Why the majority of patients who suffer from obesity also more easy to get diabetes and chronic inflammation? As we all know insulin is a hormone to regulate carbohydrate and fat metabolism in the body. Type 2 diabetes is a metabolic disorder that is characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency. From an article published on science, it figures out some parts of relevance between these two diseases.
In the article the researcher makes a contract test that when put on a high fat diet in mice, a secreted protein named Sfrp5 is decreased. This is the way how Sfrp5 works then you may know why obesity can increase the susceptibility of diabetes. First there is a group of proteins named Wnt, which are a family of secreted glycoproteins that signal through a cell surface receptor called frizzled (Fz). The Fz can stimulate the signaling pathway to stimulate guanosing triphosphatases (Rho A and Rac1), leading to activation of the JNK1. In short the Wnt activates JNK1, which triggered a proinflammatory response. Second in insulin target cell like fat cell, activated JNK1 can impair the activity of an insulin receptor substrate protein, leading to decreased insulin signaling and the development of insulin resistance. Then Sfrp5 can act as a decoy receptor that binds and sequester Wnt, thus preventing activation of Fz. In that case less JNK1 will be produced. Less JNK1 means less impairment of insulin receptor. Of course it will improve insulin sensitivity.
This observation can help the development of therapeutics, which could use Sfrp5 to treat obesity-related insulin resistance. From this article we also can know once you get a disease, other impairments will come along.
Posted by Minhui Dai
