Testosterone acts on fat cells through molecules known as androgen receptors, which enable the testosterone to activate genes linked to obesity and diabetes. Kerry McInnes, from the University of Edinburgh (United Kingdom), and colleagues have found mice in which the function of testosterone in fat tissue was impaired were more likely to be insulin resistant than mice in which the role of testosterone was not hindered. Mice that did not have androgen receptors in fat tissue for testosterone to attach to, were more likely to show signs of insulin resistance than other mice. The researchers also found that mice without androgen receptors in fat tissue also became fatter than other mice and developed full insulin resistance when both types were fed a high-fat diet. In that a protein called RBP4 (retinol binding protein 4) is thought to play a crucial role in regulating insulin resistance when testosterone is impaired, the team observed that levels of RBP4 were higher in mice in which the role of testosterone was impaired.
Low Levels of Testosterone May Raise Men’s Diabetes Risk
McInnes KJ, Smith LB, Hunger NI, Saunders PT, Andrew R, Walker BR. “Deletion of the androgen receptor in adipose tissue in male mice elevates retinol binding protein 4 and reveals independent effects on visceral fat mass and on glucose homeostasis.” Diabetes. May 2012;61(5):1072-81.
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