From Our 2010 Archives

Changes in Fat Cells May Pave Way for Type 2 Diabetes

TUESDAY, July 6 (HealthDay News) -- Cellular changes in fat tissue play a major role in the development of type 2 diabetes, a new study shows.

University of Cincinnati researchers found that these changes in fat cells -- not the immune system, as previously thought -- are linked to the "hyperinflammation" seen in obesity-related glucose intolerance and type 2 diabetes. The findings, they said, may eventually lead to the development of new drugs to treat type 2 diabetes and may also offer insights into the formation of aggressive cancers.

"This finding is quite novel because current drug development efforts target immune cells (macrophages, T-cells) to eliminate this hyperinflammation," said Jorge Moscat, the study's principal investigator and chair of UC's cancer and cell biology department, in a university news release. "Our research suggests obesity-related glucose intolerance has nothing to do with the immune system. It may be more effective to target (fat cells)."

In laboratory animals, the researchers found that a gene known as protein kinase C (PKC)-zeta plays a dual role in molecular signaling associated with inflammation. Obesity, they said, can switch the gene from acting as an inflammation regulator to an agent promoting inflammation. PKC-zeta does this by causing fat cells to secrete a substance called interleukin-6 (IL6), which streams to the liver in large quantities to cause insulin resistance.

The study appears in the July 7 issue of the journal Cell Metabolism.

Previous research has linked PKC-zeta to the development of malignant tumors. Researchers say it may do so in a manner similar to the way in which it triggers the inflammation associated with diabetes.

"Now we are trying to understand how PKC-zeta regulates IL6 to better determine how we can manipulate the protein to help prevent diabetes and cancer," Moscat said.

-- Robert Preidt

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SOURCE: University of Cincinnati Academic Health Center, July 6, 2010, news release.