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Betaine supplementation in maternal diet modulates the epigenetic regulation of hepatic gluconeogenic genes in neonatal piglets.

ABSTRACT: In this study, gestational sows were fed control or betaine-supplemented diets (3 g/kg) throughout the pregnancy, and the newborn piglets were used to elucidate whether maternal dietary betaine affected offspring hepatic gluconeogenic genes through epigenetic mechanisms. Neonatal piglets born to betaine-supplemented sows had significantly higher serum and hepatic betaine contents, together with significantly greater expression of methionine metabolic enzymes in the liver. Interestingly, significantly higher serum concentrations of lactic acid and glucogenic amino acids, including serine, glutamate, methionine and histidine, were detected in the piglets born to betaine-supplemented sows, which were coincident with higher hepatic glycogen content and PEPCK1 enzyme activity, as well as greater protein expression of gluconeogenic enzymes, pyruvate carboxylase (PC), cytoplasmic phosphoenolpyruvate carboxykinase (PEPCK1), mitochondrional phosphoenolpyruvate carboxykinase (PEPCK2) and fructose-1, 6-bisphosphatase (FBP1). Moreover, maternal betaine significantly changed the methylation status of both CpGs and histones on the promoter of gluconeogenic genes. The lower PEPCK1 mRNA was associated with DNA hypermethylation and more enriched repression histone mark H3K27me3, while the up-regulated PEPCK2 and FBP1 mRNA was associated with DNA hypomethylation and more enriched activation histone mark H3K4me3. Furthermore, the expression of two miRNAs predicted to target PC and 6 miRNAs predicted to target PEPCK1 was dramatically suppressed in the liver of piglets born to betaine-supplemented sows. Our results provide the first evidence that maternal betaine supplementation affects hepatic gluconeogenic genes expression in newborn piglets through enhanced hepatic methionine metabolism and epigenetic regulations, which involve DNA and histone methylations, and possibly miRNAs-mediated post-transcriptional mechanism.

SUBMITTER: Cai D

PROVIDER: S-EPMC4143294 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

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Betaine supplementation in maternal diet modulates the epigenetic regulation of hepatic gluconeogenic genes in neonatal piglets.

Cai Demin D Jia Yimin Y Song Haogang H Sui Shiyan S Lu Jingyu J Jiang Zheng Z Zhao Ruqian R

PloS one 20140825 8

In this study, gestational sows were fed control or betaine-supplemented diets (3 g/kg) throughout the pregnancy, and the newborn piglets were used to elucidate whether maternal dietary betaine affected offspring hepatic gluconeogenic genes through epigenetic mechanisms. Neonatal piglets born to betaine-supplemented sows had significantly higher serum and hepatic betaine contents, together with significantly greater expression of methionine metabolic enzymes in the liver. Interestingly, signific ...[more]

PMID: 25153319

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Project description:Background/objectivesPrevious research has shown maternal betaine supplementation alleviates fetal-derived hepatic steatosis. Therefore, this study examined the anti-inflammatory effect of maternal betaine intake in offspring mice and its mechanism.Materials/methodsFemale C57BL/6J mice and their offspring were randomly divided into 3 groups according to the treatment received during gestation and lactation: control diet (CD), fatty liver disease (FLD), and fatty liver disease + 1% betaine (FLD-BET). The FLD group was given a high-fat diet and streptozotocin (HFD + STZ), and the FLD-BET group was treated with HFD + STZ + 1% betaine. After weaning, the offspring mice were given a normal diet for 5 weeks and then dissected to measure the relevant indexes.ResultsCompared to the CD group, the offspring mice in the FLD group revealed obvious hepatic steatosis and increased serum levels of alanine aminotransferase, interleukin (IL)-6, and tumor necrosis factor (TNF)-α; maternal betaine supplementation reversed these changes. The hepatic mRNA expression levels of IL-6, IL-18, and Caspase-1 were significantly higher in the FLD group than in the CD group. Maternal betaine supplementation reduced the expression of IL-1β, IL-6, IL-18, and apoptosis-associated speck-like protein containing C-terminal caspase recruitment domain (ASC). Maternal betaine supplementation also reversed the increasing protein expressions of nitric oxide dioxygenase-like receptor family pyrin domain containing 3 (NLRP3), ASC, Caspase-1, IL-1β, and IL-18 in offspring mice exposed to HFD + STZ. Maternal betaine supplementation decreased the homocysteine (Hcy) and s-adenosine homocysteine (SAH) levels significantly in the livers. Furthermore, the hepatic Hcy concentrations showed significant inverse relationships with the mRNA expression of TNF-α, NLRP3, ASC, and IL-18. The hepatic SAH concentration was inversely associated with the IL-1β mRNA expression.ConclusionsThe lipotropic and anti-inflammatory effect of maternal betaine supplementation may be associated with the inhibition of NLRP3 inflammasome in the livers of the offspring mice.

Project description:The present study was conducted to investigate the effects of maternal probiotic or synbiotic supplementation during gestation and lactation on antioxidant capacity, mitochondrial function, and intestinal microbiota abundance in offspring weaned piglets. A total of 64 pregnant Bama mini-sows were randomly allocated into the control group (basal diet), antibiotic group (basal diet + 50 g/t virginiamycin), probiotic group (basal diet + 200 mL/d probiotics per pig), or synbiotic group (basal diet + 200 mL/d probiotics per pig + 500 g/t xylo-oligosaccharides). On day 30 of post-weaning, eight piglets per group with average body weight were selected for sample collection. The results showed that maternal probiotic supplementation increased the catalase (CAT) activity in plasma and glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities in plasma, jejunum, and colon of piglets while decreased the malondialdehyde (MDA) and H2O2 concentrations in plasma compared with the control group (P < 0.05). Moreover, maternal synbiotic supplementation increased the plasma CAT activity, jejunal glutathione and GSH-Px activities, jejunal and colonic total antioxidant capacity activity, and plasma and colonic SOD activity while decreased the colonic MDA concentration of offspring piglets compared with the control group (P < 0.05). The mRNA levels of antioxidant enzyme-related genes (copper- and zinc-containing superoxide dismutase, nuclear factor erythroid 2-related factor 1, and nuclear factor erythroid 2-related factor 2) and mitochondrial-related genes (adenosine triphosphate synthase alpha subunit, adenosine triphosphate synthase β, and mitochondrial transcription factor A) in the jejunal mucosa were significantly upregulated, while the level of colonic peroxisome proliferator-activated receptor γ coactivator-1α was downregulated by maternal synbiotic supplementation (P < 0.05). Maternal probiotic supplementation increased (P < 0.05) the Bacteroidetes abundance in the jejunum and Bifidobacterium abundance in the jejunum and colon, and synbiotic supplementation increased (P < 0.05) the abundances of Firmicutes, Bacteroidetes, Bifidobacterium, and Lactobacillus in the jejunum of piglets. Furthermore, correlation analysis revealed that intestinal microbiota abundances were significantly correlated with antioxidant enzyme activities and mitochondrial-related indexes. These findings indicated that maternal probiotic or synbiotic supplementation might be a promising strategy to improve the antioxidant capacity and mitochondrial function of offspring weaned piglets by altering the intestinal microbiota.

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Betaine supplementation in maternal diet modulates the epigenetic regulation of hepatic gluconeogenic genes in neonatal piglets.

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Betaine supplementation in maternal diet modulates the epigenetic regulation of hepatic gluconeogenic genes in neonatal piglets.

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