Role of oxidative stress and inflammation in the origin of Type 2 diabetes--a paradigm shift.

In Type 2 diabetes the body either produces too little insulin, or does not respond well to it. Current pharmacological treatments, which are less than optimal, either target defective insulin secretion (sulfonylureas, glinides) or insulin resistance (metformin, thiazolidinediones). Exciting new research is now helping us to understand novel pathways that may contribute to defective insulin secretion as well as decreased response to insulin. Such pathways may explain the development of diabetes and associated complications (atherosclerosis and diabetic nephropathy). Understanding the way a cell metabolises glucose may be the key to understanding how cells secrete insulin and respond to it.