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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]
  • Obesity alters the uterine environment before pregnancy
    • Abstract: Publication date: Available online 19 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): MV Bazzano, GB Sarrible, N Martinez, M Berón de Astrada, EM EliaAbstractObesity is a metabolic disorder that predisposes to numerous diseases and has become a major global public-health concern. Cafeteria diet (CAF) is the animal model used for the study of obesity that more closely reflects western diet habits. Previously we described that CAF administration for 60 days induces obesity in female rats and theirs fetuses develop macrosomia. Given that in our model rats are not genetically modified and that obese mothers were fed standard chow during pregnancy, the aim of the current study was to test the hypothesis that obesity alters the intrauterine environment prior to pregnancy; and this may explain the exacerbated fetal weight gain. We found that uteri from obese rats during the oestrous phase developed insulin resistance through mechanisms that involve the induction of uterine hypoxia and the downregulation of the insulin receptor gene. Moreover, uterine cell proliferation was induced by obesity concomitantly with the reduction in the uterine contractile response to a β2 AR agonist, Salbutamol; and this may be consequence of the downregulation in the uterine β2 AR expression. We conclude that CAF-induced obesity alters the uterine environment in rats during the oestrous phase and may cause the fetal macrosomia previously described by us in obese animals. The lower sensitivity of the uterus to a relaxation stimulus (Salbutamol) is not a minor fact given that for implantation to occur the uterus must be relaxed for embryo nidation. Thus, the alteration in the uterine quiescence may impair implantation and, consequently, the foregoing pregnancy.
       
  • Astaxanthin exerts anti-inflammatory and antioxidant effects in
           macrophages in NRF2-dependent and independent manners
    • Abstract: Publication date: Available online 19 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Callie Farruggia, Mi-Bo Kim, Minkyung Bae, Yoojin Lee, Tho X. Pham, Yue Yang, Myung Joo Han, Young-Ki Park, Ji-Young LeeAbstractAlthough anti-inflammatory effects of astaxanthin (ASTX) have been suggested, the underlying mechanisms have not been fully understood. Particularly, the modulatory action of ASTX in the interplay between nuclear factor E2-related factor 2 (NRF2) and nuclear factor κB (NFκB) to exert its anti-inflammatory effect in macrophages is unknown. The effect of ASTX on mRNA and protein expression of pro-inflammatory and antioxidant genes and/or cellular reactive oxygen species (ROS) accumulation were determined in RAW 264.7 macrophages, bone marrow-derived macrophages (BMDM) from wild-type and Nrf2 deficient mice, and/or splenocytes and peritoneal macrophages of obese mice fed ASTX. The effect of ASTX on M1 and M2 macrophage polarization was evaluated in BMDM. ASTX significantly decreased LPS-induced mRNA expression of interleukin 6 (Il-6) and Il-1β by inhibiting nuclear translocation of NFκB p65; and attenuated LPS-induced ROS with an increase in NRF2 nuclear translocation, concomitantly decreasing NADPH oxidase 2 expression in RAW 264.7 macrophages. In BMDM of WT and Nrf2-deficient mice, ASTX decreased basal and LPS-induced ROS accumulation. The induction of Il-6 mRNA by LPS was repressed by ASTX in both types of BMDM while Il-1β mRNA was decreased only in WT BMDM. Furthermore, ASTX consumption lowered LPS sensitivity of splenocytes in obese mice. ASTX decreased M1 polarization of BMDM while increasing M2 polarization. ASTX exerts its anti-inflammatory effect by inhibiting nuclear translocation of NFκB p65 and by preventing ROS accumulation in NRF2-dependent and -independent mechanisms. Thus, ASTX is an agent with anti-inflammatory and antioxidant properties that may be used for the prevention of inflammatory conditions.
       
  • Long-term exposure to high-sucrose diet downregulates hepatic endoplasmic
           reticulum-stress adaptive pathways and potentiates de novo lipogenesis in
           weaned male mice
    • Abstract: Publication date: Available online 19 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Karla Frida Torres Flister, Bruno Araújo Serra, Lucas Martins França, Caio Fernando Ferreira Coêlho, Pâmela Costa dos Santos, Caroline Castro Vale, Daniela Kajihara, Victor Debbas, Francisco Rafael Martins Laurindo, Antonio Marcus de Andrade PaesAbstractChildhood consumption of added sugars, such as sucrose, has been associated to increased risk of metabolic syndrome (MetS) and non-alcoholic fatty liver disease (NAFLD). Although the mechanisms underlying NAFLD onset are incompletely defined, recent evidence has proposed a role for the endoplasmic reticulum (ER) stress. Thus, the present study sought to investigate the metabolic outcomes of high-sucrose intake on weaned Swiss mice fed a 25% sucrose diet for 30-, 60- and 90-days in comparison to regular chow fed controls. High-sucrose feeding promoted progressive metabolic and oxidative disturbances, starting from fasting and fed hyperglycemia, hyperinsulinemia, glucose intolerance, and increased adiposity at 30-days; passing by insulin resistance, hypertriglyceridemia and NAFLD onset at 60-days; until late hepatic oxidative damage at 90-days. In parallel, assessment of transcriptional and/or translational levels of de novo lipogenesis (DNL) and ER stress markers showed upregulation of both fatty acid synthesis (ChREBP and SCD1) and oxidation (PPARα and CPT-1α), as well as overexpression of unfolded protein response sensors (IRE1α, PERK and ATF6), chaperones (GRP78 and PDIA1) and antioxidant defense (NRF2) genes at 30-days. At 60-days, fatty acid oxidation genes were downregulated and ER stress switched over toward a pro-apoptotic pattern via upregulation of BAK protein and CHOP gene levels. Finally, downregulation of both NRF2 and CPT-1α protein levels led to late upregulation of SREBP-1c and exponential raise of fatty acids synthesis. In conclusion, our study originally demonstrates a temporal relationship between DNL and ER stress pathways toward MetS and NAFLD development on weaned rats fed a high-sucrose diet.
       
  • Saturated fatty acid alters embryonic cortical neurogenesis through
           modulation of gene expression in neural stem cells
    • Abstract: Publication date: Available online 19 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Mustafa T. Ardah, Shama Parween, Divya S. Varghese, Bright Starling Emerald, Suraiya A. AnsariAbstractA perturbed maternal metabolic environment such as chronically elevated circulating free fatty acids have been shown to affect stem cell fate during embryonic neurogenesis. However, molecular mechanisms behind this are not well defined, especially in human. Here in using directed differentiation of human embryonic stem cells (hESCs) into cortical neurons as model, we show that chronically elevated saturated fatty acid (palmitate) results in decreased proliferation of neural stem cells and increased differentiation into neurons. This phenotype could be due to palmitate mediated increased expression of key genes needed for neuronal differentiation such as EOMES, TBR1, NEUROD1 and RELN and reduced expression of SREBP regulated lipogenic genes at early stages of cortical differentiation. Furthermore, palmitate treatment increased histone acetylation globally and at select gene promoters among affected genes. We also found differential expression of several lncRNAs associated with cellular stress and metabolic diseases in the presence of palmitate including BDNF-AS suggesting the contribution of additional epigenetic regulatory mechanisms. Together, our results show that saturated fatty acid affects developmental neurogenesis through modulation of gene expression and through epigenetic regulatory mechanisms.
       
  • Common gut microbial metabolites of dietary flavonoids exert potent
           protective activities in β-cells and skeletal muscle cells
    • Abstract: Publication date: Available online 15 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Benjamin F. Bitner, Jason D. Ray, Kyle B. Kener, Jacob A. Herring, Josie A. Tueller, Deborah K. Johnson, Claudia M. Tellez Freitas, Dane W. Fausnacht, Mitchell E. Allen, Alexander H. Thomson, K. Scott Weber, Ryan P. McMillan, Matthew W. Hulver, David A. Brown, Jeffery S. Tessem, Andrew P. NeilsonAbstractFlavonoids are dietary compounds with potential anti-diabetes activities. Many flavonoids have poor bioavailability and thus low circulating concentrations. Unabsorbed flavonoids are metabolized by the gut microbiota to smaller metabolites, which are more bioavailable than their precursors. The activities of these metabolites may be partly responsible for associations between flavonoids and health. However, these activities remain poorly understood. We investigated bioactivities of flavonoid microbial metabolites [hippuric acid (HA), homovanillic acid (HVA), and 5-phenylvaleric acid (5PVA)] in primary skeletal muscle and β-cells compared to a native flavonoid ([(−)-epicatechin, EC]. In muscle, EC was the most potent stimulator of glucose oxidation, while 5PVA and HA simulated glucose metabolism at 25 μM, and all compounds preserved mitochondrial function after insult. However, EC and the metabolites did not uncouple mitochonndrial respiration, with the exception of 5PVA at10 μM. In β-cells, all metabolites more potently enhanced glucose-stimulated insulin secretion (GSIS) compared to EC. Unlike EC, the metabolites appear to enhance GSIS without enhancing β-cell mitochondrial respiration or increasing expression of mitochondrial electron transport chain components, and with varying effects on β-cell insulin content. The present results demonstrate the activities of flavonoid microbial metabolites for preservation of β-cell function and glucose utilization. Additionally, our data suggest that metabolites and native compounds may act by distinct mechanisms, suggesting complementary and synergistic activities in vivo which warrant further investigation. This raises the intriguing prospect that bioavailability of native dietary flavonoids may not be as critical of a limiting factor to bioactivity as previously thought.
       
  • Flavin homeostasis in the mouse retina during aging and degeneration
    • Abstract: Publication date: Available online 15 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Tirthankar Sinha, Mustafa Makia, Jianhai Du, Muna I. Naash, Muayyad R. Al-UbaidiAbstractInvolvement of flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN) in cellular homeostasis has been well established for tissues other than the retina. Here, we present an optimized method to effectively extract and quantify FAD and FMN from a single neural retina and its corresponding retinal pigment epithelium (RPE). Optimizations led to detection efficiency of 0.1 pmol for FAD and FMN while 0.01 pmol for riboflavin. Interestingly, levels of FAD and FMN in the RPE were found to be 1.7 and 12.5 folds higher than their levels in the retina, respectively. Both FAD and FMN levels in the RPE and retina gradually decline with age and preceded the age-dependent drop in the functional competence of the retina as measured by electroretinography. Further, quantifications of retinal levels of FAD and FMN in different mouse models of retinal degeneration revealed differential metabolic requirements of these two factors in relation to the rate and degree of photoreceptor degeneration. We also found 2 fold reductions in retinal levels of FAD and FMN in two mouse models of diabetic retinopathy. Altogether, our results suggest that retinal levels of FAD and FMN can be used as potential markers to determine state of health of the retina in general and more specifically the photoreceptors.
       
  • Bio-accessible milk casein derived tripeptide (LLY) mediates overlapping
           anti- inflammatory and anti-oxidative effects under cellular (Caco-2) and
           in vivo milieu
    • Abstract: Publication date: Available online 13 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Kandukuri Sowmya, Dev Mala, Mohd Iqbal Bhat, Naveen Kumar, Rajesh Kumar Bajaj, Suman Kapila, Rajeev KapilaAbstractInflammation and oxidative stress are closely linked patho-physiological processes which occur concurrently in many diseased conditions. Recently, interdependence between these two processes explains the antioxidant paradox associated with failure to select appropriate agents required for prevention of diseases known to be induced by oxidative stress. Present study established the overlapping anti-inflammatory and anti-oxidative potential along with bio-accessibility of milk casein derived tripeptide (LLY). Tripeptide exhibited anti-inflammatory response under ex vivo conditions by suppressing (P
       
  • High fat diet affects pre-gestational adiposity and glucose tolerance
           perturbing gestational placental macronutrient transporters culminating in
           an obese offspring in wild type and glucose transporter isoform 3
           heterozygous null mice
    • Abstract: Publication date: Available online 13 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Amit Ganguly, Sherin U. DevaskarAbstractWe examined the effect of a high fat diet (HFD) versus control diet (CD) upon pre-gestational and gestational wild type (wt) and glucose transporter (glut)3 heterozygous (glut3+/−) female mice and observed an increase in pre-gestational body weights, white adiposity (wt > glut3+/−), circulating cholesterol and high density lipoproteins, with glucose intolerance in both genotypes. The HFD exposed offspring displayed reduced birth weight with catch up to CD-fed in wt versus an increased birth weight persisting as such at weaning by day 21 in glut3+/− mice. To decipher the mechanism behind this genotype specific difference in the HFD offspring's phenotype, we first examined placental macronutrient transporters and noted HFD induced increase in CD36 in wt with no change in other FATPs, SNATs and LAT2 in both genotypes. In contrast, while placental Glut1 increased in both the genotypes, only Glut3 increased in the glut3+/− genotype in response to HFD. Hence we next assessed glut3+/− embryonic (ES) cells under differing stressors of low glucose, hypoxia and inhibition of oxidative phosphorylation. Reduced Glut3 mediated glucose uptake in glut3+/−versus wt ES cells culminated in deficient growth. We conclude that maternal HFD affects the in-utero growth potential of the offspring by altering placental CD36 and Glut1 concentrations. In contrast, a differential effect on placental Glut3 concentrations between glut3+/− and wt genotypes is evident, with an increase occurring in the glut3+/− genotype alone. Deficient Glut3 in ES cells interferes with glucose uptake, cell survival and growth being further exaggerated with low glucose, hypoxia and inhibition of oxidative phosphorylation.
       
  • Cranberries attenuate animal-based diet-induced changes in microbiota
           composition and functionality: A randomized crossover controlled feeding
           trial
    • Abstract: Publication date: Available online 8 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Jose Rodríguez-Morató, Nirupa R. Matthan, Jin Liu, Rafael de la Torre, C.-Y. Oliver ChenAbstractCranberries have multiple health effects but their impact on gut microbiota has not been examined in randomized controlled feeding trials. We evaluated the relationship between the microbiota and cranberries in the context of an animal-based diet. In a randomized, double-blind, cross-over, controlled design trial, 11 healthy adults consumed for 5 days each a control diet (animal-based diet plus 30 g/day placebo powder) and a cranberry diet (animal-based diet plus 30 g/day freeze-dried whole cranberry powder). The animal-based diet included meats, dairy products, and simple sugars. Stool, urine, and blood samples were obtained before and after each intervention phase. As compared to the pre-control diet, control diet modified 46 taxonomic clades, including an increase in the abundance of Firmicutes and decrease in Bacteroidetes. Moreover, it increased bacteria-derived deoxycholic acid and decreased acetate and butyrate in stool. As compared to the post-intervention phase of control diet, the cranberry diet modified 9 taxonomic clades, including a decrease in the abundance of Firmicutes and increase in Bacteroidetes. Further, the cranberry diet attenuated control diet-induced increase in secondary bile acids and decrease in short-chain fatty acids (SCFA), and increased urinary anthocyanins and bacterially derived phenolic acids. No changes were found in fecal trimethylamine and plasma cytokines. In conclusion, an animal-based diet altered the microbiota composition to a less favorable profile, increased carcinogenic bile acids, and decreased beneficial SCFA. Cranberries attenuated the impact of the animal-based diet on microbiota composition, bile acids, and SCFA, evidencing their capacity to modulate the gut microbiota.
       
  • Sodium acetate and androgen receptor blockade improve gestational androgen
           excess-induced deteriorated glucose homeostasis and antioxidant defenses
           in rats: Roles of adenosine deaminase and xanthine oxidase activities
    • Abstract: Publication date: Available online 5 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Taofeek O. Usman, Emmanuel D. Areola, Olufunto O. Badmus, InKyeom Kim, Lawrence A. OlatunjiAbstractNutritional challenges and androgen excess have been implicated in the development of gestational diabetes and poor fetal outcome, but the mechanisms are not well delineated. The effects of short chain fatty acid (SCFA) on glucose dysmetabolism and poor fetal outcome induced by gestational androgen excess is also not known. We tested the hypothesis that blockade of androgen receptor (AR) and suppression of late gestational androgen excess prevents glucose dysmetabolism and poor fetal outcome through suppression of adenosine deaminase (ADA)/xanthine oxidase (XO) pathway. Twenty-four pregnant Wistar rats were treated (sc) with olive oil, testosterone propionate (0.5 mg/kg) singly or in combination with SCFA (sodium acetate; 200 mg/kg; po) or AR blocker (flutamide; 7.5 mg/kg; po) between gestational days 14 and 19. The results showed that late gestational androgen excess led to glucose deregulation, poor fetal outcome, increased plasma and hepatic free fatty acid and lactate dehydrogenase, liver function marker enzymes, malondialdehyde, uric acid, ADA and XO activities. Conversely, gestational androgen excess resulted in reduced body weight gain, visceral adiposity, plasma and hepatic anti-oxidant defenses (glutathione peroxidase, reduced glutathione/glutathione disulphide ratio, glucose-6-phosphate dehydrogenase, adenosine and nitric oxide). However, all these effects were ameliorated by either sodium acetate or flutamide treatment. The study demonstrates that suppression of testosterone by SCFA or AR blockade protects against glucose deregulation and poor fetal outcome by improvement of anti-oxidant defenses and replenishment of hepatic oxidative capacity through suppression of ADA/XO pathway. Hence, utility of SCFA should be encouraged for prevention of glucose dysmetabolism and poor fetal outcome.
       
  • Calorie restriction attenuates hypertrophy-induced redox imbalance and
           mitochondrial ATP-sensitive K+ channel repression
    • Abstract: Publication date: Available online 5 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Cicera Edna Barbosa David, Aline Maria Brito Lucas, Maria Thalyne Silva Araújo, Beatriz Neves Coelho, Juarez Braga Soares Neto, Bruna Raysa Campos Portela, Anna Lídia Nunes Varela, Alicia J. Kowaltowski, Heberty T. FacundoOxidative stress has been implicated in the pathogenesis of cardiac hypertrophy and associated heart failure. Cardiac tissue grows in response to pressure or volume overload, leading to wall thickening or chamber enlargement. If sustained, this condition will lead to a dysfunctional cardiac tissue and oxidative stress. Calorie restriction (CR) is a powerful intervention to improve health and delay aging. Here, we investigated whether calorie restriction in mice prevented isoproterenol-induced cardiac hypertrophy in vivo by avoiding reactive oxygen species (ROS) production and maintaining antioxidant enzymatic activity. Additionally, we investigated the involvement of mitochondrial ATP-sensitive K+ channels (mitoKATP) in cardiac hypertrophy. CR was induced by 40% reduction in daily calorie ingestion. After 3 weeks on CR or ad libitum (Control) feeding, Swiss mice were treated intraperitoneally with isoproterenol (30 mg/kg/day) for 8 days to induce hypertrophy. Isoproterenol-treated mice had elevated heart weight/tibia length ratios and cardiac protein levels. These gross hypertrophic markers were significantly reduced in CR mice. Cardiac tissue from isoproterenol-treated CR mice also produced less H2O2 and had lower protein sulfydryl oxidation. Additionally, calorie restriction blocked hypertrophic-induced antioxidant enzyme (catalase, superoxide dismutase and glutathione peroxidase) activity repression during cardiac hypertrophy. MitoKATP opening was repressed in isolated mitochondria from hypertrophic hearts, in a manner sensitive to calorie restriction. Finally, mitoKATP inhibition significantly blocked the protective effects of calorie restriction. Altogether, our results suggest that CR improves intracellular redox balance during cardiac hypertrophy and prevents this process in a mechanism involving mitoKATP activation.Graphical abstractUnlabelled Image
       
  • Dietary fatty acids augment tissue levels of n-acylethanolamines in
           n-acylphosphatidylethanolamine phospholipase D (NAPE-PLD) knockout mice
    • Abstract: Publication date: Available online 5 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Lin Lin, Adam H Metherel, Alex P Kitson, Shoug M Alashmali, Kathryn E Hopperton, Marc-Olivier Trépanier, Peter J Jones, Richard P BazinetAbstractN-acylethanolamines (NAEs) are lipid signaling mediators, which can be synthesized from dietary fatty acids via n-acylphosphatidylethanolamine-phospholipase D (NAPE-PLD) and in turn influence physiological outcomes; however, the roles of NAPE-PLD upon dietary fatty acid modulation are not fully understood. Presently, we examine if NAPE-PLD is necessary to increase NAEs in response to dietary fatty acid manipulation. Post-weaning male wild-type (C57Bl/6), NAPE-PLD (−/+) and NAPE-PLD (−/−) mice received isocaloric fat diets containing either beef tallow, corn oil, canola oil or fish oil (10% wt/wt from fat) for 9 weeks. Brain docosahexaenoic acid (DHA) levels were higher (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
       
  • Soy genistein administered in soluble chitosan microcapsules maintains
           antioxidant activity and limits intestinal inflammation
    • Abstract: Publication date: Available online 1 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Vanden Braber, Novotny Nuñez, L. Bohl, C. Porporatto, FN. Nazar, MA Montenegro, SG. CorreaWe used water-soluble Chitosan obtained by Maillard reaction with glucosamine to microencapsulate soy genistein (Ge) and preserve its biological activity for oral administration. Release of Ge was pH dependent with a super Case II mechanism at pH 1.2 and an anomalous transport with non-Fickian kinetics at pH 6.8. Microencapsulated Ge retained its antioxidant properties in vitro and its daily administration to mice attenuated clinical signs of acute colitis, limited inflammatory reaction and reduced oxidative stress and tissue injury as well. Remarkably, after feeding microencapsulated Ge the production of IL-10 in colonic tissue was restored to levels of untreated controls. According to statistical multivariate analysis, this cytokine was the parameter with the highest influence on the inflammatory/oxidative status. Microencapsulation of Ge with derivatized Chitosan becomes an interesting alternative to develop therapeutic approaches for oxidative inflammatory diseases; our findings suggest that the soy isoflavone could be incorporated into any functional food for application in intestinal inflammation.Graphical abstractUnlabelled Image
       
  • Fisetin inhibits cardiac hypertrophy
    • Abstract: Publication date: Available online 1 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Bin Dong, Chen Liu, Ruicong Xue, Yan Wang, Yu Sun, Zhuomin Liang, Wendong Fan, Jingzhou Jiang, Jingjing Zhao, Qiao Su, Gang Dai, Yugang Dong, Huiling HuangAbstractCardiac hypertrophy is a pathophysiological response to various pathological stresses and ultimately leads to heart failure. Oxidative stress is one of the critical processes involved in hypertrophy development. Fisetin, a small molecular flavonoid, has been shown to have anti-oxidative, anti-proliferative and anti-inflammatory properties. However, the effect of fisetin on cardiac hypertrophy remains unknown. In our present study, we showed that fisetin inhibited pressure overload-induced cardiac hypertrophy, improved cardiac function in vivo and suppressed phenylephrine (PE)-induced cardiomyocyte hypertrophy in vitro. Reactive oxygen species (ROS) levels were markedly decreased by fisetin treatment in both hypertrophic hearts and cardiomyocytes. Moreover, fisetin significantly up-regulated the expression of antioxidative genes, including catalase (CAT), superoxide dismutase 1 (SOD1) and heme oxygenase 1 (HO-1). Furthermore, co-treatment with N-acetylcysteine (NAC; ROS scavenger) and fisetin did not have synergistic inhibitory effects on PE-induced cardiomyocyte hypertrophy, indicating that the anti-hypertrophic effects of fisetin are mainly associated with the blockade of oxidative stress. Finally, the pro-hypertrophic signaling pathways, mitogen-activated protein kinase (MAPK) and mammalian target of rapamycin (mTOR) kinase, were found to be suppressed by fisetin after pressure overload and PE treatment. In conclusion, our study revealed that fisetin protects against cardiac hypertrophy and that oxidative stress inhibition may be one of the pivotal mechanisms involved.
       
  • Testosterone represses urinary excretion of the alpha-tocopherol
           metabolite alpha-carboxymethylhydroxychroman in rats
    • Abstract: Publication date: Available online 1 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Naoko Fujita, Asako TakenakaAbstractIn rats, plasma and tissue concentrations of α-tocopherol, a predominant form of vitamin E in mammals, are known to differ between the sexes. In order to examine sex differences in α-tocopherol metabolism, we investigated urinary excretion of the α-tocopherol metabolite α- carboxymethylhydroxychroman (α-CEHC) using Wistar rats. First, we measured α-CEHC in urine of nine-week-old male and female rats in basal and α-tocopherol-administered conditions. We observed that female rats excrete significantly more α-CEHC than male rats via urine. This sex difference was observed in matured nine-week-old rats, but not in premature three-week-old rats, suggesting that the difference may relate to sex hormones. In order to confirm this, we examined the effect of ovariectomy and orchiectomy on female and male rats, respectively. The results of castration clearly demonstrated that orchiectomy enhanced urinary excretion of α-CEHC, supporting the hypothesis that testosterone repressed α-tocopherol metabolism. We then administered testosterone propionate to orchiectomized rats, and observed downregulation of α-CEHC excretion. Taken together, these results indicate that testosterone represses the metabolism and urinary excretion of α-tocopherol in rats. This is the first report to show a sex-dependent difference in urinary excretion rate of an α-tocopherol metabolite, and contributes to the understanding of vitamin E metabolism.
       
  • 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 ZhengObesity is underpinned by both genetic and environmental factors, including a high saturated fat diet. Some mice develop diet-induced obesity (DIO) but others remain diet-resistant (DR), despite intake of the same high-saturated fat diet; a phenomenon that mimics characteristics of the human obese phenotype. Microbiota-colon-brain axis regulation is important for energy metabolism and cognition. Using DIO and DR mouse models, this study aimed to examine gut microbiota, colonic inflammation and cognitive function to elucidate the role of microbiota-gut-brain regulation in diet-induced obesity. C57Bl6/J mice fed a chronic saturated palmitic acid diet for 22 weeks showed significant body weight gain differences, with the top one third gaining 48% heavier body weight than the lower one third. There was significant reduction in gut microbiota richness and diversity in DIO mice, but not in DR mice. At the phylum level, DIO mice had increased abundance of Firmicutes and Antinobacteria, and decreased abundance of Bacterioides and Proteobacteria in gut microbiota. DIO mice exhibited reduced tight junction proteins, increased plasma endotoxin lipopolysaccharide (LPS) and increased inflammation in the colon and liver. Recognition memory and spatial memory were impaired in DIO mice, associated with decreased Bacteroidetes. Further examination showed that hippocampal brain-derived neurotrophic factor (BDNF) was significantly decreased in DIO mice (vs DR). Conversely, DR mice showed no changes in the above parameters measured. Therefore, gut microbiota, colon inflammation and circulating LPS may play a major role in the development of the obese phenotype and cognitive decline associated with a chronic high saturated palmitic acid diet.Graphical abstractUnlabelled Image
       
  • Virgin coconut oil is effective to treat metabolic and inflammatory
           dysfunction induced by high refined carbohydrate-containing-diet in mice
    • Abstract: Publication date: Available online 1 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Marina Campos Zicker, Ana Letícia Malheiros Silveira, Débora Romualdo Lacerda, Débora Fernandes Rodrigues, Cíntia Tarabal Oliveira, Letícia Maria de Souza Cordeiro, Leandro Ceotto Freitas Lima, Sérgio Henrique Sousa Santos, Mauro Martins Teixeira, Adaliene Versiani Matos FerreiraAbstractThe global rise in obesity rates is alarming since this condition is associated with chronic low-grade inflammation and secondary comorbidities as glucose intolerance, cardiovascular disease and liver damage. Therefore, a lot of dietary approaches are proposed to prevent and to treat obesity and its associated disorders. Virgin coconut oil (VCO) is well known as a functional food due to its significant amounts of medium-chain triglycerides. This study aimed to evaluate the effect of VCO on adiposity, metabolic and inflammatory dysfunctions induced by a high-refined carbohydrate-containing (HC) diet in mice. Male BALB/c mice were divided into two groups and fed with control (C) or HC diet to induce obesity for eight weeks. At the 9th week mice fed with HC diet were randomly regrouped into four groups, and were kept this way until the 12th week, as following: (i) HC diet alone or HC diet supplemented with three different VCO doses (ii) 1000 mg/Kg, (iii) 3000 mg/Kg and (iv) 9000 mg/Kg. Regardless of the concentration used, VCO supplementation promoted lower adiposity and also improvement in glucose tolerance, lower serum glucose and lipid levels and decreased hepatic steatosis. Moreover, VCO intake induced a lower inflammatory response due to decreased number of leukocytes and TNF-α and IL-6 concentrations in adipose tissue, as well as reduced counts of total leukocytes, mononuclear and polymorphonuclear circulating cells. Our data showed that VCO can be considered as an interesting potential dietary approach to attenuate obesity and its metabolic and inflammatory alterations.
       
  • Alpha cell function interacts with diet to modulate prediabetes and type 2
           diabetes
    • Abstract: Publication date: Available online 1 September 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Irene Roncero-Ramos, Rosa Jimenez-Lucena, Juan F. Alcala-Diaz, Cristina Vals-Delgado, Antonio P. Arenas-Larriva, Oriol A. Rangel-Zuñiga, Ana Leon-Acuña, María M. Malagon, Javier Delgado-Lista, Pablo Perez-Martinez, Jose M. Ordovas, Antonio Camargo, Jose Lopez-MirandaAlpha- and beta-cells dysfunction is implicated in the development of type 2 diabetes mellitus (T2DM). We aimed to evaluate whether alpha- and beta-cell dysfunction may precede prediabetes (PreDM) and T2DM development. Furthermore, we explored the role of two healthy diets (Mediterranean and low-fat diets) modulating these processes. We included 462 patients from the CORDIOPREV study without T2DM at baseline, of which 272 were PreDM. During follow-up, 107 patients developed T2DM (T2DM-incident group), 30 developed PreDM (PreDM-incident group), 86 regressed to normoglycemia (PreDM-regression group) and 29 patients remained without PreDM or T2DM criteria (control group), according to the American Diabetes Association diagnosis criteria. We measured glucose, insulin, glucagon and GLP-1 plasma levels in the OGTT performed at baseline and after 2 years of follow-up. Patients were randomized to consume two healthy diets, a Mediterranean (>35%) and a low-fat (
       
  • The co-administration of proanthocyanidins and an obesogenic diet prevents
           the increase in intestinal permeability and metabolic endotoxemia derived
           to the diet
    • Abstract: Publication date: Available online 30 August 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Katherine Gil-Cardoso, Iris Ginés, Montserrat Pinent, Anna Ardévol, Mayte Blay, Ximena TerraAbstractThe consumption of Westernized diets leads to hyperphagia and obesity, as well as intestinal alterations. In the present study, we evaluated the effect of the administration of a grape seed proanthocyanidin extract (GSPE) at different time points on the modulation of intestinal barrier function (intestinal permeability and metabolic endotoxemia), in rats with high-fat/high-carbohydrate diet-induced obesity. Animals were fed a cafeteria diet (CAF) supplemented with a preventive (PRE-CAF) or simultaneously intermittent (SIT-CAF) GSPE treatment (500 mg/Kg bw). Changes in the plasma levels of an orally administered marker of intestinal permeability (ovalbumin, OVA), lipopolysaccharide (LPS) and tumor necrosis factor-α (TNF-α) were analyzed after animals were fed the obesogenic diet for 8, 12 and 17 weeks. In addition, ex vivo variations in transepithelial electrical resistance (TEER), the expression of tight junction (TJ) genes and the activity of myeloperoxidase (MPO) in the small and large intestines were monitored at the end of the experiment. The CAF diet increased OVA, LPS, MPO and TNF-α levels, accompanied by decreased TEER values in the small and large intestines. Interestingly, both GSPE treatments prevented these detrimental effects of the CAF diet, being the SIT-CAF group the most effective after 17 weeks of diet intervention. For the first time, this study provides evidence of the ameliorative effect of a proanthocyanidin extract, administered before or together with an obesogenic diet, on barrier dysfunction, as measured by intestinal permeability and metabolic endotoxemia.
       
  • Myeloperoxidase deficiency attenuates systemic and dietary Iron-induced
           adverse effects
    • Abstract: Publication date: Available online 21 August 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Xia Xiao, Piu Saha, Beng San Yeoh, Jennifer A. Hipp, Vishal Singh, Matam Vijay-KumarAbstractIron deficiency is routinely treated with oral or systemic iron supplements, which is highly reactive and could induce oxidative stress via augmenting the activity of proinflammatory enzyme, myeloperoxidase (MPO). To investigate the extent to which MPO is involved in iron-induced toxicity, acute (24 h) iron toxicity was induced by intraperitoneal administration of FeSO4 (25 mg/kg body weight) to MPO deficient (MpoKO) mice and their WT littermates. Acute iron-toxicity was also assessed in WT mice pretreated with a MPO inhibitor, 4-aminobenzoic acid hydrazide (ABAH). Systemic iron administration upregulated circulating MPO, neutrophil elastase and elevated systemic inflammatory and organ damage markers in WT mice. However, genetic deletion of MPO or its inhibition significantly reduced iron-induced organ damage and systemic inflammatory responses. In contrast to the acute model, 8 weeks of 2% carbonyl iron diet feeding to WT mice did not change the levels of circulating MPO and neutrophil elastase but promoted their accumulation in the liver. Even though both MpoKO and WT mice displayed similar levels of diet-induced hyperferremia, MpoKO mice showed significantly reduced inflammatory response and oxidative stress than the WT mice. In addition, WT bone marrow-derived neutrophils (BMDN) generated more reactive oxygen species than MPO deficient BMDN upon iron stimulation. Altogether, genetic deficiency or pharmacologic inhibition of MPO substantially attenuated acute and chronic iron-induced toxicity. Our results suggest that targeting MPO during iron supplementation is a promising approach to reduce iron-induced toxicity/side effects in vulnerable population.
       
  • Linoleic acid reduces vascular reactivity and improves the vascular
           dysfunction of the small mesentery in hypertension
    • Abstract: Publication date: Available online 17 August 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Dieli Oliveira Nunes, Vinicius Bermond Marques, Camila Cruz Pereira Almenara, Wena Marcarini Dantas, Rogério Faustino Ribeiro, Alessandra Simão PadilhaAbstractWe aimed to investigate the effect of linoleic acid (LA) treatment on the blood pressure and function of mesenteric resistance arteries (MRA) in spontaneous hypertensive rats (SHR). Male SHR were treated daily with LA (15 mg/kg) or vehicle (control) for 15 days. Compared with controls, LA treatment decreased blood pressure and showed the following in MRA: (1) increased lumen and external diameter, (2) decreased wall:lumen ratio and wall thickness, (3) decreased stiffness and (4) less collagen deposition. LA treatment reduced the contractile response to phenylephrine, although there were no changes observed in MRA in regard to the acetylcholine or sodium nitroprusside responses. Incubation with L-NAME left-shifted the reactivity to phenylephrine only in the MRA treated group, suggesting that LA treatment can improve NO bioavailability. This result was accompanied by an increase “in situ” NO production. Incubation with tiron decreased vascular reactivity to phenylephrine in MRA in LA rats, which was accompanied by decreased superoxide anion production. Moreover, incubation with indomethacin (non-selective COX inhibitor, 10 μM), NS 398 (COX-2 specific inhibitor, 1 μM), furegrelate (TXA2 synthase inhibitor, 1 μM), SQ 29.548 (TP receptor antagonist, 1 μM) and SC 19220 (EP1 receptor antagonist, 10 μM) reduced the vasoconstrictor responses to phenylephrine in MRA in the treated group. These results were accompanied by a reduction in COX-2 protein expression. In conclusion, these findings show that LA treatment decreases blood pressure. In addition, the improvement of endothelial dysfunction and structural changes in this hypertension model may be responsible for the reduction in blood pressure.
       
  • Linoleic acid derived oxylipins are elevated in kidney and liver and
           reduced in serum in rats given a high protein diet
    • Abstract: Publication date: Available online 15 August 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Md Ariful Islam, Amir Ravandi, Harold M AukemaAbstractHigh protein (HP) diets are often used as a means to reduce obesity, but their long-term effects remain unclear. In vitro studies suggest the involvement of a subset of oxylipins in the tissue response to HP diets. To examine the role of these bioactive lipids in vivo, normal adult male Sprague Dawley rats were provided isocaloric diets with LP (low protein, 8% protein by weight), NP (normal protein, 14%) or HP (50%) diets for two weeks, and targeted lipidomic analysis of oxylipins in kidney (cortex and medulla), liver and serum was performed by HPLC-MS/MS. The main group of oxylipins affected by the HP diet was the oxylipins derived from linoleic acid (LA), many of which were elevated in kidney (particularly the medulla) and liver, but reduced in serum of rats provided the HP compared to NP or LP diets. A smaller proportion of other n-6 fatty acid derived oxylipins were lower in kidney and higher in liver, and none were affected in serum, by HP feeding. Few n-3 oxylipins were affected by protein level. In liver only, the oxylipin product to substrate ratios of the soluble epoxide hydrolase enzyme were higher in LP fed rats. Differences between cortex and medulla oxylipins suggest relatively higher cortex activity of 5- and 8-lipoxygenase and cytochrome P450 hydroxylase, and higher medulla cyclooxygenase and 12- and 15-lipoxygenase activity. Further studies are needed to elucidate the physiological effects of the changes in these novel oxylipins in response to short-term dietary HP.
       
  • Resveratrol preserves mitochondrial function in a human post-mitotic cell
           model
    • Abstract: Publication date: Available online 14 August 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Gianluca Sgarbi, Francesca Liuzzi, Alessandra Baracca, Giancarlo SolainiAbstractDysfunctions caused by genetic defects in the mitochondrial DNA (mtDNA) of humans are called mitochondrial diseases; however, mtDNA mutations are also associated with aging and age-related diseases. Here, we present an original cellular model that allows to gather information on molecules that might contrast or prevent mitochondrial dysfunctions and their related diseases. This model allowed us to show that resveratrol (RSV), a phytochemical present in food, exerts protective effects at low concentrations on resting human fibroblasts carrying dysfunctional respiratory chain Complex I. Cells were maintained both in resting condition, to mimic the high energy demanding post-mitotic tissues (serum absence and gramicidin presence), and under glucose deficiency to push the synthesis of ATP via oxidative phosphorylation. Pre-incubation with RSV prolonged the viability of the fibroblasts exposed to rotenone, a well-known specific inhibitor of the respiratory chain Complex I, and decreased mitochondrial fragmentation. It significantly prevented the oxidative phosphorylation impairment indirectly caused by the rotenone-mediated Complex I inhibition, allowing for an almost complete preservation of the cellular ATP level. Indeed, RSV limited the rotenone-induced reactive oxygen species increase, allowing for the maintenance of a functional mitochondrial membrane potential. These findings indicate the potential usage of resveratrol to prevent or possibly treat many disorders, in which the bioenergetic defects and oxidative stress are the primary (mitochondrial encephalomyopathy), or the secondary (age-related diseases) causes of the pathology; and to also assist cell senescence during aging.
       
  • Green tea polyphenols modify gut-microbiota dependent metabolisms of
           energy, bile constituents and micronutrients in female Sprague–Dawley
           rats
    • Abstract: Publication date: Available online 14 August 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Jun Zhou, Lili Tang, Chwan-Li Shen, Jia-Sheng WangAbstractOur recent metagenomics analysis has uncovered remarkable modifying effects of green tea polyphenols (GTP) on gut-microbiota community structure and energy conversion related gene orthologs in rats. How these genomic changes could further influence host health is still unclear. In this work, the alterations of gut-microbiota dependent metabolites were studied in the GTP-treated rats. Six groups of female SD rats (n=12/group) were administered drinking water containing 0%, 0.5%, and 1.5% GTP (wt/vol). Their gut contents were collected at 3- and 6-month and were analyzed via high performance liquid chromatography (HPLC) and gas chromatography (GC)-mass spectrometry (MS). GC–MS based metabolomics analysis captured 2668 feature, and 57 metabolites were imputatively from top 200 differential features identified via NIST fragmentation database. A group of key metabolites were quantitated using standard calibration methods. Compared with control, the elevated components in the GTP-treated groups include niacin (8.61-fold), 3-phenyllactic acid (2.20-fold), galactose (3.13-fold), mannose (2.05-fold), pentadecanoic acid (2.15-fold), lactic acid (2.70-fold), and proline (2.15-fold); the reduced components include cholesterol (0.29-fold), cholic acid (0.62-fold), deoxycholic acid (0.41-fold), trehalose (0.14-fold), glucose (0.46-fold), fructose (0.12-fold), and alanine (0.61-fold). These results were in line with the genomic alterations of gut-microbiome previously discovered by metagenomics analysis. The alterations of these metabolites suggested the reduction of calorific carbohydrates, elevation of vitamin production, decreases of bile constituents, and modified metabolic pattern of amino acids in the GTP-treated animals. Changes in gut-microbiota associated metabolism may be a major contributor to the anti-obesity function of GTP.
       
  • Dietary grape seed procyanidin extract protects against lead-induced heart
           injury in rats involving endoplasmic reticulum stress inhibition and AKT
           activation
    • Abstract: Publication date: Available online 14 August 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Daqian Yang, Siyu Li, Li Gao, Zhanjun Lv, Qizheng Bing, Qingjie Lv, Xiaoyan Zheng, Ruobing Li, Zhigang ZhangTo investigate the protective role of grape seed procyanidin extract (GSPE) against lead-induced heart injury and the possible molecular mechanism associated with this event, Wistar rats were orally given GSPE (200 mg/kg) daily with or without lead acetate (PbA) (0.5 g/L) in drinking water for 56 d. GSPE attenuated oxidative stress, heart dysfunction, and lead accumulation in lead-exposed rat hearts. Meanwhile, GSPE inhibited the protein kinase RNA-like endoplasmic reticulum (ER) kinase /eukaryotic initiation factor 2α signaling pathway, and promoted protein kinase B (AKT) and glycogen synthase kinase 3β phosphorylation altered by lead, and regulated lead-activated apoptosis and its related signaling pathway. This study suggests that dietary GSPE ameliorates lead-induced heart injury associated with ER stress inhibition and AKT activation. Dietary GSPE may be a protector against lead-induced heart injury and a novel therapy for lead exposure.Graphical abstractUnlabelled Image
       
  • Liraglutide modulates gut microbiota and reduces NAFLD in obese mice
    • Abstract: Publication date: Available online 11 August 2018Source: The Journal of Nutritional BiochemistryAuthor(s): GV Moreira, FF Azevedo, LM Ribeiro, A Santos, D Guadagnini, P Gama, EA Liberti, MJA Saad, CRO CarvalhoAbstractMetabolic disorders such as insulin resistance and diabetes are associated with obesity and nonalcoholic fatty liver disease (NAFLD). The aggressive form of a fatty liver disease may progress to cirrhosis and hepatocellular carcinoma. Furthermore, recent studies demonstrated that there is a dysbiosis in the gut microbiota associated with early stages of metabolic disease. Therefore, the identification and repurposing of drugs already used to treat insulin resistance may be an excellent option for other disorders. We evaluated the effect of liraglutide on obesity, NAFLD and gut microbiota modulation, in two different animal models of obesity, the ob/ob mice and the high fat diet fed mice. Liraglutide treatment induced significant weight-loss in both obesity models, showed improvements in glycemic parameters, and reduced inflammatory cell infiltration in the cecum and the liver. In ob/ob mice, the liraglutide treatment was able to reduce the accumulation of liver fat, by 78%, and reversed steatosis in the HFD mice. The gut microbiota analysis showed that liraglutide changed the overall composition as well as the relative abundance of weight-relevant phylotypes such as: a reduction of Proteobacteria and an increase of Akkermansia muciniphila in the treated high fat diet (HFD) group. We show that liraglutide can lead to weight loss and gut microbiota modulations, and is associated with an improvement of NAFLD. Furthermore, by generating a profile of the intestinal microbiota, we compiled a list of potential bacterial targets that may modulate metabolism and induce a metabolic profile that is considered normal or clinically controlled.
       
  • Blueberry polyphenols extract as a potential prebiotic with anti-obesity
           effects on C57BL/6 J mice by modulating the gut microbiota
    • Abstract: Publication date: Available online 11 August 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Xinyao Jiao, Yuehua Wang, Yang Lin, Yuxi Lang, Enhui Li, Xiuyan Zhang, Qi Zhang, Ying Feng, Xianjun Meng, Bin LiPolyphenols are known for their various health benefits. Blueberries are dietary sources of polyphenols with reported health benefits. However, the role of blueberry polyphenols in alleviating obesity is not completely understood. This study investigated the potential positive effect of blueberry polyphenol extract (PPE) on high-fat diet (HFD)-induced obesity in C57BL/6 J mice by modulation of the gut microbiota. Four-week-old C57BL/6 J mice were fed a normal-fat diet or HFD with or without PPE or Orlistat for 12 weeks. Mice fed HFD exhibited increased body weight and adipose tissue weight and disordered lipid metabolism. In contrast, PPE inhibited body weight gain and returned lipid metabolism to normal. Furthermore, 16S rRNA gene sequencing of the fecal microbiota suggested that PPE changed the composition of the gut microbiota in C57BL/6 J mice and modulated specific bacteria such as Proteobacteria, Deferribacteres, Actinobacteria, Bifidobacterium, Desulfovibrio, Adlercreutzia, Helicobacter, Flexispira, and Prevotella. Orlistat also improved obesity and metabolic alterations of HFD mice and modulated the composition of the gut microbiota. Our findings suggest that PPE, as a potential prebiotic agent, influences the gut microbiota to positively affect HFD-induced obesity in C57BL/6 J mice.Graphical abstractUnlabelled Image
       
  • Dietary modulation of mitochondrial DNA damage: Implications in ageing and
           associated diseases
    • Abstract: Publication date: Available online 7 July 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Juwela Lam, Maureen McKeagueAbstractMammalian mitochondria contain small genomes (mtDNA), which encode several of the proteins that are crucial for respiration. As such, maintaining the integrity of mtDNA is essential for healthy life. Nutrition and strategies such as “Dietary Restriction” may play an important role in regulating mtDNA integrity and prolonging lifespan. In this review, we compare mitochondrial DNA with nuclear DNA damage and discuss how the resulting cell fates relate to human health. We provide a description of the mechanisms behind Dietary Restriction as an approach to induce mitochondrial processes contributing to a longer lifespan. We make connections between the current repertoire of studies to propose how nutrition may mitigate mitochondrial dysfunction and potentially reducing DNA damage. Finally, we describe nutritional-based approaches to prevent mitochondrial dysfunction with a focus on mimetics of dietary and calorie restriction.
       
  • Excessive adipogenesis in the offspring is prevented by a slow digesting
           carbohydrate diet during pregnancy
    • Abstract: Publication date: Available online 12 June 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Maria J Martin, Manuel Manzano, Pilar Bueno-Vargas, Ricardo Rueda, Rafael Salto, Maria-Dolores Giron, Jose D Vilchez, Elena Cabrera, Ainara Cano, Azucena Castro, Cesar Ramirez-Tortosa, Jose M Lopez-PedrosaAbstractAn obesogenic environment during pregnancy has been shown to increase the risk of dysregulation on adipogenesis and insulin resistance in the offspring. Being essential for the growing fetus, glucose supply is guaranteed by a number of modifications in the mother's metabolism and thus, glucose control during pregnancy especially among obese or diabetic women is paramount to prevent adverse consequences in their children.In addition to low glycemic index carbohydrate-containing diet, the rate of carbohydrate digestion could be relevant to keep a good glucose control. In the present study, we have compared the effects of two high fat diets with similar glycemic load but different rates of carbohydrate digestion given to pregnant insulin-resistant rats. After birth, all the animals were kept on a standard diet until age 14 weeks. We analyzed body composition, plasma and adipose lipidomics, lipid metabolism in adipose tissue, and insulin sensitivity. Those animals whose mothers were fed the rapid digesting carbohydrate diet exhibited an excessive adipogenesis. Thus, these animals showed a marked lipidemia, increased lipid synthesis in the adipose tissue, and reduced glucose transporter amount in the adipose. On the contrary, those animals whose mothers were fed slow digesting carbohydrate diet showed a profile in the measured parameters closer to that of healthy animals. These results support the hypothesis that not only glycemic index but the rate of carbohydrate digestion during gestation may be critical to regulate the programming of adipogenesis in the offspring.
       
  • Systematic review and meta-analysis of preclinical trials demonstrate
           robust beneficial effects of prebiotics in induced inflammatory bowel
           disease
    • Abstract: Publication date: Available online 7 June 2018Source: The Journal of Nutritional BiochemistryAuthor(s): Marcos Natal Rufino, Gabriel Francisco Pereira Aleixo, Ingrid Eloise Trombine-Batista, Rogério Giuffrida, Rogéria Keller, Hermann Bremer-Neto
       
 
 
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