Changes in adipose tissue – and not in the immune system – are to blame for the massive inflammation characteristic of obesity-related glucose intolerance and type 2 diabetes, argue US scientists in the pages of Cell Metabolism.
Experts in cell and cancer biology say that the new discovery of the cellular mechanisms leading to glucose intolerance has the potential to contribute to the development of an effective treatment for type 2 diabetes and should help understand how cancer arises.
Dr. Jorge Moscat and Dr. Maria Diaz-Meco of the University of Cincinnati studied the function of the gene encoding a protein called protein kinase C – zeta (PKC-zeta), which is known to be essential for the growth of malignant tumors. In animal studies, scientists found that PKC-zeta, depending on its conditions, can play two different roles in the development of inflammation – either controlling inflammation or exacerbating it.
In normal cells, PKC-zeta regulates the balance of inflammatory factors in response to changes in glucose levels. During obesity-induced inflammation, the role of PKC-zeta changes and this protein intensifies inflammatory changes, prompting adipose tissue cells (adipocytes) to secrete interleukin-6, which enters the liver and causes insulin resistance (i.e. cell insensitivity to insulin) .
The researchers say their research shows that obesity-related glucose intolerance has nothing to do with the immune system. In their opinion, in the treatment of type 2 diabetes, one should focus on influencing adipocytes.
Researchers also believe that a similar mechanism may be involved in the development of malignant neoplasms. Now they are trying to explain how PKC-zeta regulates the level of interleukin-6, which would allow to manipulate the level of this protein and prevent the development of diabetes and cancer (PAP).