Back in 2000, researchers at the University of Alberta in Edmonton, Canada transplanted islet cells in the livers of people with type 1, known as the Edmonton Protocol. Each islet transplant required several cadaver donors. The transplants worked for awhile, but approximately 80 percent of patients required insulin after a couple years. It was assumed the transplanted cells were rejected, but new research points to a new possible culprit -- fat.

Dr. Roger Unger and colleagues of the University of Texas Southwestern Medical Center in Dallas performed the Edmonton Protocol in rats with type 1. Fat built up around the transplanted cells in only a month. The cells stopped producing insulin and the rats died after 15 weeks. Dr. Unger explained the liver creates fatty acids from food, and islet transplants in the liver are surrounded by too much fat. He proved his point by repeating the transplant in a separate group of type 1 rats, but this time the rats were on a strict diet. A third group of rats received leptin, a hormone involved in increasing metabolism and decreasing appetite. These rats had an improved response, although the Reuters story does not provide specifics. Here's the study abstract in Diabetes, but ya gotta pay for the full text article.

Bummer. You get an islet cell transplant, but still have to stay away from the Ben & Jerry's. A next step could be testing this theory in human islet cell transplants via a low-calorie, low-sugar diet following transplantation. Read more in Reuters.

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.

What is the purpose of body fat? We all have it, some of us a little more than others. As we grow older, some of our diets fall out of balance with our energy needs causing our white fat cells to become swollen.

White fat cells secrete leptin, adiponectin and resistin. Leptin and adiponectin work together in suppressing appetite. Resistin is the newest discovered - and has been found to participate in the inflammatory response and resistence to insulin. It also triggers an immune response to irritation, so it may be the fat cells attempt to shut your piehole because we're not gonna take it. As the white fat cells take on excessive calories they begin swelling, resulting in an inflammatory response.

Inflammation, by definition, is a protective attempt to remove the injurious stimuli (excess calories) and initiate the healing process. As the fat cells dispatch hormones signaling inflammation - one could hypothesize that Type 2 diabetes is a response to an imbalanced diet - calories in versus calories out. So what do our white fat cells do for us? They are designed to store energy for use in times of need. When your body is sending out DEFCON signals of inflammation - I'd say that is a time of need, indeed. Would inducing ketosis till the swelling goes down help?

Elixir Pharmaceuticals is a company focused on age-related diseases such as diabetes and obesity. Elixir released new data on research that ultimately could lead to a treatment for type 2 diabetes.

The research explains the role of ghrelin, a hormone secreted by the stomach. Ghrelin controls appetite by increasing levels before meals and decreasing levels after meals. A lack of sleep produces ghrelin, which stimulates appetite and creates less leptin which, amongst its many other effects, suppresses appetite. Research scientists have developed an anti-obesity vaccine, which is directed against the hormone ghrelin. The vaccine uses the immune system antibodies to prevent ghrelin from reaching the central nervous system, thus producing a desired reduction in weight gain.

The research conducted by Elixir, as well as the obesity vaccination, shows compelling evidence that ghrelin plays a pivotal role in metabolic regulation. Scientists have shown pharmacologic inhibition of the ghrelin receptor results in a reduction in fasting glucose levels, reduction in insulin resistance, and weight loss. This could lead to victorious battle for science in the war on obesity.