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JCI table of contents November 1, 2004

ondria 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.

TITLE: Mitochondrial remodeling in adipose tissue associated with obesity and treatment with rosiglitazone

AUTHOR CONTACT:
Silvia Corvera,
University of Massachusetts Medical School, 373 Plantation Street, Worcester, MA 01601, USA
Phone: 508-856-6898; Fax: 508-856-1617; E-mail: silvia.corvera@umassmed.edu

View the PDF of this article at: https://www.the-jci.org/press/21752.pdf


Imatinib May Aid in Combating Idiopathic Pulmonary Fibrosis

Idiopathic pulmonary fibrosis (IPF) is a rapidly progressing lung disease that has a survival rate of fewer than three years. Recent work suggests an underlying mechanism of pathogenesis of IPF may work through cytokines that can promote the formation of excessive fiberous tissue, such as TGF-b and PDGF. Edward Leof and colleagues , from the Mayo Clinic, examined TGF-bin
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Contact: Laurie Goodman
press_releases@the-jci.org
212-342-4159
Journal of Clinical Investigation
1-Nov-2004


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