Ming Jiang
Last active: 7/6/2016

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

Jiang M, Strand DW, Franco OE, Clark PE, Hayward SW
Differentiation. 2011 82 (4-5): 220-36

PMID: 21645960 · PMCID: PMC3174339 · DOI:10.1016/j.diff.2011.05.008

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.

Copyright © 2011 International Society of Differentiation. Published by Elsevier B.V. All rights reserved.

MeSH Terms (14)

Animals Diabetes Mellitus, Type 2 Disease Models, Animal Dyslipidemias Humans Inflammation Lower Urinary Tract Symptoms Male Mice Molecular Targeted Therapy PPAR gamma Prostate Prostatic Hyperplasia Signal Transduction

Connections (3)

This publication is referenced by other Labnodes entities: