Complications associated with obesity stands out for its special relevance to the development of insulin resistance in skeletal muscle, the first link in a broad condition known as type II diabetes. It has been proposed to adipocitokine TNF-α as the link between obesity and the development of insulin resistance, which is a defect in signaling of the same at various levels. In this study, led by Margarita Lorenzo, Faculty of Pharmacy of the Complutense University of Madrid, has identified the tyrosine phosphatase PTP1B, a negative regulator of insulin signaling, as a target of action of TNF-α.


Treatment with adipocitokine increases, both in myocytes and in skeletal muscle, the expression and activity of this phosphatase. Since for PTP1B gene deletion mice were generated immortalized myocyte lines showing increased insulin sensitivity with respect to the wild lines and do not develop resistance to it by TNF-α.


The study also describes that PTP1B deficiency confers protection in mice when subjected to the tests of glucose tolerance and insulin after treatment with adipocitokine. In conclusion, modulation of genes such as PTP1B may contribute to the pathogenesis caused by TNF-α in skeletal muscle, and genetic ablation of PTP1B in this tissue may confer protection against insulin resistance by this adipocitokine.