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
This is a Cholic Acid Treatment in Hypertriglyceridemia Models protocol using mouse as the model organism. The procedure involves 3 procedural steps, 1 materials. Extracted from a 2004 paper published in Journal of Clinical Investigation.
Model and subjects
mouse • Not specified in provided text • unknown • Not specified in provided text • Not specified in provided text
Study window
Estimated timing pending
Core workflow
Cholic acid treatment • Molecular analysis • Genetic analysis using mouse mutants
Primary readouts
- Hepatic triglyceride accumulation
- VLDL secretion
- Serum triglyceride levels
- Hepatic expression of SREBP-1c
Key equipment and reagents
Verified items
0
Direct vendor links
0
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Protocol Steps
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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”