Table of Contents Author Guidelines Submit a Manuscript
PPAR Research
Volume 2008 (2008), Article ID 651419, 10 pages
Research Article

Activation of Penile Proadipogenic Peroxisome Proliferator-Activated Receptor 𝛾 with an Estrogen: Interaction with Estrogen Receptor Alpha during Postnatal Development

1Departments of Anatomy, Physiology, and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, AL 36849, USA
2Department of Biomedical Sciences, Tuskegee University, Tuskegee, AL 36088, USA
3Cellular and Molecular Biosciences Program, Department of Animal Sciences, Auburn University, Auburn, AL 36849, USA

Received 23 April 2008; Accepted 14 July 2008

Academic Editor: Carolyn Komar

Copyright © 2008 Mahmoud M. 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.


Exposure to the estrogen receptor alpha (ER 𝛼 ) ligand diethylstilbesterol (DES) between neonatal days 2 to 12 induces penile adipogenesis and adult infertility in rats. The objective of this study was to investigate the in vivo interaction between DES-activated ER 𝛼 and the proadipogenic transcription factor peroxisome proliferator-activated receptor gamma (PPAR 𝛾 ). Transcripts for PPARs 𝛼 , 𝛽 , and 𝛾 and 𝛾 1a splice variant were detected in Sprague-Dawley normal rat penis with PPAR 𝛾 predominating. In addition, PPAR 𝛾 1b and PPAR 𝛾 2 were newly induced by DES. The PPAR 𝛾 transcripts were significantly upregulated with DES and reduced by antiestrogen ICI 182, 780. At the cellular level, PPAR 𝛾 protein was detected in urethral transitional epithelium and stromal, endothelial, neuronal, and smooth muscular cells. Treatment with DES activated ER 𝛼 and induced adipocyte differentiation in corpus cavernosum penis. Those adipocytes exhibited strong nuclear PPAR 𝛾 expression. These results suggest a biological overlap between PPAR 𝛾 and ER 𝛼 and highlight a mechanism for endocrine disruption.