Fat cells play a key role in type 2 diabetes

Cellular changes in adipose tissue leads to the "hyperinflammation" feature of glucose intolerance related to obesity and type 2 diabetes, according to new research from the University of Cincinnati (UC), the United States.

Experts in cell biology and cancer say that this new discovery about the cellular mechanisms can provide a different target for drugs to treat type 2 diabetes as well as show how the aggressive cancers are formed.

For this study, the leader Jorge Moscat and his partner Maria Diaz-Meco, evaluated the role of a specific gene known as protein kinase C (PKC) zeta, which has been implicated as a major contributor to the malignant tumor cell growth. Using a preclinical animal model, they found that PKC-zeta played a double role in molecular signaling that leads to inflammation.

"This finding is fairly new, considering the efforts to develop new drugs to target the immune cells (macrophages, T-cells), eliminating this hyperinflammation. Our research suggests that the glucose intolerance associated with obesity not has nothing to do with the immune system. It may be more effective in achieving adipocytes (fat cells) "explains Moscat.

In normal cells, PKC-zeta regulates the balance between cellular inflammatory responses to maintain glucose control. During inflammation induced by obesity, however, the function of PKC-zeta molecule begins to change and promote inflammation, causing the fat cells secrete a substance (IL-6) that travels in large quantities in the liver, causing resistance to insulin.

"We believe that a similar mechanism of action is at stake in the development of malignant tumors. Now we are trying to understand how PKC-zeta regulates IL6 to best determine how to manipulate the protein and help to prevent diabetes and cancer," he adds.

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