New research into the development of type 2 diabetes has found that it may not just be the immune system to blame for the metabolic condition, but that fat cells may also be involved. The study, undertaken by scientists at the University of Cincinnati, revealed that cellular changes in fat tissue can lead to the state of hyperinflammation, a characteristic of type 2 diabetes and obese-related glucose intolerance.
It is hoped that this breakthrough will provide a different target for drugs to treat patients with type 2 diabetes, and potentially greater insight into how aggressive cancers form.
The researchers examined the role of a specific gene known as protein Kinase C or PKC-zeta, by using a preclinical animal model. PKC-zeta has already been implicated as a key cellular contributor to the malignant growth of tumours.
The research has found that PKC-zeta has a dual role, moving from a regulator of inflammation to a proinflammation agent depending on the circumstances. When there is inflammation caused by obesity, PKC-zeta changes and the molecule starts to promote inflammation by causing adipocytes to secrete a substance that travels in large quantities to the liver to cause insulin resistance.
Jorge Moscat, chair of the university’s cancer and cell biology department, said “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 fat cells.”

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