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 κ 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.
Keywords: Corpus cavernosum, Erectile dysfunction, Diabetes, Endothelium, Neuropathy, Nitric oxide, Oxidative stress, Advanced glycation, Protein kinase C, Rho-kinase
Current Diabetes Reviews
Title: Erectile Dysfunction and Diabetes Mellitus: Mechanistic Considerations from Studies in Experimental Models
Volume: 3 Issue: 3
Author(s): Norman E. Cameron and Mary A. Cotter
Affiliation:
Keywords: Corpus cavernosum, Erectile dysfunction, Diabetes, Endothelium, Neuropathy, Nitric oxide, Oxidative stress, Advanced glycation, Protein kinase C, Rho-kinase
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 κ 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.
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Cite this article as:
Norman E. Cameron and Mary A. Cotter , Erectile Dysfunction and Diabetes Mellitus: Mechanistic Considerations from Studies in Experimental Models, Current Diabetes Reviews 2007; 3 (3) . https://dx.doi.org/10.2174/157339907781368977
DOI https://dx.doi.org/10.2174/157339907781368977 |
Print ISSN 1573-3998 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6417 |
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