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High glucose promotes benign prostatic hyperplasia by downregulating PDK4 expression.

Pengyu Wei1,2, Dongxu Lin1,2, Changcheng Luo1,2

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High glucose levels may promote benign prostatic hyperplasia (BPH) by reducing pyruvate dehydrogenase kinase 4 (PDK4) expression. Lowering PDK4 mimics BPH progression, suggesting PDK4 as a potential therapeutic target for BPH.

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Area of Science:

  • Urology
  • Endocrinology
  • Molecular Biology

Background:

  • Benign prostatic hyperplasia (BPH) is a common condition in aging men.
  • Diabetes is a potential risk factor for BPH development.
  • Pyruvate dehydrogenase kinase 4 (PDK4) is involved in glucose metabolism and disease progression.

Purpose of the Study:

  • To investigate the direct effects of high glucose on prostate epithelial cells.
  • To determine the role of PDK4 expression in high glucose-induced BPH.
  • To explore PDK4 as a potential therapeutic target for BPH.

Main Methods:

  • Prostate epithelial cells (RWPE-1 and BPH-1) were treated with high glucose (50 mM).
  • PDK4 expression was manipulated using siRNA and expression plasmids.
  • Rosiglitazone (RG), a PPARγ agonist, was used to modulate PDK4 levels.
  • PDK4 expression was analyzed in human prostate samples.

Main Results:

  • High glucose enhanced proliferation, epithelial-mesenchymal transition (EMT), and suppressed apoptosis in prostate cells.
  • High glucose treatment and diabetes-related BPH samples showed reduced PDK4 expression.
  • PDK4 knockdown mimicked high glucose effects, while PDK4 overexpression reversed them.
  • Rosiglitazone increased PDK4 expression and may offer therapeutic potential for BPH.

Conclusions:

  • High glucose environments may promote BPH development, potentially through PDK4 down-regulation.
  • PDK4 expression levels are inversely correlated with BPH progression.
  • PDK4 represents a promising therapeutic target for managing BPH.