Objectives: 

Endoglin is a transmembrane auxiliary receptor for transforming growth factor-beta(TGF-beta) that is predominantly expressed on proliferating endothelial cells. It plays a wide range of physiological roles but its importance on energy balance or insulin sensitivity has been unexplored.

Materials: 

Heterozygous deficient mice were fed standard chow or high fat diet during 16 weeks.RNA was extracted using Trizol® reagent followed by reverse-transcription reaction.For the analysis of gene expression we used real-time reverse-transcription polymerase chain reaction.Western blots were performed to measure the protein levels of NFkB, PTEN, pAKT and Glut4.Blood glucose levels were measured after an intraperitoneal injection of either D-glucose or insulin.

Results: 

We report for first time that heterozygous endoglin deficiency in mice protects against high fat diet-induced insulin resistance.At molecular level, we failed to detect relevant changes in the insulin signalling pathway in liver, muscle or adipose tissues that could explain the insulin-dependent effect. However, we found increased protein levels of the glucose transporter Glut4 in the adipose tissue of endoglin heterozygous mice fed on high fat diet in comparison to their wild type littermates.

Conclusions: 

Our findings indicate that endoglin is a potentially important physiological mediator of insulin sensitivity and this effect on insulin action is independent of changes in body weight or adiposity