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Maternal betaine supplementation attenuates glucocorticoid-induced hepatic lipid accumulation through epigenetic modification in adult offspring rats
Affiliation:1. MOE Joint International Research Laboratory of Animal Health & Food Safety, Nanjing Agricultural University, Nanjing 210095, P. R. China;2. Key Laboratory of Animal Physiology & Biochemistry, Nanjing Agricultural University, Nanjing 210095, P. R. China;1. MOE Joint International Research Laboratory of Animal Health & Food Safety, Nanjing Agricultural University, Nanjing 210095, PR China;2. Key Laboratory of Animal Physiology & Biochemistry, Nanjing Agricultural University, Nanjing 210095, PR China;3. Jiangsu Collaborative Innovation Centre of Meat Production and Processing, Quality and Safety Control, Nanjing 210095, PR China;1. Neuropharmacology and Neurochemistry Research Unit, Department of Biochemistry, University of Karachi, Karachi 75270, Pakistan;2. Department of Biological and Biomedical Sciences, Aga Khan University, Karachi, Pakistan;1. Key Laboratory of Animal Physiology & Biochemistry, Nanjing Agricultural University, Nanjing 210095, P. R. China;2. Department of Medical cell biology, University of Uppsala, Uppsala SE-75123, Sweden;1. Departamento de Ciencias Químico-Biológicas y Agropecuarias, Universidad de Sonora, Unidad Regional Sur, Navojoa, Sonora, Mexico;2. Centro de Investigación en Alimentación y Desarrollo A.C., Hermosillo 83304, Sonora, Mexico
Abstract:There are lots of reports about alleviation of NAFLD by dietary supplements of betaine. However, it remains unclear whether maternal betaine supplementation can also ameliorate NAFLD in offspring. Hence, twenty pregnant rats were fed with a basal diet with or without betaine (1%), and then the female offspring rats were raised at 3 months of age followed by 3 weeks of physiological saline or dexamethasone in a dose of 0.1 mg/kg body mass every day via intraperitoneal injection. In this study, maternal betaine supplementation significantly (P<.05) reduced the increase of hepatic triglycerides concentration in dexamethasone-induced rats, which is associated with the expression of hepatic lipogenic genes (ACC1, FASN and SCD1). Moreover, the hypomethylation of lipogenic genes in dexamethasone-induced rats were reserved by prenatal betaine exposure. Furthermore, the increase of hepatic GR or SP1 content in dexamethasone-injected rats were significantly decreased (P<.05), which were in line with the binding of GR or SP1 to lipogenic genes, in betaine -exposed rats. Together, these results suggest that maternal betaine supplementation attenuates dexamethason-induced fatty liver in the female adult offspring rats, which may be attributed to DNA methylation and GR or SP1-mediated the regulation of lipogenic genes.
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