B Jin1, X Chen1, L Xing1, W Xu1, X Fu1, J Zhu1, X Mou2, Z Wang2, J Shu1. 1. a Department of Reproductive Endocrinology , Zhejiang Provincial People's Hospital , Hangzhou , Zhejiang , PR China. 2. b Clinical Research Institute , Zhejiang Provincial People's Hospital , Hangzhou , Zhejiang , PR China.
Abstract
OBJECTIVE: Elevated fat mass and redistribution of body fat are commonly observed in postmenopausal women. Aquaporin 7 (AQP7), a unique glycerol permeable integral membrane protein, has been associated with the onset of obesity. We hypothesized that estrogen supplementation could counteract this fat accumulation and redistribution through tissue-specific modulation of AQP7. METHODS: We measured fat depot weight, adipocyte size, and the expression of AQP7 and glycerol kinase (GK) in visceral and subcutaneous fat tissues of ovariectomized mice supplemented with or without 17β-estradiol. RESULTS: Removal of the ovaries resulted in a significant decrease in AQP7 expression and an increase in GK expression in visceral adipocyte tissue; expression of AQP7 and GK in subcutaneous adipose tissue remained unaltered. Supplementation with estrogen significantly restored the visceral, but not subcutaneous, fat depot mass and adipocyte size to those of sham-operated mice. A marked increase in the expression of AQP7 and a reduction of GK were observed selectively in the visceral fat depots in estrogen-treated mice. CONCLUSIONS: Our results suggest that estrogen has tissue-specific effects on AQP7 expression, and modulation of AQP7 by estrogen alters the balance of adipocyte metabolism between adipose tissue depots.
OBJECTIVE: Elevated fat mass and redistribution of body fat are commonly observed in postmenopausal women. Aquaporin 7 (AQP7), a unique glycerol permeable integral membrane protein, has been associated with the onset of obesity. We hypothesized that estrogen supplementation could counteract this fat accumulation and redistribution through tissue-specific modulation of AQP7. METHODS: We measured fat depot weight, adipocyte size, and the expression of AQP7 and glycerol kinase (GK) in visceral and subcutaneous fat tissues of ovariectomized mice supplemented with or without 17β-estradiol. RESULTS: Removal of the ovaries resulted in a significant decrease in AQP7 expression and an increase in GK expression in visceral adipocyte tissue; expression of AQP7 and GK in subcutaneous adipose tissue remained unaltered. Supplementation with estrogen significantly restored the visceral, but not subcutaneous, fat depot mass and adipocyte size to those of sham-operated mice. A marked increase in the expression of AQP7 and a reduction of GK were observed selectively in the visceral fat depots in estrogen-treated mice. CONCLUSIONS: Our results suggest that estrogen has tissue-specific effects on AQP7 expression, and modulation of AQP7 by estrogen alters the balance of adipocyte metabolism between adipose tissue depots.