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Fat cells play key role in development of type 2 diabetes

http://www.eurekalert.org

Cellular changes in fat tissue—not the immune system—lead to the "hyperinflammation" characteristic of obesity-related glucose intolerance and type 2 diabetes, according to new research from the University of Cincinnati (UC). Cancer and cell biology experts say this new discovery about the cellular mechanisms behind glucose intolerance may provide a different target for drugs to treat type 2 diabetes as well as insights into how aggressive cancers form. The study, led by Jorge Moscat, PhD, is reported in the July 7, 2010, issue of the scientific journal Cell Metabolism. For this study, Moscat and his UC collaborator Maria Diaz-Meco, PhD, looked at the role of a specific gene known as protein kinase C (PKC)-zeta, which has been implicated as a key cellular contributor to malignant tumor growth. Using a preclinical animal model, they found that PKC-zeta had a dual role in the molecular signaling that leads to inflammation, switching from acting as a regulator of inflammation to a proinflammation agent in different circumstances. "This finding is quite novel because current drug development efforts target immune cells (macrophages, T-cells) to eliminate this hyperinflammation.

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Fat cells play key role in development of type 2 diabetes