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

被引:43
作者
Jiang, Ming
Strand, Douglas W.
Franco, Omar E.
Clark, Peter E.
Hayward, Simon W. [1 ,2 ]
机构
[1] Vanderbilt Univ, Med Ctr, Dept Urol Surg, MCN, Nashville, TN 37232 USA
[2] Vanderbilt Ingram Canc Ctr, Dept Canc Biol, Nashville, TN USA
关键词
BPH; LUTS; Co-morbidities; Metabolism; Inflammation; PPAR gamma; URINARY-TRACT SYMPTOMS; ACTIVATED-RECEPTOR-GAMMA; TYPE-2; DIABETES-MELLITUS; ADIPOSE-TISSUE EXPANDABILITY; CARCINOMATOUS HUMAN-PROSTATE; ISCHEMIA-REPERFUSION INJURY; UROGENITAL SINUS MESENCHYME; IMPROVES GLYCEMIC CONTROL; FACTOR BINDING PROTEIN-3; CANCER PREVENTION TRIAL;
D O I
10.1016/j.diff.2011.05.008
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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. PPAR gamma 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. (C) 2011 International Society of Differentiation. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:220 / 236
页数:17
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