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Betaine modulates high carbohydrate diet‐induced fatty liver in mice
Author(s) -
Liu Rui,
Chen Linda,
McClain Craig
Publication year - 2006
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.20.4.a183-a
Subject(s) - betaine , endocrinology , medicine , adiponectin , chemistry , steatosis , fatty liver , glutathione , steatohepatitis , lipid peroxidation , liver injury , oxidative stress , alanine transaminase , biochemistry , insulin resistance , biology , insulin , enzyme , disease
There is a surge in obesity in the USA. It is associated with non‐alcoholic fatty liver disease (NAFLD), which may evolve into non‐alcoholic steatohepatitis (NASH). Betaine may act as an antioxidant since it is involved in glutathione (GSH) metabolism. The objective of this study was to determine whether betaine might modulate mediators, nuclear factor‐kB (NF‐kB) and adiponectin, which are involved in the molecular mechanism of NAFLD. Fifteen C57BL/6 male mice were fed for 5 months in 3 groups: (1) a standard diet with water; (2) a high carbohydrate diet (HCD) with water; and (3) a HCD with betaine drink (2.5 g betaine dissolved in 500 ml water). The mice were killed 2 hours after iv administration of lipopolysaccharide (LPS). The HCD‐induced fatty liver mouse model was established. Betaine markedly reduced fatty liver and the elevated levels of plasma triglycerides and cholesterol induced by HCD. The HCD‐induced oxidative stress was manifested by increased liver lipid peroxidation (LP) and decreased GSH levels, and HCD also led to increased plasma alanine transaminase (ALT) activity and adiponectin levels. Betaine decreased LP and ALT activity, and increased GSH and adiponectin levels. Furthermore, HCD‐induced release of tumor necrosis factor‐a (TNF‐a) and NF‐kB activation in the liver, shown by the translocation of subunit P65 and elevated phosphorylated IkB‐a levels, were decreased by betaine. In conclusion, this study suggests that betaine partly modulates hepatic steatosis by blocking NF‐kB activation and adiponectin secretion, and that betaine can improve antioxidant status and plasma lipid profile in mice fed HCD. Our findings provide a rationale for further exploration of the potential use of betaine in the treatment of NAFLD/NASH. Supported by NIH grants AA01762 and AA10496.