Cholic Acid Treatment in Hypertriglyceridemia Models
Objective: To assess the effects of cholic acid on hepatic triglyceride accumulation, VLDL secretion, and serum triglyceride levels in mouse models of hypertriglyceridemia, and to elucidate the molecular pathway involving FXR, SHP, and SREBP-1c
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Materials1
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Protocol Steps
Cholic acid treatment
Administer cholic acid to mouse models of hypertriglyceridemia
Note: Treatment aimed at preventing hepatic triglyceride accumulation and VLDL secretion
View evidence from paper
“Cholic acid (CA) prevents hepatic TG accumulation, VLDL secretion, and elevated serum TG in mouse models of hypertriglyceridemia”
Molecular analysis
Measure hepatic expression of SREBP-1c and its lipogenic target genes
Note: Cholic acid decreases hepatic expression of SREBP-1c and its lipogenic target genes
View evidence from paper
“At the molecular level, CA decreases hepatic expression of SREBP-1c and its lipogenic target genes”
Genetic analysis using mouse mutants
Use mouse mutants for short heterodimer partner (SHP) and liver X receptor (LXR) α and β to demonstrate critical dependence of SREBP-1c reduction
Note: Demonstrates the critical dependence of the reduction of SREBP-1c expression by FXR agonists on both SHP and LXRα and LXRβ
View evidence from paper
“Through the use of mouse mutants for the short heterodimer partner (SHP) and liver X receptor (LXR) α and β, we demonstrate the critical dependence of the reduction of SREBP-1c expression by either natural or synthetic farnesoid X receptor (FXR) agonists on both SHP and LXRα and LXRβ”