Obesity is closely associated with insulin resistance and is one of the leading risk factors for type 2 diabetes. Both affect more than 50 percent of the U.S. population. Little has been known about the molecular mechanisms linking these two metabolic diseases. Both are associated with a wide range of inflammatory molecular activity in fatty tissue. This activity puts into motion the JNK genes that interfere with insulin sensitivity. Type 2 diabetes usually occurs after age 40. People with this type of diabetes do not produce adequate amounts of insulin for the needs of the body and/or cannot use insulin effectively. To test the role of JNK in decreasing insulin sensitivity in a variety of obesity models, a research team bred mice lacking either form of the gene JNK1 or JNK2 and mice possessing the JNK genes. Weight gain rose the sharpest over an eight-week span for the mice on a high-fat diet but particularly for those with the JNK genes. In studying total body fat composition, JNK-deficient mice had significantly decreased total body fat accumulation in comparison. The research findings appeared in the Nov. 21, 2002 issue of the journal Nature.