%0 Journal Article
%T Obesity Affects Mitochondrial Citrate Synthase in Human Omental Adipose Tissue
%A Martine Christe
%A Estelle Hirzel
%A Andrea Lindinger
%A Beatrice Kern
%A Markus von Fl¨še
%A Ralph Peterli
%A Thomas Peters
%A Alex N. Eberle
%A Peter W. Lindinger
%J ISRN Obesity
%D 2013
%R 10.1155/2013/826027
%X The activities of some key enzymes in mitochondria from 135 human omental adipose tissue samples of obese and nonobese patients were analyzed for potential association with the patientsĄ¯ state of obesity. The activities of respiratory complexes I and II as well as citrate synthase in isolated mitochondria were measured using spectrophotometric enzyme assays. ATP generation of mitochondria was determined with a bioluminescence assay. Protein levels of citrate synthase were quantified by western blot. The rates of ATP generation and the enzymatic activities of complexes I and II did not display associations with age, gender, obesity, or diabetes. By contrast, the enzymatic activities of citrate synthase and its protein levels were significantly reduced in obesity as compared to controls. In diabetic patients, protein levels but not enzymatic activities of citrate synthase were elevated. Thus, this investigation based on enzymatic assay and determination of protein levels revealed that the development of obesity is associated with a significant impact on citrate synthase in mitochondria of human omental adipose tissue. The state of obesity appears to affect mitochondrial function in human omental adipose tissue by limiting this key enzyme of the tricarboxylic acid cycle rather than by limiting the activities of respiratory chain enzymes. 1. Introduction The human adipose tissue is recognized as a multifunctional organ; it stores lipids and with its brown tissue islets also plays an important role in thermogenesis [1, 2]. Furthermore, intra-abdominal and omental adipose tissue compartments exert various endocrine functions [3] by secreting different peptide hormones and adipokines such as adiponectin, plasminogen activator inhibitor-1, interleukin-6, leptin, resistin, or visfatin [4]. The dysregulation of endocrine factors and other functional entities, including mitochondria, are known to be associated with the development of metabolic disorders such as obesity, insulin resistance, metabolic syndrome, and type 2 diabetes [5¨C10]. Lipid storage and mobilization in adipocytes are tightly linked to the functional state of the mitochondria. Energy expenditure depends on an intact electron transfer chain located in the inner mitochondrial membrane and requires a proton gradient to synthesize ATP from ADP and phosphate [11]. This tightly regulated process can be uncoupled by uncoupling proteins resulting in thermogenesis in brown adipocytes [12] but not in white adipocytes [13]. Different types of cell or tissue contain heterogeneous populations of mitochondria
%U http://www.hindawi.com/journals/isrn.obesity/2013/826027/