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

Fingerprint

Erectile Dysfunction
Endothelium
Diabetes Mellitus
Nitric Oxide
Theoretical Models
Advanced Glycosylation End Products
Vascular Endothelium
Dyslipidemias
Vascular Diseases
Mitogens
Nitric Oxide Synthase
Hyperglycemia
Protein Kinase C
Oxidative Stress
Phosphotransferases
Therapeutics

Keywords

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

Cite this

Erectile Dysfunction and Diabetes Mellitus : Mechanistic Considerations from Studies in Experimental Models. / Cameron, Norman E; Cotter, Mary Anne.

In: Current Diabetes Reviews, Vol. 3, No. 3, 08.2007, p. 149-158.

Research output: Contribution to journalArticle

@article{9e68dd62b5af4ad19f6a06c5b50ede1f,
title = "Erectile Dysfunction and Diabetes Mellitus: Mechanistic Considerations from Studies in Experimental Models",
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.",
keywords = "corpus cavernosum, erectile dysfunction, diabetes, endothelium, neuropathy, nitric oxide, oxidative stress, advanced glycation, protein kinase C, Rho-kinase",
author = "Cameron, {Norman E} and Cotter, {Mary Anne}",
year = "2007",
month = "8",
doi = "10.2174/157339907781368977",
language = "English",
volume = "3",
pages = "149--158",
journal = "Current Diabetes Reviews",
issn = "1573-3998",
publisher = "Bentham Science Publishers B.V.",
number = "3",

}

TY - JOUR

T1 - Erectile Dysfunction and Diabetes Mellitus

T2 - Mechanistic Considerations from Studies in Experimental Models

AU - Cameron, Norman E

AU - Cotter, Mary Anne

PY - 2007/8

Y1 - 2007/8

N2 - 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.

AB - 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.

KW - corpus cavernosum

KW - erectile dysfunction

KW - diabetes

KW - endothelium

KW - neuropathy

KW - nitric oxide

KW - oxidative stress

KW - advanced glycation

KW - protein kinase C

KW - Rho-kinase

U2 - 10.2174/157339907781368977

DO - 10.2174/157339907781368977

M3 - Article

VL - 3

SP - 149

EP - 158

JO - Current Diabetes Reviews

JF - Current Diabetes Reviews

SN - 1573-3998

IS - 3

ER -