New research may help break the link between obesity and diabetes. Although overweight and obesity confer significant risk for developing type 2 diabetes, the precise mechanisms underlying the relationship between body fat and diabetes remain unclear. An accumulation of research over the last several years, however, implicates the chronic, low-grade inflammation which typically accompanies obesity, in promoting insulin resistance, which is a precursor to type 2 diabetes. Earlier work found a type of immune system cell, the macrophage, is abundant in the fat tissues of obese mice (and humans). Macrophages are responsible for producing some of the chemical signals that trigger the inflammatory response. Now, new research highlights a role for a different type of immune system cell, called the CD4+Foxp3+ Regulatory T (Treg) cell. Such Treg cells are found in the fat of lean mice, but not in those that are overweight. Experimentally depleting Treg cells from lean mice increased their resistance to insulin. Importantly, the researchers found that the Treg cells produce chemical signals which attenuate the inflammatory response when experimentally introduced into fat mice, helping restore the animals to a more normal metabolic state. This suggests that restoring normal immune regulatory signals in people at risk for type 2 diabetes may one day interrupt the development of insulin resistance and help them prevent the disease.
Feuerer M, Herrero L, Cipolletta D, Naaz A, Wong J, Nayer A, Lee J, Goldfine AB, Benoist C, Shoelson S, and Mathis D: Lean, but not obese, fat is enriched for a unique population of regulatory T cells that affect metabolic parameters. Nat Med 15: 930-939, 2009.
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