It has been a common opinion that inflammation in adipose tissue may cause insulin resistance, and thereby type 2 diabetes. However, recent research from the Swedish medical university Karolinska Institutet, published in the New England Journal of Medicine, question the theory that inflammation in the body fat is only pernicious. Instead the findings suggest that a certain form of body fat inflammation is necessary for fat cell turnover in the lean, healthy state.
In 2008 the same group of researchers showed that adult humans constantly produce new fat cells to replace equally rapid break down of the already existing fat cells due to cell death, and that overweight people generate and replace more fat cells than do lean. It is also well established that obesity is a very strong risk factor for the most common form of diabetes (type 2). The mechanisms linking obesity to diabetes are not clear, but it is believed that disturbances in the function of adipose tissue which are induced by obesity impair the action of insulin on carbohydrate and lipid metabolism (insulin resistance) thereby causing type 2 diabetes.
One of the most investigated pathogenic factors behind the link between insulin resistance and obesity is inflammation of adipose tissue (i.e. where the body fat is stored). Adipose inflammation is pronounced among obese and even more so when obesity is accompanied by type 2 diabetes.
"The hypothesis has been that inflammation in adipose tissue indirectly causes insulin resistance and thereby type 2 diabetes", says Professor Peter Arner, who led the study. "However, when we investigated adipose tissue from healthy and lean young women, we found that inflammation also is necessary for fat cell turnover in the lean, healthy state."
The researchers determined the expression of a number of inflammatory factors produced by the adipose tissue. The most important of these factors in adipose tissue is the signal protei
|Contact: Katarina Sternudd|