Display Settings:

Format

Send to:

Choose Destination

    Androgen deficiency, diabetes, and the metabolic syndrome in men.

    Source

    Division of Endocrinology and Metabolism, Johns Hopkins School of Medicine, Baltimore, Maryland 21287, USA.

    Abstract

    PURPOSE OF REVIEW:

    The burden of androgen deficiency in men with diabetes and the metabolic syndrome has become increasingly apparent in population-based studies. This article focuses on the mechanisms underlying the interdependent relationship between these conditions.

    RECENT FINDINGS:

    Various definitions of hypogonadism, the metabolic syndrome and diabetes have been proposed and are used in the literature. Cross-sectional studies have found that between 20 and 64% of men with diabetes have hypogonadism, with higher prevalence rates found in the elderly. Hypogonadism can be a risk factor for the development of diabetes and the metabolic syndrome through various mechanisms including changes in body composition; androgen receptor polymorphisms; glucose transport; and reduced antioxidant effect. Conversely, diabetes and the metabolic syndrome can be risk factors for hypogonadism through some similar but mostly distinct mechanisms, such as increased body weight; decreased sex hormone binding globulin levels; suppression of gonadotrophin release or Leydig cell testosterone production; cytokine-mediated inhibition of testicular steroid production; and increased aromatase activity contributing to relative estrogen excess.

    SUMMARY:

    The relationship between diabetes, the metabolic syndrome and androgen deficiency is complex. Testosterone supplementation, by either oral or intramuscular routes and through exogenous or endogenous delivery, has a promising role in this population although further clinical trials are needed.

    PMID:
    17940444
    [PubMed - indexed for MEDLINE]

      Supplemental Content

      Recent activity

      Your browsing activity is empty.

      Activity recording is turned off.

      Turn recording back on

      See more...
      Write to the Help Desk