9-Jul-10 10:00 AM CST

Study Ties Gene in Fat Cells to Type 2 Diabetes

Jorge Moscat, PhD, Chair of UC Cancer and Cell Biology Department, hopes that understanding the role PKC-zeta plays in Type 2 Diabetes and tumor growth will lead to new drugs that can help prevent both diseases.

A new study by researchers at the University of Cincinnati (UC) suggests that a specific gene in found in the fat cells could play a major role in the development of Type 2 Diabetes.

According to the UC study, led by Dr. Jorge Moscat, Ph.D., chair of the University of Cincinnati cancer cell and biology department, fat cells are regulated by a gene known as protein kinase C-zeta (PKC-zeta). Obesity, however, can cause the fat cells to become inflamed, which causes PKC-zeta to release a substance called IL-6. IL-6 travels to the liver, eventually causing the insulin resistance that leads to Type 2 Diabetes.

Moscat says this research is unique in that earlier studies had said a different gene called JNK1, known to regulate immune cells, also regulated fat cells and therefore was behind the inflammation in fat cells that could ultimately lead to Type 2 Diabetes.

"This finding is quite novel because current drug development efforts target immune 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 a UC press release.

Type 2 Diabetes affects more than 23 million Americans, according to the CDC. According to Moscat, drug developers are currently working on treatments for Type 2 Diabetes that target JNK1, so these treatments could affect the both fat cells and immune cells. However, if PKC-zeta is what is really causing fat cells to become inflamed, drug developers will be able to produce pharmaceuticals that can treat Type 2 Diabetes without compromising the immune system.

Moscat and his colleagues are currently working with the University of Cincinnati’s Drug Discovery Department to develop compounds that regulate PKC-zeta for further research. In addition to treating Type 2 Diabetes, Moscat hopes that this research can help explain the role PKC-zeta plays in tumor growth and help researchers develop new drugs to prevent certain cancers.

“We believe a similar mechanism of action is at play in malignant tumor development,” Moscat said. “Now we are trying to understand how PKC-zeta regulates IL-6 to better determine how we can manipulate the protein to help prevent diabetes and cancer.”

The study is available online in the July issue of Cell Metabolism.

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