in gene expression, as well as gene expression associated with liver disease. Overall our data indicates that the repression or inhibition of CYP2B may exacerbate metabolic disorders and cause obesity by perturbing fatty acid metabolism, especially in males.Graphical abstractUnlabelled Image
       
  • Naringenin ameliorates progression of endometriosis by modulating
           Nrf2/Keap1/ HO1 axis and inducing apoptosis in rats
    • Abstract: Publication date: Available online 21 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Radhika Kapoor, Vijay Kumar Sirohi, Kanchan Gupta, Anila Dwivedi Endometriosis is mainly characterized by the presence of endometrial tissue exterior to the uterus, however the exact pathophysiology of this disease still remains uncertain. Moreover, the incidence significantly contributes to infertility among women and hence, a novel treatment for endometriosis is widely investigated. Naringenin is a plant-derived flavonoid having anti-proliferative, anti-inflammatory, and anti-angiogenic properties in chronic and metabolic diseases. The study was planned with an objective to demonstrate the anti-endometriotic therapeutic potential of naringenin in rats and to examine its impact on various cellular aspects with a view to define the mechanism involved. The endometrial implant volumes, weight, TNF-α level in serum and the histopathologic scores were significantly reduced in the naringenin treated group as compared to the endometriotic control group. Naringenin ameliorated the expression of prognostic markers (TAK1, PAK1, VEGF and PCNA) involved in development and progression of endometriotic cells. Naringenin caused dose-dependent loss of mitochondrial membrane potential, induced apoptosis and inhibited proliferation in these cells. Further, a significant increase in level of Nrf2 and its downstream molecules (NQO1, HO-1) was found in endometriotic lesion, with a subsequent decrease in its repressor molecule Keap-1. Naringenin significantly modulated the expression of Nrf2 and its effector molecules downstream. It also inhibited the invasion of endometrial cells by inhibiting the expression of MMP-2 and MMP-9 in in-vitro primary culture. We conclude that naringenin may have a therapeutic potential in the treatment of endometriosis via induction of ROS-mediated apoptosis and its anti-invasive effects.
       
  • Ginger prevents obesity through regulation of energy metabolism and
           activation of browning in high-fat diet-induced obese mice
    • Abstract: Publication date: Available online 21 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Jing Wang, Daotong Li, Pan Wang, Xiaosong Hu, Fang Chen Numerous natural herbs have been proven as safe anti-obesity resources. Ginger, one of the most widely consumed spices, has shown beneficial effects against obesity and related metabolic disorders. The present study aimed to examine whether the antiobesity effect of ginger is associated with energy metabolism. Mice were maintained on either a normal control diet or a high-fat diet (HFD) with or without 500 mg/kg (w/w) ginger supplementation. After 16 weeks, ginger supplementation alleviated the HFD-induced increases in body weight, fat accumulation, and levels of serum glucose, triglyceride and cholesterol. Indirect calorimetry showed that ginger administration significantly increased the respiratory exchange ratio (RER) and heat production in both diet models. Furthermore, ginger administration corrected the HFD-induced changes in concentrations of intermediates in glycolysis and the TCA cycle. Moreover, ginger enhanced brown adipose tissue function and activated white adipose tissue browning by altering the gene expression and protein levels of some brown and beige adipocyte-selective markers. Additionally, stimulation of the browning program by ginger may be partly regulated by the sirtuin-1 (SIRT1)/AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) pathway. Taken together, these results indicate that dietary ginger prevents body weight gain by remodeling whole-body energy metabolism and inducing browning of white adipose tissue (WAT). Thus, ginger is an edible plant that plays a role in the therapeutic treatment of obesity and related disorders.
       
  • Riboflavin deficiency affects lipid metabolism partly by reducing
           apolipoprotein B100 synthesis in rats
    • Abstract: Publication date: Available online 14 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Xiangyu Bian, Weina Gao, Yawen Wang, Zhanxin Yao, Qingao Xu, Changjiang Guo, Bailin Li Lipid metabolism is dependent on riboflavin status. Apolipoprotein B100 plays an important role in lipids transportation. This study was aimed to investigate the effect of riboflavin status on lipid metabolism and explore its association with apolipoprotein B100 synthesis in vivo. Riboflavin deficiency was developed in rats by feeding riboflavin-deficient diets. Compared to the control rats, the mRNA and protein expressions of apolipoprotein B100 were significantly reduced in riboflavin-deficient rats. Endoplasmic reticulum oxidoreductin 1 (ERO1) and protein disulfide isomerase (PDI), two enzymes involved in the oxidative folding of apolipoprotein B100, were also lowered remarkably in expression at protein level. Meanwhile, total cholesterol and triglyceride levels were decreased in the plasma and increased in the liver of riboflavin-deficient rats. The plasma very low-density lipoprotein cholesterol (VLDL-c) and low-density lipoprotein cholesterol (LDL-c) were also reduced in riboflavin-deficient rats. Our findings demonstrate that riboflavin deficiency affects lipid metabolism partly by reducing apolipoprotein B100 synthesis.Graphical abstractUnlabelled Image
       
  • Ascorbic acid deficiency increases hepatic expression of acute phase
           proteins through the intestine-derived IL-6 and hepatic STAT3 pathway in
           ODS rats
    • Abstract: Publication date: Available online 14 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Noe Kawade, Atsushi Murai, Wakana Suzuki, Yuki Tokuda, Misato Kobayashi, Fumihiko Horio We have previously shown that ascorbic acid (AsA) deficiency elevates hepatic expression of acute phase proteins (APPs), inflammatory markers, in Osteogenic Disorder Shionogi (ODS) rats, which are unable to synthesize AsA. However, the precise mechanisms of this elevation are unknown. Signal transducer and activator of transcription 3 (STAT3) is one of the transcription factors inducing the expression of APPs and is activated by several cytokines including interleukin-6 (IL-6). The aim of this study was to determine whether AsA deficiency stimulates hepatic STAT3 activation and increases intestinal production of proinflammatory cytokines such as IL-6. Male ODS rats (six weeks old) were fed either a basal diet containing 300 mg AsA/kg (control group) or an AsA-free diet (AsA-deficient group) for 18 days. AsA deficiency gradually and simultaneously elevated both mRNA levels of APPs (haptoglobin, α1-acid glycoprotein, C-reactive protein and α2-macroglobulin) and nuclear level of phosphorylated STAT3 (activated STAT3) in the liver. These results showed that the AsA deficiency-induced expression of hepatic APPs is stimulated by proinflammatory cytokines activating STAT3. On day 14, AsA deficiency significantly elevated IL-6 mRNA level in the ileum and the concentration of IL-6 in portal blood. Furthermore, the portal concentration of IL-6 positively correlated with hepatic mRNA levels of STAT3-regulated genes. These findings suggest that IL-6, produced in the intestine as a result of AsA deficiency, is recruited to the liver via the portal vein and contributes to hepatic STAT3 activation and the elevated expression of APPs.Graphical abstractUnlabelled Image
       
  • A genetic epidemiological study in British adults and older adults shows a
           high heritability of the combined indicator of vitamin B12 status (cB12)
           and connects B12 status with utilisation of mitochondrial substrates and
           energy metabolism.
    • Abstract: Publication date: Available online 14 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Anupriya Dalmia, Marie-Joe Dib, Hannah Maude, Dominic J Harrington, Agata Sobczyńska-Malefora, Toby Andrew, Kourosh R Ahmadi Vitamin B12 deficiency is common among older adults. However, the most commonly used marker of deficiency, total serum vitamin B12 (B12), is not sensitive enough to diagnose true deficiency in a significant proportion of the population. The combined indicator of B12 status (cB12), formulated as a composite score of various biomarkers of vitamin B12 status (which also accounts for low folate status and age) has been shown to offer a more robust and powerful test to diagnose B12 deficiency.There are no epidemiological studies of cB12 variability in older adults. We carried out a twin study to characterise the relative contribution of heritable (h2) and environmental factors to the observed variability in cB12 score in an adult and older adult population (n=378). Furthermore, we tested for association between variability in cB12 and candidate polymorphisms and genes previously associated with B12 biomarker levels characterised in-silico the mechanism linking the genetic variants and cB12 variability.We found the variability in cB12 and its constituents to be highly heritable (h2=55%–64%). The SNP rs291466 in HIBCH, previously associated with variation in MMA, was significantly associated with cB12 (R2=5% P=5E-04). Furthermore, variants in MTRR, MMAB, and MUT, underlying inborn errors of B12 metabolism, were nominally associated with variation in cB12. Pathway accompanied by expression quantitative trait loci (eQTL) analysis revealed that HIBCH rs291466 influences the concentration of MMA via the valine degradation pathway.Our study provides etiological insight into how B12 deficiency can manifest into impaired mitochondrial function through perturbations in mitochondrial “fuel” usage.
       
  • Dietary patterns influence Epicardial adipose tissue fatty acid
           composition and inflammatory gene expression in the Ossabaw pig
    • Abstract: Publication date: Available online 14 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Maura E. Walker, Nirupa R. Matthan, Audrey Goldbaum, Huicui Meng, Stefania Lamon-Fava, Sukla Lakshman, Saebyeol Jang, Aleksey Molokin, Gloria Solano-Aguilar, Joseph F. Urban, Alice H. Lichtenstein Epicardial adipose tissue (EAT) inflammation is implicated in the development and progression of coronary atherosclerosis. Dietary saturated and polyunsaturated fatty acids (SFAs and PUFA) can influence adipose tissue inflammation. We investigated the influence of dietary patterns, with emphasis on dietary fat type, and statin therapy, on EAT fatty acid (FA) composition and inflammatory gene expression. Thirty-two Ossabaw pigs were fed isocaloric amounts of a Heart Healthy (high in unsaturated fat) or Western (high in saturated fat) diets +/− atorvastatin for 6 months. EAT FA composition reflected dietary fat composition. There was no significant effect of atorvastatin on EAT FA composition. Total and long-chain SFAs were positively associated with inflammatory signaling (TLR2) and a gene involved in lipid mediator biosynthesis (PTGS2) (P
       
  • Vitamin D intervention does not improve vascular regeneration in
           diet-induced obese male mice with peripheral ischemia
    • Abstract: Publication date: Available online 10 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Kia M. Peters, Richard Zhang, Chanho Park, Zengxuan Nong, Hao Yin, Rachel B. Wilson, Brian G. Sutherland, Cynthia G. Sawyez, J. Geoffrey Pickering, Nica M. Borradaile Vitamin D appears to either promote or inhibit neovascularization in a disease context-dependent manner. The effects of vitamin D, alone or in combination with niacin, on endothelial cell (EC) angiogenic function, and on revascularization in obese animals with peripheral ischemia are unknown. Here, we report that supplementation of high palmitate medium with vitamin D, niacin, or both vitamins, increased EC tube formation, which relies primarily on cell migration, and also maintained tube stability over time. Transcriptomic analyses revealed that both vitamins increased stress response and anti-inflammatory gene expression. However, vitamin D decreased cell cycle gene expression and inhibited proliferation, while niacin induced stable expression of miR-126-3p and -5p, and maintained cell proliferation in high palmitate. To assess vascular regeneration, diet-induced obese mice received vitamin D, niacin, or both vitamins following hind limb ischemic injury. Niacin, but not vitamin D or combined treatment, improved recovery of hind limb use. Histology of tibialis anterior sections revealed no improvements in revascularization, regeneration, inflammation, or fibrosis with vitamin D or combined treatment. In summary, although both vitamin D and niacin increased angiogenic function of EC cultures in high fat, only niacin improved recovery of hind limb use following ischemic injury in obese mice. It is possible that inhibition of cell proliferation by vitamin D in high fat conditions limits vascular regeneration and recovery from peripheral ischemia in obesity.
       
  • Navy bean supplemented high fat diet improves intestinal health,
           epithelial barrier integrity and critical aspects of the obese
           inflammatory phenotype
    • Abstract: Publication date: Available online 10 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Jennifer M. Monk, Wenqing Wu, Dion Lepp, Hannah R. Wellings, Amber L. Hutchinson, Danyelle M. Liddle, Daniela Graf, K. Peter Pauls, Lindsay E. Robinson, Krista A. Power Obesity is associated with impaired intestinal epithelial barrier function and an altered microbiota community structure, which contribute to host systemic inflammation and metabolic dysfunction. Fiber-rich common beans (Phaseolus vulgaris) promote intestinal health (microbiota and host epithelial barrier integrity) in lean mice. The objective was to assess the gut health promoting effects of navy bean supplementation during high fat diet-induced obesity. Male C57BL/6 mice were fed either a high fat diet (HF, 60% fat as kcal) or an isocaloric HF supplemented with 15.7% (by weight) cooked navy bean powder (HF + B) for 12 weeks. Compared to HF, the HF + B diet altered the fecal microbiota community structure (16S rRNA gene sequencing), most notably increasing abundance of Akkermansia muciniphila (+19-fold), whose abundance typically decreases in obese humans and rodents. Additionally, HF + B fecal abundance of carbohydrate fermenting, short chain fatty acid (SCFA) producing Prevotella (+332-fold) and S24–7 (+1.6-fold) and fecal SCFA levels were increased. HF + B improved intestinal health and epithelial barrier integrity versus HF, evidenced by reduced serum fluorescein isothiocyanate (FITC)-dextran concentration in an in vivo gut permeability test, and increased intestinal mRNA expression of tight junction components (ZO-1, occludin), anti-microbial defenses (Reg3γ, IgA, Defα5, Defβ2) and mucins (Muc2). Additionally, HF + B improved the systemic obese phenotype via reduced serum HOMA-IR and leptin:adiponectin ratio, and locally via attenuation of epididymal adipose tissue crown-like structure formation, adipocyte size, and inflammatory transcription factor (NFκBp65 and STAT3) activation. Therefore, HF + B improved obese intestinal health (microbiota and epithelial barrier integrity) and attenuated the severity of the obese phenotype.
       
  • Insufficient zinc intake enhances lung inflammation in response to
           agricultural organic dust exposure.
    • Abstract: Publication date: Available online 3 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Daren L. Knoell, Deandra A. Smith, Muna Sapkota, Art J. Heires, Corrine K. Hanson, Lynette M. Smith, Jill A. Poole, Todd A. Wyatt, Debra J. Romberger Organic dust exposure particularly within hog confinement facilities is a significant cause of airway inflammation and lung disease. In a cohort of Midwestern veterans with COPD and agricultural work exposure we observed reduced zinc intakes which was associated with decreased lung function. Because insufficient zinc intake is common within the U.S. and a potent modulator of innate immune function, we sought to determine whether deficits in zinc intake would impact the airway inflammatory response to hog confinement facility dust extract (HDE). Adult male C57BL/6 mice were randomized to zinc deficient or matched zinc sufficient diets for 3 weeks and subsequently treated with intranasal HDE inhalation or saline once or daily for 3 weeks while maintained on specific diets. Lavage fluid and lung tissue was collected. Conditions of zinc deficiency were also studied in macrophages exposed to HDE. Single and repetitive HDE inhalation exposure resulted in increased influx of total cells and neutrophils, increased mediator hyper-responsiveness (TNFα, IL-6, CXCL1, and amphiregulin), and enhanced tissue pathology that was more pronounced in zinc deficient mice compared to normal dietary counterparts. Airway inflammation was most pronounced in zinc deficient mice treated with repetitive HDE for 3 weeks. Similarly, macrophages maintained in a zinc deficient environment exhibited increased CXCL1 and IL-23 production as a result of increased NF-κB activation.Conclusion: Given the relatively high incidence of dietary deficiencies in agriculture workers, we anticipate that zinc intake, or a lack thereof, may play an important role in modulating the host response to organic dust exposure.
       
  • Response to the photoperiod in the white and brown adipose tissues of
           Fischer 344 rats fed a standard or cafeteria diet
    • Abstract: Publication date: Available online 3 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Albert Gibert-Ramos, Maria Ibars, M. Josepa Salvadó, Anna Crescenti Researchers are identifying new factors that contribute to the obesity epidemic, with changes in the photoperiod as one promising risk factor. To study the influence of the photoperiod on adipose tissue, Fischer 344 rats were treated for fourteen weeks with a long day (18 h light:6 h dark; LD) or a short day (6 h light:18 h dark; SD) and fed a standard diet (STD). Biometric measures, postprandial plasmatic parameters, gene expression in the retroperitoneal white adipose tissue (RWAT) and brown adipose tissue (BAT) and histology of the RWAT were analyzed. A second experiment with the same conditions and analysis was performed for eleven weeks with rats fed a cafeteria diet (CAF). In the STD experiment, the SD increased triglycerides and showed a tendency to reduce fat compared to the LD. In the RWAT, genes implicated in adipogenesis, lipogenesis and lipolysis were downregulated and the histological results showed a higher percentage of small adipocytes in the SD, without changes in their total number. In the CAF experiment, lipogenesis and adipogenesis gene expression were increased in the SD, while adipocytes were smaller and their number increased. Both experiments showed in the SD a decrease in the BAT expression of lipid uptake and β-oxidation genes, while only the STD additionally showed a reduction in Ucp1 expression. In conclusion, the RWAT morphology and the expression of key genes for lipid metabolism in RWAT and BAT were influenced by the photoperiod; however, the changes observed in the RWAT were different depending on the diet.
       
  • A critical review on anti-angiogenic property of phytochemicals
    • Abstract: Publication date: Available online 3 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Janani Rajasekar, Madan Kumar Perumal, Baskaran Vallikannan Angiogenesis, a process involved in neovascularization, has been found to be associated with several metabolic diseases like cancer, retinopathy etc. Thus, currently, the focus on anti-angiogenic therapy for treatment and prevention of diseases has gained significant attention. Currently available Food and Drug Administration (FDA) approved drugs are targeting either vascular endothelial growth factor or it’s receptor, but in the long term, these approaches were shown to cause several side effects and the chances of developing resistance to these drugs is also high. Therefore, identification of safe and cost-effective anti-angiogenic molecules is highly imperative. Over the past decades, dietary based natural compounds have been studied for their anti-angiogenic potential which provided avenues in improving the angiogenesis based therapy. In this review, major emphasis is given to the molecular mechanism behind anti-angiogenic effect of natural compounds from dietary sources.
       
  • MD2 blockade prevents oxLDL-induced renal epithelial cell injury and
           protects against high fat diet-induced kidney dysfunction
    • Abstract: Publication date: Available online 2 May 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Sujing Xu, Wu Luo, Xiaohong Xu, Yuanyuan Qian, Zheng Xu, Weihui Yu, Xiaoou Shan, Xinfu Guan, Hazel Lum, Huiping Zhou, Yi Wang There is a strong epidemiological link between obesity, a growing world-wide concern, and kidney disease. Emerging evidence indicates that the pathogenic basis of obesity-related kidney disease may be attributed to Toll-like receptor 4 (TLR4) of the innate immune system. We hypothesized that renal epithelial cell injury in response to oxidized low density lipoprotein (oxLDL) requires MD2 (myeloid differentiation factor 2), a co-receptor of TLR4. Moreover, we also hypothesized that renal dysfunction is MD2-dependent in the high fat diet (HFD) mouse model. Results indicated that the MD2 selective inhibitor (L6H21) abrogated the oxLDL-induced formation of MD2-TLR4 dimerization in the renal proximal tubular epithelial cell line, NRK-52E. Further, MD2 blockade in NRK-52E cells using siRNA target sequences or L6H21 prevented oxLDL-induced cell injury as indicated by expression of pro-fibrotic molecules, autophagic activity, and apoptosis. Similarly, TLR4 knockdown in NRK-52E cells using siRNA target sequences prevented oxLDL-induced cell injury. In the HFD mouse model, MD2 knockout protected against development of kidney dysfunction and renal tissue injury, corroborating the observations observed in NRK-52E cells. Thus, the oxLDL-induced renal tubular epithelial cell pro-fibrotic responses, autophagy, and apoptosis were dependent on MD2, as were the renal dysfunction and tissue impairment in HFD mice. These are new findings indicating that the MD2-TLR4 immune signaling complex is a critical pathogenic factor in the development of kidney disease related to obesity or metabolic syndrome.
       
  • The concomitant lower concentrations of vitamins B6, B9 and B12 may cause
           methylation deficiency in autistic children
    • Abstract: Publication date: Available online 24 April 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Antonio Belardo, Federica Gevi, Lello Zolla Autism spectrum disorder (ASD) is characterized by severe and persistent difficulties in social communication and social interaction at multiple levels. Recently, metabolic disorders have been associated with most cases of patients with ASD. The aim of this study was to investigate, through a new and more sophisticated mass technique, such as UHPLC-mass spectrometry (Q-exactive analyzer), alteration in metabolisms analyzing ASD children urine samples from children showing simultaneous vitamin B6, B9 and B12 deficiencies. This in order to study how these concurrent deficiencies may influence some phenotypic aspects of autistic disorder. Thus, urinary metabolic patterns specific to ASD were explored at an early age in sixty children with ASD, showing lower three vitamins levels, and sixty corresponding controls (age group 3–8, M: F=42:18). The results showed significant block of cystathionine formation with consequent accumulation of homocysteine. A lower glutathione levels (GSH), with reduction of essential intracellular reducing environment required for normal immune function, detoxification capacity and redox-sensitive enzyme activity. Increased concentration of 5-methyltetrahydrofolate, which leads to a lower availability of methyl group and significant decrease in urinary methionine and S-adenosyl-L-methionine (SAM) concentrations, the major methyl donor. The latter justify the well-known reduction in protein and DNA methylation reported in autistic children. As a final consideration, the concomitant deficiencies of all three B vitamins, recorded in a significant number of autistic children, suggests that intestinal dysbiosis in these patients may be the main cause of a reduction in their absorption, in addition to the genetic mutation of a specific gene.
       
  • The attenuating effects of pyridoxamine on adipocyte hypertrophy and
           inflammation differ by adipocyte location
    • Abstract: Publication date: Available online 24 April 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Seyeon Oh, Hyosang Ahn, Hyunjin Park, Jae-Ik Lee, Kook Yang Park, Daehee Hwang, Sojung Lee, Kuk Hui Son, Kyunghee Byun It is known that receptor for advanced glycation end products (RAGE) and its ligands accumulate in the fat tissues of obese individuals, and RAGE ligands induce M1 macrophage polarization, which in turn induces inflammation. We evaluated the effect of pyridoxamine on RAGE ligand accumulation and M1 polarization in the visceral, subcutaneous, and perivascular fat tissues of Sprague–Dawley rats fed a high fat diet (HFD).Pyridoxamine reduced HFD-induced weight gain, attenuated adipocyte size increases, RAGE ligand accumulations, RAGE-RAGE ligands binding, decreased macrophage M1 polarization and increased M2 polarization in visceral fat tissues, but not in subcutaneous tissues. Pyridoxamine induced glyoxalase 1 (Glo-1) expression in visceral fat in the HFD group, whereas pyridoxamine induced Glo-1 expression in perivascular fat tissues was no higher than that observed in the normal fat diet (NFD) controls. In vitro, pyridoxamine suppressed the release of RAGE ligands from AGE treated macrophages, but non-significantly attenuated RAGE ligands release in AGE treated adipocytes.Pyridoxamine was found to suppress weight increases and M1 polarization, and to increase Glo-1 expression through the RAGE pathway in perivascular and visceral fat tissues of HFD-induced obese rats. These findings suggest pyridoxamine is a candidate for the treatment of obesity or complications related to obesity-induced inflammation.
       
  • Resveratrol prevents combined prenatal NG-nitro-L-arginine-methyl ester
           (L-NAME) treatment plus postnatal high-fat diet induced programmed
           hypertension in adult rat offspring: Interplay between nutrient-sensing
           signals, oxidative stress and gut microbiota
    • Abstract: Publication date: Available online 24 April 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Hung-En Chen, Yu-Ju Lin, I-Chun Lin, Hong-Ren Yu, Jiunn-Ming Sheen, Ching-Chou Tsai, Li-Tung Huang, You-Lin Tain Oxidative stress, nutrient-sensing signals, high-fat (HF) intake, and dysbiosis of gut microbiota are involved in the development of hypertension, a disorder that can originate in early life. We examined whether postnatal HF diet can aggravate maternal NG-nitro-L-arginine-methyl ester (L-NAME) treatment-induced programmed hypertension and whether resveratrol therapy can prevent it. Pregnant Sprague–Dawley rats received L-NAME administration at 60 mg/kg/day subcutaneously during pregnancy alone, or with additional resveratrol (R) 50 mg/L in drinking water during the pregnancy and lactation. The offspring were onto either regular chow or HF diet (D12331) from weaning to 16 weeks of age. Male offspring rats were assigned to five groups (N=8/group): control, L-NAME, HF, L-NAME+HF, and L-NAME+HF + R at weaning at 3 weeks of age. Rats were sacrificed at 16 weeks of age. We observed that postnatal HF diet exacerbates maternal L-NAME treatment-induced programmed hypertension in male adult offspring, which resveratrol attenuated. Combined L-LAME and HF diet-induced hypertension is related to increased oxidative stress, inhibiting AMP-activated protein kinase (AMPK)/ peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) pathway, and altered gut microbiota compositions. L-NAME+HF caused an increase of the Firmicutes to Bacteroidetes ratio, which resveratrol therapy prevented. Additionally, the abundances of phylum Verrucomicrobia and genus Akkermansia were amplified by resveratrol therapy. Conclusively, our data highlighted the interactions between maternal NO deficiency, HF diet, AMPK/PGC-1α pathway, and gut microbiota in which the blood pressure of adult offspring can be modified by resveratrol. Resveratrol might be a useful reprogramming strategy to prevent L-NAME and HF diet-induced hypertension of developmental origin.
       
  • The role of diet and intestinal microbiota in the development of metabolic
           syndrome
    • Abstract: Publication date: Available online 8 April 2019Source: The Journal of Nutritional BiochemistryAuthor(s): Jose A. Santos-Marcos, Francisco Perez-Jimenez, Antonio Camargo Metabolic syndrome (MetS) is a cluster of metabolic factors that increase the risk of cardiovascular disease and type 2 diabetes mellitus (T2DM), which is in itself a major cardiovascular disease risk factor. The aim of this review is to summarize the data related to the influence of the gut microbiota on the development of obesity and the MetS, highlighting the role of diet in controlling the MetS by modifying the gut microbiota. The main alterations in the gut microbiota of individuals with MetS consist of an increased Firmicutes/Bacteriodetes ratio and a reduced capacity to degrade carbohydrates to short-chain fatty acids, which in turn is related with the metabolic dysfunction of the host organism rather than with obesity itself. In addition to a low-fat, high-carbohydrate diet, with its high fiber intake, a diet with 30% fat content but with a high content in fruit and vegetables, such as the Mediterranean diet, is beneficial and partially restores the dysbiosis found in individuals with MetS. Overall, the shaping of the gut microbiota through the administration of prebiotics or probiotics increases the short-chain fatty acid production, and is therefore a valid alternative in MetS treatment.
       
  • 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
       
 
 
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