期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 113, 期 10, 页码 1408-1418出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI200421025
关键词
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资金
- NIDDK NIH HHS [P01 DK059820, 1P01 DK59820-01] Funding Source: Medline
We explored the effects of bile acids on triglyceride (TG) homeostasis using a combination of molecular, cellular, and animal models. Cholic acid (CA) prevents hepatic TG accumulation, VLDL secretion, and elevated serum TG in mouse models of hypertriglyceridemia. At the molecular level, CA decreases hepatic expression of SREBP-1c and its lipogenic target genes. Through the use of mouse mutants for the short heterodimer partner (SHP) and liver X receptor (LXR) alpha and beta, we demonstrate the critical dependence of the reduction of SR-EBP-1c expression by either natural or synthetic farnesoid X receptor (FXR) agonists on both SHP and LXRalpha and LXRbeta. These results suggest that strategies aimed at increasing FXR activity and the repressive effects of SHP should be explored to correct hypertriglyceridemia.
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