Testosterone, the metabolic syndrome and diabetes mellitus

Abstract 

Both cross-sectional and longitudinal epidemiological studies have convincingly established that low plasma levels of testosterone and sex hormone binding globulin (SHBG) are correlated with / predict the metabolic syndrome and diabetes mellitus. Visceral obesity with its associated hyperinsulinism suppresses SHBG synthesis and, concomitantly, circulating testosterone levels. It also may impair the strength of LH signaling to the testis. Further, insulin and leptin have a suppressive effect on testicular steroidogenesis. Thus, there are reasons to consider adiposity a significant factor capable of lowering circulating levels of testosterone. Conversely, low levels of testosterone predict the development of the metabolic syndrome and diabetes mellitus type2. This notion is supported by the appearance of a metabolic syndrome-like condition in men with prostate cancer whose plasma testosterone levels are rendered low. Furthermore, the observation that differentiation of pluripotent stem cells is androgen dependent (adipogenic in a low testosterone milieu and myogenic with normal levels of testosterone) provides a unifying explanation for the reciprocal effects of androgens on muscle and fat mass in men.

Administration of testosterone has been found to improve insulin sensitivity in non-diabetic and diabetic men, although this has not been universally the case. Our own study in men with diabetes mellitus and low androgen status found an improvement of glycemic control upon testosterone administration. When combined with proper nutrition, physical activity and resistance training, administration of testosterone may improve body composition (reduction of fat mass / increase of lean body mass) and may thus contribute to better metabolic control and reduction of cardiovascular risks.

Keywords: Testosterone, Glycemic control, Diabetes mellitus, Metabolic syndrome