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Date of release: 28 March, 2011

Endogenous androgens and effects on body fat and insulin resistance


In a recently published study, Casson and colleagues evaluated endogenous serum androgens and sex hormone binding globulin (SHBG) in 29 normal, non-obese, naturally occurring postmenopausal women whose ages ranged from 52 to 70 years [1]. Correlations were then evaluated between serum androgens and SHBG and insulin sensitivity, whole-body fat and lean body mass, visceral/abdominal fat areas per meter and aerobic capacity. Increased serum testosterone levels were related to greater maximal aerobic capacity and reduced adiposity. Higher serum levels of dihydrotestosterone, dehydroepiandrosterone sulfate (DHEAS), androstenedione, and androstenetriol glucuronidate were correlated with greater insulin sensitivity.

Comment

The use of replacement androgens, specifically transdermal testosterone and oral methyltestosterone, has principally been advocated in women with low libido or hypoactive sexual desire disorder [2,3]. Studies of transdermal testosterone have used women with and without intact ovaries, and the outcome has been to maintain serum testosterone in the physiologic range; the effects on libido have been measured with validated instruments. Concerns have been raised over cardiovascular outcomes and breast cancer, although there is little evidence to support or refute these concerns. Excess serum androgens, specifically testosterone, have been associated with the metabolic and morphologic changes associated with the polycystic ovarian syndrome (PCOS). Casson and colleagues [1] find that, in non-obese, postmenopausal women, testosterone is associated with a reduction in adiposity in contrast to that seen in the woman with PCOS. Testosterone levels also correlated with a better aerobic capacity. The authors speculate that these findings could represent just the general better health of the participants in the study. Testosterone in males and females does appear to reduce visceral adiposity, but the effects in women are inconsistent, with testosterone reducing the estrogen-associated reduction in visceral adiposity [4,5]. The effect of transdermal testosterone on weight and cardiovascular risk factors such as lipids is negligible in the clinical trials [3,6]. How testosterone affects the visceral adipocyte is unknown, but the clinical implications of reducing visceral fat accumulation are significant. Dehydroepiandrosterone and its sulfate (DHEA and DHEAS) are synthesized principally in the adrenal zona reticularis, and serum levels decline with age [7]. DHEA and DHEAS have been evaluated in only limited numbers of women in clinical trials; these have shown general improvement in well-being but no significant improvement in any disease process [8,9]. Serum levels of DHEAS, dihydrotestosterone, androstenedione and androstenetriol glucuronidate in the current article were associated with improved insulin sensitivity [1]. DHEA administration to women with impaired glucose intolerance was not found to alter insulin sensitivity [10]. The use of transdermal testosterone in women with low libido had no effect on serum hemoglobin A1c or fasting insulin levels [11]. A cross-sectional study of endogenous hormones in postmenopausal women who had no identifiable factors that would have affected their endogenous hormone levels did not find any correlations between serum DHEAS, testosterone, androstenedione and cardiovascular risk profiles [12]. Thus, the precise effect of DHEAS on insulin and its role in cardiovascular disease are unclear. In summary, declines in endogenous hormones with aging have been hypothesized to play a role in the occurrence of cardiovascular disease. Current evidence in support of this hypothesis is highly variable and limited, making it difficult to draw any meaningful conclusion. The role of adrenal androgens in postmenopausal health deserves greater investigation in order to clarify their role in age-related occurrence of disease.

Comentario

David F. Archer
Professor of Obstetrics and Gynecology, Eastern Virginia Medical School, Norfolk, Virginia, USA

    References

  1. Casson PR, Toth MJ, Johnson JV, et al. Correlation of serum androgens with anthropometric and metabolic indices in healthy, nonobese postmenopausal women. J Clin Endocrinol Metab 2010;95:4276-82.
    http://www.ncbi.nlm.nih.gov/pubmed/20566621

  2. Davis SR, Moreau M, Kroll R, et al. Testosterone for low libido in postmenopausal women not taking estrogen. N Engl J Med 2008;359:2005-17.
    http://www.ncbi.nlm.nih.gov/pubmed/18987368

  3. Shifren JL, Braunstein GD, Simon JA, et al. Transdermal testosterone treatment in women with impaired sexual function after oophorectomy. N Engl J Med 2000;343:682-8.
    http://www.ncbi.nlm.nih.gov/pubmed/10974131

  4. Davis SR, Walker KZ, Strauss BJ. Effects of estradiol with and without testosterone on body composition and relationships with lipids in postmenopausal women. Menopause 2000;7:395-401.
    http://www.ncbi.nlm.nih.gov/pubmed/11127762

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    http://www.ncbi.nlm.nih.gov/pubmed/19645638

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  8. Grimley Evans J, Malouf R, Huppert F, van Niekerk JK. Dehydroepiandrosterone (DHEA) supplementation for cognitive function in healthy elderly people. Cochrane Database of Systematic Reviews 2006;(4):CD006221.
    http://www.ncbi.nlm.nih.gov/pubmed/17054283

  9. Tchernof A, Labrie F. Dehydroepiandrosterone, obesity and cardiovascular disease risk: a review of human studies. Eur J Endocrinol 2004;151:1-14.
    http://www.ncbi.nlm.nih.gov/pubmed/15248817

  10. Talaei A, Amini M, Siavash M, Zare M. The effect of dehydroepiandrosterone on insulin resistance in patients with impaired glucose tolerance. Hormones 2010;9:326-31.
    http://www.ncbi.nlm.nih.gov/pubmed/21112864

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    http://www.ncbi.nlm.nih.gov/pubmed/17224854