Poster Topical Area: Obesity
Location: Hall D
Poster Board Number: 693
Objectives: We previously discovered that female mice deficient for GPR30, a membrane-associated estrogen receptor, were protected from high-fat diet-induced obesity, glucose intolerance, and insulin resistance with increased core temperature and energy expenditure. As enhanced formation of beige adipocytes within the white adipose tissue is associated with improved energy expenditure and metabolic phenotypes, we explored in the present study whether GPR30 regulates beige adipogenesis.
Methods: Stromal vascular fraction cells in subcutaneous fat depots of the mice were isolated and induced for beige adipogenesis. Thermogenic uncoupling protein-1 (UCP-1) gene expression was determined by real time-qPCR and its protein was probed with western blotting.
Results: Deletion of GPR30 enhanced the differentiation of stromal cells into beige adipocytes. UCP-1 gene expression in GPR30-/- beige adipocytes was significantly higher as compared with WT cells in response to cold exposure. Consistently, deletion of GPR30- enhanced cold-stimulated UCP-1 protein expression in subcutaneous white adipose of mice, whereas UCP-1 protein levels in brown adipose tissue were not altered.
Conclusion: These findings provide further evidence that GPR30 plays a role in energy homeostasis and obesity development in females.