Hypogonadism and metabolic syndrome

Abstract

Background: The relationship between metabolic syndrome (MetS), male hypogonadism and their possible interaction in cardiovascular (CV) risk stratification are not completely understood.

Aim: We reviewed relationships between testosterone (T) and MetS emphasizing their possible interaction in the pathogenesis of CV diseases.

Materials and methods: A systematic search of published evidence was performed using Medline (1969 to January 2011).

Results: Cross-sectional data have shown that subjects with MetS have lower levels of total T (TT) (about 3 nmol/l), as hypogonadism is more evident in subjects with than in those without erectile dysfunction (ED) than in those without. Longitudinal evidence shows that low T is allocated with a higher risk of subsequent development of MetS, although the reverse condition is also possible. Which are the factors in MetS responsible for the low T is not completely clarified. In clinical studies, increased waist circumference is the major determinant of MetS-associated hypogonadism. Our experiments in rabbits do not support the idea that visceral fat is the main determinant of MetS-associated male hypogonadism. Only few randomized clinical trials have evaluated the impact of T replacement therapy (TRT) in patients with MetS. Available evidence suggests that TRT decreases visceral fat accumulation and ameliorates insulin sensitivity, whereas androgen deprivation increases abdominal adiposity.

Conclusions: The clinical significance of the MetS-associated hypogonadism needs further clarifications. In particular, it has not been completely clarified if low T might be considered a cause or a consequence of MetS. The benefit of TRT in term of the reduction of CV risk needs to be confirmed in larger and longer studies.