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PPAR Research
Volume 2009, Article ID 101857, 8 pages
Research Article

Activation of PPAR 𝛾 by Rosiglitazone Does Not Negatively Impact Male Sex Steroid Hormones in Diabetic Rats

Department of Anatomy, Physiology and Pharmacology, Auburn University, AL 36849, USA

Received 22 December 2008; Revised 17 March 2009; Accepted 29 April 2009

Academic Editor: Carolyn Komar

Copyright © 2009 Mahmoud Mansour et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Peroxisome proliferator-activated receptor gamma (PPAR 𝛾 ) activation decreased serum testosterone (T) in women with hyperthecosis and/or polycystic ovary syndrome and reduced the conversion of androgens to estradiol (E2) in female rats. This implies modulation of female sex steroid hormones by PPAR 𝛾 . It is not clear if PPAR 𝛾 modulates sex steroid hormones in diabetic males. Because PPAR 𝛾 activation by thiazolidinedione increased insulin sensitivity in type 2 diabetes, understanding the long term impact of PPAR 𝛾 activation on steroid sex hormones in males is critical. Our objective was to determine the effect of PPAR 𝛾 activation on serum and intratesticular T, luteinizing hormone (LH), follicle stimulating hormone (FSH) and E2 concentrations in male Zucker diabetic fatty (ZDF) rats treated with the PPAR 𝛾 agonist rosiglitazone (a thiazolidinedione). Treatment for eight weeks increased PPAR 𝛾 mRNA and protein in the testis and elevated serum adiponectin, an adipokine marker for PPAR 𝛾 activation. PPAR 𝛾 activation did not alter serum or intratesticular T concentrations. In contrast, serum T level but not intratesticular T was reduced by diabetes. Neither diabetes nor PPAR 𝛾 activation altered serum E2 or gonadotropins FSH and LH concentrations. The results suggest that activation of PPAR 𝛾 by rosiglitazone has no negative impact on sex hormones in male ZDF rats.