期刊
STEROIDS
卷 77, 期 6, 页码 659-665出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.steroids.2012.02.012
关键词
White adipose tissue; Ovariectomy; E2 replacement; Mitochondria; Adiponectin; Sex
资金
- Direccion General de Investigacion y Gestion del Plan Nacional de I+D+i [SAF2010-21792]
- Fondo de Investigaciones Sanitarias of the Spanish Government [PIO60293]
- Comunitat Autonoma de les Illes Balears
Sexual dimorphism has been previously found both in mitochondrial biogenesis and function and in adiponectin expression of retroperitoneal WAT. However, little is known about the E2 effects on WAT mitochondrial function. Accordingly, the aim of this study was to examine in greater depth the role of estrogens in sexual dimorphism. This was accomplished by studying the effects of ovariectomy and E2 replacement on retroperitoneal WAT mitochondrial function. Fourteen-week-old female and ovariectomized (OVX) female Wistar rats were used in this study. The ovariectomy was performed at 5 weeks of age and at 10 weeks of age OVX rats were divided into two experimental groups: OVX, and OVX treated with 17 beta-estradiol (E2) (OVX + E2). Subcutaneous injections of E2 (10 mu g/kg/48 h) were administered to the OVX + E2 rats for 4 weeks previous to the sacrifice whereas OVX rats were treated only with the vehicle. Levels of the main markers for mitochondrial biogenesis and function and those representatives of the antioxidant defense system and insulin sensitivity were determined. Additionally, the mRNA levels of the alpha and beta estrogen receptors and of some adipocyte differentiation markers were studied. Our results indicate that retroperitoneal WAT was able to adapt itself to ovariectomy without any changes in mitochondrial function markers or for the adiponectin levels. However, E2 supplementation led to an unexpected decrease in: TFAM protein levels, in LPL, PPAR gamma and adiponectin gene expression and in the systemic HMW adiponectin levels. This decrease is probably due to the down-regulation of the ER alpha mRNA expression to avoid an over-stimulation by E2. (c) 2012 Elsevier Inc. All rights reserved.
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