Related Experiment Video
Updated: Jun 4, 2025

A Protocol for Housing Mice in an Enriched Environment
Published on: June 8, 2015
IDOL alleviates the body weight by upregulating UCP-1 in mice
Hua Guan1,2, Le Wang2, Chengcheng Tang2
1State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Engineering Research Center for Dental Materials and Advanced Manufacture, Department of Anesthesiology, School of Stomatology, The Fourth Military Medical University, Xi'an, China.
Inducible degrader of the low density lipoprotein receptor (IDOL) overexpression in brown adipose tissue (BAT) reduced body weight. IDOL promotes BAT lipolysis by increasing UCP-1 and ATGL, offering a potential anti-obesity strategy.
Area of Science:
- Metabolic research
- Adipose tissue biology
- Molecular endocrinology
Background:
- Brown adipose tissue (BAT) activation stimulates energy expenditure, presenting an anti-obesity treatment avenue.
- Adenoviral delivery was used to investigate the role of inducible degrader of the low density lipoprotein receptor (IDOL) in BAT formation.
Purpose of the Study:
- To determine the effect of inducible degrader of the low density lipoprotein receptor (IDOL) on brown adipose tissue (BAT) formation and function.
- To explore IDOL's potential as an anti-obesity therapeutic target.
Main Methods:
- Adenovirus-mediated overexpression of IDOL in C57BL/6J mice fed a high-fat diet for 12 weeks.
- Analysis of body weight, adipose tissue morphology, lipid profiles, adipogenesis markers, and gene expression via RNA sequencing and Western blot.
Main Results:
- IDOL overexpression significantly reduced body weight, adipose tissue mass, and serum FGF21/leptin levels.
- Increased expression of ATGL, perilipin 1, and UCP-1 in BAT, alongside elevated PGAM2, G6PC1, and phosphorylated AMPK.
- RNA sequencing revealed 1256 differentially expressed genes enriched in nine signaling pathways.
Conclusions:
- IDOL overexpression alleviates body weight by promoting BAT lipolysis.
- This effect is mediated by the phosphorylation of AMPK, leading to upregulation of UCP-1 and ATGL in brown adipose tissue.

