Proteomic study of periovarian adipose tissue in 17β-estradiol-treated and untreated ovariectomized rats

被引:5
作者
Amengual-Cladera, Emilia [1 ,2 ]
Capllonch-Amer, Gabriela [1 ]
Llado, Isabel [1 ,2 ]
Gianotti, Magdalena [1 ,2 ]
Proenza, Ana M. [1 ,2 ]
机构
[1] Univ Illes Balears, Inst Univ Invest Ciencies Salut IUNICS, Dept Biol Fonamental & Ciencies Salut, Grp Metab Energet & Nutr, Palma de Mallorca, Spain
[2] Inst Salud Carlos III, Ctr Invest Biomed Red Fisiopatol Obesidad & Nutr, C Sinesio Delgado 4, Madrid 28029, Spain
关键词
white adipose tissue; 17; beta-estradiol; mitochondria; ovariectomy; proteomics; SEX-DEPENDENT DIFFERENCES; MITOCHONDRIAL-FUNCTION; ER-ALPHA; INSULIN-RESISTANCE; CARBONIC-ANHYDRASE; SKELETAL-MUSCLE; METABOLISM; GLUCOSE; BETA; INFLAMMATION;
D O I
10.1139/bcb-2015-0077
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Taking into account the sexual dimorphism previously found in white adipose tissue (WAT) regarding mitochondrial function and biogenesis, as well as insulin sensitivity, the aim of this study was to go further into the role of sex hormones in this dimorphism. To achieve this objective, we used ovariectomized rats and performed a screening by means of proteomic analyses of the periovarian WAT, combined with a study of the protein levels of specific factors involved in mitochondrial function. Rats were ovariectomized at 5 weeks of age and subcutaneously injected every 48 h with corn-oil (OVX group) or with 17 beta-estradiol (E2, 10 mu g/kg body mass; OVX + E2 group) for 4 weeks prior to sacrifice. Beside proteomic analysis, protein levels of Transcription Factor A, Mitochondrial (TFAM), cytochrome oxidase (COX) II, and COXIV were determined by Western blot, and mRNA levels of peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1 alpha, ER alpha, ER beta, lipoprotein lipase (LPL), peroxisome proliferator-activated receptor-gamma (PPAR gamma), and adiponectin were quantified by real-time PCR. Our results show that ovariectomy leads to an increase in anabolic processes and inflammatory protein levels as well as to a decrease in some of the markers of mitochondrial function, which are restored, at least in part, by E2 supplementation. Indeed, this E2 supplementation seems to be counteracted by a decline in ER alpha and in the ER alpha to ER beta ratio values that could be directed to avoid an over-stimulation of the E2 signaling pathway, given the possibility of an activation of extra-gonadal steroid biosynthetic pathways.
引用
收藏
页码:167 / 175
页数:9
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