Deletion of S6K1 confers increased insulin sensitivity in mice: A potential target for the treatment of type 2 diabetes?
(June 18, 2015) Currently, there are more than 350 million type 2 diabetics and according to the World Health Organization (WHO) by 2030 it will be the 7th leading cause of death worldwide.
The hallmark of type 2 diabetes is insulin resistance, which is initially compensated for by an increase in beta cell size (responsible for producing insulin). However, the beta cells of such patients will eventually collapse and die, leading to full blown type 2 diabetes.
Researchers from the Laboratory of Cancer Metabolism at IDIBELL, led by Sara Kozma, have shown in animal models that inhibition of S6K1 protein may be a potential treatment for type 2 diabetes.