Abstract
Several endocrine factors, including sex-steroid hormones are known to influence adiponectin secretion. Our purpose was to evaluate the influence of testosterone and of the synthetic non-aromatizable/non-5α reducible androgen 17β-hydroxyestra-4,9,11-trien-3-one (trenbolone) on circulating adiponectin and adiponectin protein expression within visceral fat. Young male and female F344 rats underwent sham surgery (SHAM), gonadectomy (GX), or GX plus supraphysiologic testosterone-enanthate (TE) administration. Total circulating adiponectin was 39% higher in intact SHAM females than SHAM males (p<0.05). GX increased total adiponectin by 29–34% in both sexes (p<0.05), while TE reduced adiponectin to concentrations that were 46–53% below respective SHAMs (p≤0.001) and ablated the difference in adiponectin between sexes. No differences in high molecular weight (HMW) adiponectin were observed between sexes or treatments. Adiponectin concentrations were highly and negatively associated with serum testosterone (males: r = −0.746 and females: r = −0.742, p≤0.001); however, no association was present between adiponectin and estradiol. In separate experiments, trenbolone-enanthate (TREN) prevented the GX-induced increase in serum adiponectin (p≤0.001) in young animals, with Low-dose TREN restoring adiponectin to the level of SHAMs and higher doses of TREN reducing adiponectin to below SHAM concentrations (p≤0.001). Similarly, TREN reduced adiponectin protein expression within visceral fat (p<0.05). In adult GX males, Low-dose TREN also reduced total adiponectin and visceral fat mass to a similar magnitude as TE, while increasing serum HMW adiponectin above SHAM and GX animals (p<0.05). Serum adiponectin was positively associated with visceral fat mass in young (r = 0.596, p≤0.001) and adult animals (r = 0.657, p≤0.001). Our results indicate that androgens reduce circulating total adiponectin concentrations in a dose-dependent manner, while maintaining HMW adiponectin. This change is directionally similar to the androgen-induced lipolytic effects on visceral adiposity and equal in magnitude between TE and TREN, suggesting that neither the aromatization nor the 5α reduction of androgens is required for this effect.
Highlights
Adiponectin is an 30 kDa insulin sensitizing adipokine [1] that is primarily secreted by visceral adipose tissue [2] and typically the serum concentration is inversely proportional to fat mass [3]
Serum adiponectin was lower in intact males when compared with intact females (SHAM males and females were analyzed separately (Males): 52606288 ng/ml vs. Sham operated (SHAM) Females: 79996840 ng/ml; p,0.05)
Previous reports indicate that testosterone lowers total adiponectin within the circulation [6,13,17,18,34], which is surprising given the known lipolytic [11,15,16] and insulin sensitizing [35] effects of testosterone
Summary
Adiponectin is an 30 kDa insulin sensitizing adipokine [1] that is primarily secreted by visceral adipose tissue [2] and typically the serum concentration is inversely proportional to fat mass [3]. Within the circulation adiponectin is present as high molecular weight (HMW) and lower molecular weight oligomeric isoforms, with the HMW isoform producing the primary hepatic insulin sensitizing activity associated with adiponectin [4]. Testosterone is the primary endogenous androgen in tissues lacking 5a reductase enzymes [10] and this androgen exerts potent lipolytic effects. In tissues that express any of the 5a reductase isozymes, dihydrotestosterone (DHT) is the most potent androgen [10]. The lipolytic effects of testosterone are, at least partially, influenced by its ability to direct pluripotent stem cells towards the myogenic lineage and away from the adipogenic lineage [11]; it remains unclear whether this is a direct androgen-mediated effect of testosterone or whether this effect requires testosterone to undergo 5a reduction prior to androgen signaling [12]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
