DALLAS Aug. 23, 2007 The worlds fattest mice can overeat without developing insulin resistance or diabetes thanks to a glut of a key hormone, a dichotomy that helps explain why not all obese people are diabetic, a UT Southwestern Medical Center researcher has found.
Consuming excess calories usually spurs insulin resistance and diabetes. But in a multicenter study appearing online today in the Journal of Clinical Investigation, scientists show how an abundance of adiponectin, a hormone that controls sensitivity to insulin, and a lack of leptin, a hormone that curbs appetite, enables mice to store excess calories in fat tissue instead of in liver, heart or muscle tissue places where excess fat can lead to inflammation, diabetes and heart disease.
The mice get morbidly obese, but are insulin-sensitive with normal blood-glucose levels.
The message isnt that its good to be obese, but that expanded fat mass, when stored in the right places, can help prevent diabetes and reduce the risk of heart disease, said Dr. Philipp Scherer, professor of internal medicine and the studys senior author. In fact, these are the first mice to directly show that fat-mass expansion has antidiabetic effects. Dr. Scherer directs the Touchstone Center for Diabetes Research at UT Southwestern.
Fat tissue, which was largely perceived as a useless storage bin until the early 1990s, has been found to release hormones, including adiponectin, that play integral roles in metabolism and obesity. Adiponectin levels decline as a person accumulates more fat, making the levels a good predictor of future risk of developing diabetes, heart disease and cancer, said Dr. Scherer, who discovered the hormone in 1994.
But what would happen if, despite overeating, adiponection levels increased"
To find out, Dr. Scherer and other researchers in this study genetically engineered mice to produce an overabundance of adiponectin while lacking
|Contact: Amanda Siegfried|
UT Southwestern Medical Center