Insulin is a hormone that is produced by the pancreas and allows cells of the body to use blood glucose effectively. In conditions such as Type 2 diabetes, obesity or excessively reduced body fat, cells can become resistant to the effects of insulin through a mechanism that is not completely clear. A compound that was able to reverse the effects of insulin resistance would therefore be useful in these conditions and in the August issue of Nature Medicine (Vol. 7, No. 8), two teams of scientists report the discovery of one compound with this potential - adiponectin.
Takashi Kadowaki and colleagues at the University of Tokyo administered adiponectin to obese mice fed a high fat diet and to mice that had reduced levels of body fat (lipoatrophy). They found that the hormone improved insulin resistance and lowered blood glucose levels in both sets of mice. They further discovered that adiponectin works by reducing triglyceride levels in skeletal muscle. Because of its ability to lower blood glucose levels in the fact of insulin resistance, Kadowaki's team concludes that "adiponectin has potential as an anti-diabetic drug."
A separate team working at Albert Einstein College of Medicine in New York, led by Philipp E. Scherer, have also discovered that injection of adiponectin lowers blood glucose levels in obese and diabetic mice. Alan Saltiel of the University of Michigan School of Medicine puts the findings into context in an accompanying News & Views article.
Dr. Alan R. Saltiel
Life Sciences Institute
Department of Medicine
University of Michigan School of Medicine
Ann Arbor, Michigan, USA
Tel: (+1) 734 615-9787
Fax: (+1) 734 936-2888
Dr. Takashi Kadowaki
Department of Internal Medicine
Graduate School of Medicine
University of Tokyo
Tel: (+81) 3 5800 8818
Fax (+81) 3 5689 7209
Dr. Philipp E. Scherer
Department of Cell Biology and
Diabetes Research and Training Center
Albert Einstein College of Medicine
1300 Morris Park Avenue
Bronx, NY, USA
Tel: (+1)718 430-2928
Fax (+1) 718 430 8574
(C) Nature Medicine press release.
Message posted by: Trevor M. D'Souza