How come type 2 diabetes does not affect all obese people? A study recently published in the Journal of Clinical Investigation may explain why. Adiponectin is a hormone that controls insulin sensitivity. Leptin is a hormone which lessens appetite. Too much adiponectin allows mice to store excess calories in fat tissue instead of in more dangerous areas -- the liver, heart or muscle tissue -- where extra fat may lead to inflammation, diabetes and heart disease. Unfortunately adiponectin levels decline as people get fatter. So researchers wondered "what if overeating mice had high levels of adiponectin?"

Researchers genetically engineered mice to produce lots of adiponectin and a lack of leptin. The mice overate and became obese, but their high levels of adiponectin enabled them to dump their fat into fat tissue, which has antidiabetic effects. Dr. Philipp Scherer, senior author, stated the inability to appropriately expand fat mass while overeating may be an underlying cause of insulin resistance, diabetes and cardiovascular disease. Low adiponectin levels don't allow fat cells to accept fat, so the fat builds up in inflammatory locations.

Considering 66 percent of American adults are overweight or obese, Dr. Scherer stated researchers need to find way to deposit extra calories in the least harmful places. He plans to investigate how to maximize good fat areas and shrink bad ones. This solution is disturbing to me -- don't we need to get rid of the fat in the first place? Read more in Health News Digest and check out Diane's recent post on upper body fat's link to insulin resistance.