The research team found that failure of glucose absorption by adipocytes could be a trigger for type 2 diabetes.

The innovative strategy would allow in a context of insulin-resistant patients to reduce blood glucose levels by specifically targeting adipocytes.

Within adipocytes, the central protein ALMS1 combines with two key proteins (TBC1D4 and αPKC) to regulate glucose entry. In the absence of insulin, ALMS1 interacts with αPKC. This interaction is disrupted by the insulin signalling pathway. ALMS1 will then interact with TBC1D4, resulting in glucose absorption in the adipocytes.