The tumour suppressor p53 is crucial for the development of insulin resistance, a hallmark of diabetes, reports a study in this week's Nature Medicine.
Issei Komuro and his colleagues found that excessive calorie intake led to inflammation, insulin resistance and increased expression of p53 in mice. Inhibition of p53 activity specifically in fat tissue, decreased the inflammatory response and improved insulin resistance. Conversely, forced expression of p53 in the fat caused an inflammatory response that led to insulin resistance, and fat tissue from patients with diabetes showed similar responses.
These results illustrate a new role for p53 in the regulation of insulin resistance, raising the possibility that cellular changes linked to p53 activity could be new targets for the treatment of diabetes.