2-Heptyl-Formononetin Increases Cholesterol and Induces Hepatic Steatosis in Mice
Figure 4
Hepatic gene expression measured by RT-PCR in C57BL/6 mice fed chow, cholesterol, or cholesterol supplemented formononetin or 2-heptyl-formonetin (C7F) for five weeks (Experiment 2). (A) Genes involved in lipogenesis (Srebf1 (sterol regulatory element-binding protein-1c), Mlxipl (carbohydrate response element binding protein), Acaca (acyl-CoA carboxylase 1), Fasn (fatty acid synthase), and Scd1 (stearoyl-CoA desaturase 1)) and synthesis of triglycerides (Gpam (glycerol phosphate acyltransferase) and Dgat2 (diglyceride acyltransferase 2)). (B) Genes involved in hydrolysis and beta-oxidation of fatty acids, Atgl (adipose triglyceride lipase), Ppara (peroxisome proliferator-activated receptor α), Cpt1a (carnitine palmitoyltransferase 1a), and Acox1 (acyl CoA oxidase). (C) Genes involved in lipoprotein metabolism, Acat2 (acetyl-CoA acetyltransferase), Mttp (microsomal triglyceride transfer protein), and Ldlr (low-density lipoprotein receptor). (D) Genes involved in cholesterol metabolism, Hmgcr (3-hydroxy-3-methyl-glutaryl-CoA reductase), Cyp7a1 (cholesterol 7 alpha-hydroxylase), Nr1 h3 (liver X receptor), and Nr1 h3 (farnesoid X receptor). Data is normalised to 18S ribosomal RNA and presented relative to the expression in chow (). Graphs show mean ± SEM. Different letters (a, b, c) denote significant difference () between the groups.
