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Effects of androgens on adipocyte differentiation and adipose tissue explant metabolism in men and women

Authors


André Tchernof, Endocrinology and Genomics, Laval University Medical Research Center, 2705 Laurier Blvd. (T3-67), Québec, QC, Canada G1V 4G2. Tel: (+1) 418 654 2296; Fax: (+1) 418 654 2761; E-mail: andre.tchernof@crchul.ulaval.ca

Summary

Objective  To examine the effects of aromatizable or nonaromatizable androgens on abdominal subcutaneous (SC) and omental (OM) adipose tissue lipid metabolism and adipogenesis in men and women.

Design and subjects  Primary organ and preadipocyte cultures were established from surgical samples obtained in men (= 22) and women undergoing biliopancreatic diversions (= 12) or gynaecological surgeries (= 8). Cultures were treated with testosterone, dihydrotestosterone (DHT) and methyltrienolone (R1881).

Measurements  Heparin-releasable lipoprotein lipase (HR-LPL) activity, glycerol release, adiponectin secretion, glycerol-3-phosphate dehydrogenase activity and lipid accumulation were measured.

Results  In organ cultures from men, DHT had a statistically significant inhibitory effect on HR-LPL activity in the OM compartment. Testosterone significantly inhibited HR-LPL activity in SC and OM cultures. In women, high DHT concentrations tended to inhibit HR-LPL activity in OM cultures. Minor androgenic effects were observed for basal and isoproterenol-stimulated lipolysis as well as adiponectin release in men. On the other hand, adipocyte differentiation was significantly and dose-dependently inhibited by DHT, testosterone and R1881 in SC and OM cultures from both sexes. These effects did not differ according to adipose tissue depot but appeared to be more pronounced in women than in men.

Conclusions  Androgens slightly decreased HR-LPL activity in adipose tissue organ cultures, but markedly inhibited adipogenesis in SC and OM primary preadipocyte cultures in both sexes. Androgenic effects on adipose tissue in men vs. women may not differ in terms of direction but in the magnitude of their negative impact on adipogenesis and lipid synthesis.

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