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Research Links Changes in Fat Cells to Diabetes
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.
For this study, lead author Jorge Moscat and his UC collaborator Maria Diaz-Meco, 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. Our research suggests obesity-related glucose intolerance has nothing to do with the immune system. It may be more effective to target adipocytes (fat cells)," said Moscat.
In normal cells, explains Moscat, PKC-zeta regulates the balance between cellular inflammatory responses to maintain glucose control. During obesity-induced inflammation, however, the function of PKC-zeta changes and the molecule begins to promote inflammation by causing adipocytes to secrete a substance (IL-6) that travels in large quantities to the liver to cause insulin resistance.
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