Erectile Dysfunction and Diabetes Mellitus: Mechanistic Considerations from Studies in Experimental Models

Norman E Cameron, Mary Anne Cotter

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Diabetes is a major risk factor for erectile dysfunction. The condition degrades both neural and vascular endothelium penile control systems. Experimental and epidemiological evidence suggest that both hyperglycemia and dyslipidemia contribute to the etiology. These are the driving forces for elevated oxidative stress and the formation of advanced glycation and lipoxygenation end products, the major target being the nitric oxide systems of nerve and endothelium. This causes reversible functional loss followed by less reversible degenerative changes. These mechanisms have direct effects, such as the nitric oxide quenching, but perhaps more importantly, indirect effects on the regulation of nitric oxide synthase expression and activity, which can involve recruitment of proinflammatory cell signaling pathways. The latter include protein kinase C, mitogen-activated kinases, and the nuclear factor ¿ B cascade. Diabetes also changes the trophic influences on nerve and endothelium. Together, these form potential therapeutic targets against diabetic erectile function, and indeed vascular disease in general.
Original languageEnglish
Pages (from-to)149-158
Number of pages10
JournalCurrent Diabetes Reviews
Volume3
Issue number3
DOIs
Publication statusPublished - Aug 2007

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Keywords

  • corpus cavernosum
  • erectile dysfunction
  • diabetes
  • endothelium
  • neuropathy
  • nitric oxide
  • oxidative stress
  • advanced glycation
  • protein kinase C
  • Rho-kinase

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