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Induction of non‐alcoholic fatty liver is prevented by betaine supplementation in rats
Author(s) -
Ahn Chul Won,
Kwon Do Young,
Kim Sun Ju,
Kim Young Chul
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1106.1
Subject(s) - betaine , medicine , endocrinology , fatty liver , steatosis , chemistry , triglyceride , homocysteine , very low density lipoprotein , cholesterol , lipoprotein , biochemistry , biology , disease
Previous work in this laboratory showed that betaine supplementation inhibited fat accumulation in liver of rats fed a high fat diet. In this study we examined the hepatoprotective mechanism of betaine against induction of non‐alcoholic fatty liver. Male rats were fed a high fat (HF) liquid diet for 3 wks. Betaine (1 % w/v) supplementation reduced the elevation of hepatic triglyceride (TG) significantly while increasing serum total cholesterol and TG levels. The decrease in phosphorylation of adenosine monophosphate‐activated protein kinase and acetyl‐CoA carboxylase in fatty liver was blocked by betaine supplementation. The elevated translocation of lipogenic transcription factors, sterol regulatory element binding protein‐1c and liver X receptor‐alpha, was normalized in the betaine‐treated rats. The HF diet intake resulted in reduction of betaine‐homocysteine methyltransferase expression and elevation of hepatic homocysteine, which was inhibited by betaine. Meanwhile, betaine supplementation increased hepatic apolipoprotein B protein expression, the obligatory platform for assembly of very‐low density lipoprotein (VLDL), and serum phosphatidylcholine, a component of VLDL particles. Taken together, the results suggest that the beneficial effects of betaine against hepatic steatosis may be accounted for by inhibition of lipid synthesis as well as by enhancement of its secretion.