Karin Stenkula

Hjelt grant holder 2020

Lund University

Obesity is one of the main risk factors behind type 2 diabetes and cardiovascular diseases. Both obesity and type 2 diabetes are characterized by an insulin resistance, which means that even though insulin is released into the blood, it does not stimulate uptake of fat and glucose into the cells. This results in elevated blood glucose levels, which can develop into type 2 diabetes. Still, it is not known how an increased fat tissue mass is linked with onset of these diseases.

Recently, the protein EHD2 was shown to promote both insulin sensitivity and fat cell function. In the present proposal, we hypothesize that EHD2 is central for regulating uptake of both glucose and fat from the blood. To test our hypothesis, we will apply a variety of cell biology- and microscopy techniques to monitor cellular insulin response, and nutritional uptake. To specifically address the role of EHD2 for these processes, we will analyze fat cells isolated from both normal, wild-type mice and a recently established mouse model lacking EHD2. 

Possibly, knowledge of how EHD2 contributes to maintain intact fat cell function can result in new strategies to improve insulin sensitivity and lipid storage capacity in fat cells. This will be useful to both prevent and improve adipocyte dysfunction, with beneficial effects on whole-body glucose homeostasis.