Role of estrogen-related receptor alpha in adipocyes lipolysis.
- Author:
Dapeng JU
1
;
Jingjing HE
;
Xueli ZHENG
;
Lili ZHAO
;
Gongshe YANG
Author Information
1. Laboratory of Animal Fat Deposition and Muscle Development, College of Animal Science and Technology, Northwest Sci-Tech University of Agriculture and Forestry, Yangling 712100, China.
- Publication Type:Journal Article
- MeSH:
Adipocytes;
cytology;
metabolism;
Animals;
Animals, Newborn;
Cells, Cultured;
Glycerol;
analysis;
Lipase;
metabolism;
Lipolysis;
physiology;
Receptors, Estrogen;
metabolism;
physiology;
Sterol Esterase;
metabolism;
Swine;
Triglycerides;
analysis
- From:
Chinese Journal of Biotechnology
2011;27(1):18-25
- CountryChina
- Language:Chinese
-
Abstract:
Estrogen-related receptor a (ERRalpha) is a key regulator for energy metabolism and adipogenesis. However, its role in lipolysis is unknown. To study the function of ERRalpha in lipolysis, primary cultured differentiated porcine adipocytes were treated by a specific inverse agonist XCT790 or infected with adenoviral vector expressed ERRalpha for 48 h, in the absence and/or presence of specific protein kinase A (PKA) inhibitor or extracellular signal-related kinase (ERK) inhibitor. Then, we measured the triglyceride (TG) content and the glycerol release into the culture media to analysis the effect of ERRalpha on lipolysis; Further, we analyzed the expression of PPARgamma, perilipin A, p-perilipin A, HSL and ATGL with Western blotting. Here, we found that ERRalpha significantly increased adipocytes differentiation, TG accumulation and glycerol release. Separately or simultaneously block the PKA and ERK pathway do not significantly altered the effect of ERRalpha on glycerol release. ERRalpha significantly up-regulated the proteins expression of PPARgamma, perilipin A, HSL and ATGL, while the p-perilipin A protein level was not significantly changed. These findings imply that ERRalpha could increase lipolysis via up-regulating HSL and ATGL, thereby to supply more FFA as substrate for a larger turnover of cellular triglyceride pool during adipocytes differentiation.
