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New understanding of insulin's complexities needed to conquer diabetes

Major advances in signal-transduction research have contributed greatly to understanding the complexities of insulin action, which, when disrupted, can lead to diabetes and other health problems. According to Howard Hughes Medical Institute investigator Morris F. White, however, further progress is needed to integrate our expanding knowledge with human physiology if the diabetes epidemic that is escalating throughout the world is to be conquered.

It is important to understand the molecular links between obesity, peripheral insulin action and the function of insulin-producing beta cells, said White, who is at the Joslin Diabetes Center and Harvard Medical School. White, the author of a Viewpoints article published in the December 5, 2003, issue of the journal Science , argues that a much better understanding of insulin-regulatory pathways is needed to distinguish between pathways that can be manipulated to enhance health and those whose manipulation would endanger health.

Insulin, produced by beta cells in the pancreas, is best known for its role in regulating glucose levels in the bloodstream. However, insulin signaling also controls embryonic growth and development, reproduction, and appetite regulation. The widespread influence of insulin and the vulnerability of its signaling pathways to inhibition make understanding insulin signaling an important research goal, White noted.

Improper regulation of these pathways can lead to a range of systemic disorders. The most recognized of these, diabetes, comes in two basic forms: type 1 diabetes usually occurs in children and is caused by an absolute lack of insulin; and type 2 diabetes, which historically occurred in middle age, but today appears with alarming frequency in children and adolescents. It is caused mainly by insulin resistance in tissues and is closely associated with obesity. In addition, defects in insu
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Contact: Jim Keeley
keeleyj@hhmi.org
301-215-8858
Howard Hughes Medical Institute
4-Dec-2003


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