Insulin resistance is the hallmarker of Type 2 diabetes and accumulating evidence show that inflammation plays a key role in obesity associated insulin resistance. Recently,Cellpublished the latest finding in Prof. Li Pingping's lab about inflammatory factor Galectin-3 (Gal3),Which is mainly secreted by macrophages. Prof. Li's group showed that Gal3 can directly bind to the insulin receptor and impair insulin signaling pathway in hepatocyte, adipocyte, and myocyte, then lead to the insulin resistance and glucose intolerance. Whereas inhibition of Gal3, through either genetic or pharmacologic loss of function, improved insulin sensitivity in obese mice. In the clinical setting, obese and insulin resistant patients have higher serum Gal3 levels compared to lean subjects. These observations elucidate a novel role for Gal3 in insulin resistance, suggesting that Gal3 can link inflammation to decreased insulin sensitivity. Inhibition of Gal3 could be a new approach to treat insulin resistance.
This research was accomplished by Prof. Li Pingping's group of State Key Laboratory of Bioactive Substance and Function of Natural Medicines in Institute of Materia Medica Chinese Acadey of Medical Science and Peking Union Medical College, Prof. Olefsky's group of University of California, San Diago, and Prof. Shen Zhufang's lab ofInstitute of Materia Medica. Prof. Li has been dedicated to the research of insulin resistance and diabetes for 15 years. Her work was published on peer reviewed scientific journal, includingCell, Nature Medicine, Cell Metabolism, DiabetesandPNASet. al. And her research group will continue the study on insulin resistance and diabetes and the development of therapeutic drugs of Type 2 diabetes.
