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Insulin's Double-Edged Sword Explained

  January, 11 2005 8:59
your information resource in human molecular genetics
The mechanisms leading to insulin resistance in type II diabetes have puzzled scientists for years. In people who suffer from this form of the disease, insulin is unable to control blood sugar levels but still seems capable of shutting off the switch that promotes burning of fat stores in the liver. Hence, diabetics suffer from the consequences of increased glucose levels and abnormal accumulation of fat. A paper published in the 23 Dec 04 issue of Nature (Vol. 432, No. 7020, pp. 1027-1032) reveals that some cell switches are more sensitive to insulin than others, creating new possibilities for diabetes therapies.

Markus Stoffel and his colleagues examined distinct switches within cells that control glucose and fat metabolism. The team focused on the fact that insulin inactivates the protein Foxa2, which regulates fatty-acid breakdown, and Foxo1, which promotes the formation of glucose from non-carbohydrate sources. The group found that Foxa2 seems to be much more sensitive to insulin than Foxo1, explaining how the hormone acts as a double-edged sword in type II diabetes.

"The results potentially explain how insulin can have different effects on glucose and fat metabolism, and provide interesting clues to how hepatic steatosis develops and leads to diabetes," say Marc Montminy and Seung-Hoi Koo in an accompanying News and Views article. Because type II diabetes affects 5% of adults in developed countries, a better understanding of the disease could improve the lives of many people. According to Stoffel and his team, pharmacological interventions to inhibit Foxa2 inactivation may be an effective treatment for type II diabetes.


Markus Stoffel (Rockefeller University, New York, NY, USA)
Tel: +1 212 327 8797
E-mail: stoffel@rockvax.rockefeller.edu

Marc Montminy (Salk Institute, La Jolla, CA, USA)
Tel: +1 858 453 4100 x 1394
E-mail: Montminy@salk.edu

(C) Nature press release.

Message posted by: Trevor M. D'Souza

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