作者: C. A. Ihunnah , T. Wada , B. J. Philips , S. K. Ravuri , R. B. Gibbs
DOI: 10.1128/MCB.01147-13
关键词:
摘要: Estrogen sulfotransferase (EST/SULT1E1) is known to catalyze the sulfoconjugation and deactivation of estrogens. The goal this study determine whether how EST plays a role in human adipogenesis. By using primary adipose-derived stem cells (ASCs) whole-fat tissues from abdominal subcutaneous fat obese nonobese subjects, we showed that expression was low preadipocytes but increased upon differentiation. Overexpression knockdown ASCs promoted inhibited differentiation, respectively. proadipogenic activity humans opposite antiadipogenic effect same enzyme rodents. Mechanistically, adipogenesis by deactivating can be recapitulated an estrogen receptor (ER) antagonist or ERα knockdown. In contrast, activation ER decreasing recruitment adipogenic peroxisome proliferator-activated γ (PPARγ) onto its target gene promoters, whereas antagonism PPARγ promoters. Linear regression analysis revealed positive correlation between body mass index (BMI), as well negative BMI. We conclude factor which may serve druggable inhibit turnover accumulation adipocytes patients.