Mitochondrial remodeling in adipose tissue associated with obesity and treatment with rosiglitazone
Energy homeostasis is controlled by a complex series of cellular and hormonal interactions. White fat tissue has been shown by mouse-knockout studies and the identification of fat-specific secreted factors to be central to this process. Drugs for type 2 diabetes that enhance sensitivity to insulin, such as rosiglitazone, work through mechanisms that involve fat. Cell culture work has indicated that rosiglitazone alters the mitochondria of fat cells, both in their structural features and in the types of proteins they produce. Mitochondria are what make the cell's energy. Silvia Corvera and colleagues, from University of Massachusetts Medical School, examined in live animals the effects of rosiglitazone through studies on white fat tissue in an obesity mouse model called ob/ob mice. The authors found that at the onset of obesity in the ob/ob mice, there was decreased expression of about 50% of the mitochondrial protein genes. When these mice were treated with rosiglitazone, half of these genes showed increased expression. Additionally, the mitochondria in the white fat cells of treated ob/ob mice had increased size and altered structure. The oxygen consumption, reflecting energy use, of these cells was also significantly higher. The work here provides live animal evidence that rosiglitazone treatment works by modifying mitochondrial structure and increasing white fat cell tissue energy, which indicates that increased lipid utilization by fat cells improves insulin sensitivity and alters whole-body energy homeostasis.
Source: Eurekalert & othersLast reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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