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. Author manuscript; available in PMC: 2017 Oct 30.
Published in final edited form as: Hepatology. 2015 Oct 10;63(1):95–106. doi: 10.1002/hep.28124

Figure 1. Lrh-1−/− mice are resistant to hepatitis and liver fibrosis induced by methyl-pool alterations.

Figure 1

A. Schematic of methyl-group cycling. SAM, S-adenosylmethionine; Gnmt, glycine-n-methyltransferase; Gamt, guanidinoacetate-n-methyltransferase; Pemt, phosphatidylethanolamine-n-methyltransferase; phosphatidylcholine, PC; SAH, S-adenosylhomocysteine; MCD, Methionine-choline deficient diet; Mdr2/Abcb4, multidrug-resistance protein 2; PE, phosphatidylethanolamine; THF, tetrahydrofolate; B,C. Wildtype (WT) and liver specific LRH-1 knockout (Lrh-1−/−) mice were fed MCD diet for 2 weeks and markers of liver injury (ALT serum levels (B)) and inflammation (hepatic TNFα and Icam mRNA (C)) were measured. n=7-9 mice per group. D. Wildtype (WT) and liver specific LRH-1 knockout (Lrh-1−/−) mice were fed MCD diet for 8 weeks and markers of fibrosis (hepatic Col1a1 mRNA and hydroxyproline content) were determined. n=4 mice per group. * p<0.05, chow vs. MCD; # p<0.05, WT vs. Lrh-1−/− . Error bars represent means ± standard deviation.