Dietary betaine supplementation to gestational sows enhances hippocampal IGF2 expression in newborn piglets with modified DNA methylation of the differentially methylated regions

Li, Xi; Sun, Qinwei; Li, Xian; Cai, Demin; Sui, Shiyan; Jia, Yimin; Hu, Song; Zhao, Ruqian

doi:10.1007/s00394-014-0799-4

Cited by 30 publications

(25 citation statements)

References 54 publications

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“…In this study, maternal betaine supplementation significantly upregulated BHMT at both mRNA and protein levels in F1 offspring. Similar findings have been reported that maternal betaine supplementation during gestation enhanced BHMT expression in liver , skeletal muscle , and hippocampus of neonatal piglets. However, this change was not detected in F2 offspring.…”

Section: Discussionsupporting

confidence: 90%

Maternal betaine supplementation in rats induces intergenerational changes in hepatic IGF‐1 expression and DNA methylation

Zhao

Yang

et al. 2017

Molecular Nutrition Food Res

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Section: Discussionsupporting

confidence: 90%

Maternal betaine supplementation in rats induces intergenerational changes in hepatic IGF‐1 expression and DNA methylation

Zhao

Yang

et al. 2017

Molecular Nutrition Food Res

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“…Betaine, a methyl donor, is an important component of the methionine cycle which is essential for the epigenetic gene regulation through DNA methylation and histone modifications192021. It is well-documented that betaine can promote growth and improve carcass characteristics and meat quality in livestock animals2223 and broiler chickens2425.…”

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confidence: 99%

In ovo injection of betaine alleviates corticosterone-induced fatty liver in chickens through epigenetic modifications

Sun

Liu

et al. 2017

Sci Rep

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Betaine alleviates high-fat diet-induced fatty liver and prenatal betaine programs offspring hepatic lipid metabolism. Excessive corticosterone (CORT) exposure causes fatty liver in chickens, yet it remains unknown whether and how prenatal betaine modulates the susceptibility of CORT-induced fatty liver later in life. In this study, fertilized eggs were injected with saline or betaine before incubation, and the hatchlings were raised at 8 weeks of age followed by 7 days of subcutaneous CORT injection. CORT-induced fatty liver was less severe in betaine-treated chickens, with significantly reduced oil-red staining and hepatic triglyceride content (P < 0.05). The protective effect of prenatal betaine was associated with significantly up-regulated expression of PPARα and CPT1α, as well as mitochondrial DNA (mtDNA)-encoded genes (P < 0.05). Moreover, betaine rescued CORT-induced alterations in methionine cycle genes, which coincided with modifications of CpG methylation on CPT1α gene promoter and mtDNA D-loop regions. Furthermore, the elevation of hepatic GR protein content after CORT treatment was significantly reduced (P < 0.05), while the reduction of GR binding to the control region of affected genes was significantly increased (P < 0.05), in betaine-treated chickens. These results indicate that in ovo betaine injection protects the juvenile chickens from CORT-induced fatty liver.

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“…Total protein was extracted from 50 mg frozen liver samples, as previously described . Protein concentrations were measured using bicinchoninic acid (BCA) Protein Assay kit (No.…”

Section: Methodsmentioning

confidence: 95%

Grandmaternal betaine supplementation enhances hepatic IGF2 expression in F2 rat offspring through modification of promoter DNA methylation

et al. 2019

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BACKGROUND: We reported previously that maternal betaine promotes hepatic insulin-like growth factor (IGF2) expression in F1 offspring rats through hypermethylation of the IGF2/H19 imprinting control region (ICR). It remains unknown whether this acquired trait can be transmitted to the F2 generation. This study aimed to determine whether dietary betaine supplementation to grand dams affects the hepatic IGF2 expression in F2 rat offspring and how it is related to alterations in DNA methylation. F2 rat offspring derived from grand dams fed basal or betaine-supplemented diet (10 g kg −1 ) were examined at weaning. Serum IGF2 concentration was measured with enzyme-linked immunosorbent assay (ELISA). Hepatic expression of IGF2, together with other proliferation and apoptosis markers, was determined by using quantitative polymerase chain reaction (qPCR), western blot, and immunohistochemistry. The methylation status of the IGF2/H19 ICR and the promoters of IGF2 gene were detected by methylated DNA immunoprecipitation quantitative polymerase chain reaction (MeDIP-qPCR). RESULTS: The maternal betaine-induced up-regulation of hepatic IGF2 expression in F1 ratoffspring was transmitted to the F2 generation. The F2 rats from the betaine group demonstrated enhanced hepatic IGF2 expression at both mRNA and protein levels, in association with higher serum IGF2 concentration. No alterations were observed in the ICR methylation of the IGF2/H19 locus, and hypomethylation was detected in promoters of IGF2 gene in betaine group. CONCLUSION: These results indicate that maternal betaine enhances hepatic IGF2 expression in F2 rat offspring through modification of DNA methylation on IGF2 promoters.Immunohistochemical staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) apoptosis assay Proliferating cell nuclear antigen and IGF2 immunoreactive cells were stained with immunohistochemistry in liver sections as

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Dietary betaine supplementation to gestational sows enhances hippocampal IGF2 expression in newborn piglets with modified DNA methylation of the differentially methylated regions

Cited by 30 publications

References 54 publications

Maternal betaine supplementation in rats induces intergenerational changes in hepatic IGF‐1 expression and DNA methylation

Maternal betaine supplementation in rats induces intergenerational changes in hepatic IGF‐1 expression and DNA methylation

In ovo injection of betaine alleviates corticosterone-induced fatty liver in chickens through epigenetic modifications

Grandmaternal betaine supplementation enhances hepatic IGF2 expression in F2 rat offspring through modification of promoter DNA methylation

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