TUESDAY, July 6, 2010 (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.
The U.S. National Institute of Diabetes and Digestive and Kidney Diseases has more about type 2 diabetes.