PPARγ: a molecular link between systemic metabolic disease and benign prostate hyperplasia

Differentiation. Nov-Dec 2011;82(4-5):220-36. doi: 10.1016/j.diff.2011.05.008. Epub 2011 Jun 8.

Abstract

The emergent epidemic of metabolic syndrome and its complex list of sequelae mandate a more thorough understanding of benign prostatic hyperplasia and lower urinary tract symptoms (BPH/LUTS) in the context of systemic metabolic disease. Here we discuss the nature and origins of BPH, examine its role as a component of LUTS and review retrospective clinical studies that have drawn associations between BPH/LUTS and type II diabetes, inflammation and dyslipidemia. PPARγ signaling, which sits at the nexus of systemic metabolic disease and BPH/LUTS through its regulation of inflammation and insulin resistance, is proposed as a candidate for molecular manipulation in regard to BPH/LUTS. Finally, we introduce new cell and animal models that are being used to study the consequences of obesity, diabetes and inflammation on benign prostatic growth.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Animals
  • Diabetes Mellitus, Type 2 / complications
  • Diabetes Mellitus, Type 2 / pathology
  • Disease Models, Animal
  • Dyslipidemias / complications
  • Dyslipidemias / pathology
  • Humans
  • Inflammation / complications
  • Inflammation / pathology
  • Lower Urinary Tract Symptoms / complications
  • Lower Urinary Tract Symptoms / metabolism*
  • Lower Urinary Tract Symptoms / pathology
  • Male
  • Mice
  • Molecular Targeted Therapy
  • PPAR gamma / genetics*
  • PPAR gamma / metabolism*
  • Prostate / anatomy & histology
  • Prostate / growth & development
  • Prostate / pathology*
  • Prostatic Hyperplasia / complications
  • Prostatic Hyperplasia / metabolism*
  • Prostatic Hyperplasia / pathology
  • Signal Transduction

Substances

  • PPAR gamma