Changes in endothelial dysfunction and associated cardiovascular disease morbidity markers in GH-IGF axis pathology

Michael R. Graham, Peter Evans, Non-Eleri Thomas, Bruce Davies, Julien S. Baker

Research output: Contribution to journalArticle

Abstract

Arterial endothelial dysfunction is an early event in the pathogenesis of atherosclerosis and predisposes individuals to the deposition of unstable atherosclerotic plaques. It can also lead to increased arterial stiffness, which is an accepted cause of increased arterial pulse wave velocity (APWV). Endothelial dysfunction is reversed by recombinant human growth hormone (rhGH) therapy in patients with growth hormone (GH) deficiency (GHD), favorably influencing the risk for atherogenesis. Endogenous human growth hormone (hGH), secreted by the anterior pituitary, and levels of insulin-like growth factor-I (IGF-I), produced in response to hGH stimulation of the liver, peak during early adulthood, but decline throughout adulthood. It is suspected that low-grade inflammatory cardiovascular pathophysiologic markers such as homocysteine, nitric oxide, C-reactive protein (CRP), and fibrinogen and plasminogen activator inhibitor along with changes in lipid and glucose metabolism may all contribute to GHD-associated metabolic and cardiovascular complications. These effects are associated with increased APWV, but are attenuated by rhGH therapy in GHD. GH replacement increases IGF-I levels and reduces CRP and large-artery stiffness. Reviews of rhGH in the somatopause have not been overtly favorable. Whereas reviews of rhGH/rhIGF-I combinations in GH resistance are more positive than those for rhGH alone, their combined use in the somatopause is limited. Senescent individuals may benefit from such a combination.
Original languageEnglish
Pages (from-to)371-381
Number of pages11
JournalAmerican Journal of Cardiovascular Drugs
Volume9
Issue number6
DOIs
Publication statusPublished - 1 Dec 2009

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Human Growth Hormone
Growth Hormone
Cardiovascular Diseases
Pathology
Morbidity
Pulse Wave Analysis
Insulin-Like Growth Factor I
C-Reactive Protein
Atherosclerosis
Plasminogen Inactivators
Vascular Stiffness
Homocysteine
Atherosclerotic Plaques
Lipid Metabolism
Fibrinogen
Nitric Oxide
Arteries
Glucose
Liver
Therapeutics

Cite this

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title = "Changes in endothelial dysfunction and associated cardiovascular disease morbidity markers in GH-IGF axis pathology",
abstract = "Arterial endothelial dysfunction is an early event in the pathogenesis of atherosclerosis and predisposes individuals to the deposition of unstable atherosclerotic plaques. It can also lead to increased arterial stiffness, which is an accepted cause of increased arterial pulse wave velocity (APWV). Endothelial dysfunction is reversed by recombinant human growth hormone (rhGH) therapy in patients with growth hormone (GH) deficiency (GHD), favorably influencing the risk for atherogenesis. Endogenous human growth hormone (hGH), secreted by the anterior pituitary, and levels of insulin-like growth factor-I (IGF-I), produced in response to hGH stimulation of the liver, peak during early adulthood, but decline throughout adulthood. It is suspected that low-grade inflammatory cardiovascular pathophysiologic markers such as homocysteine, nitric oxide, C-reactive protein (CRP), and fibrinogen and plasminogen activator inhibitor along with changes in lipid and glucose metabolism may all contribute to GHD-associated metabolic and cardiovascular complications. These effects are associated with increased APWV, but are attenuated by rhGH therapy in GHD. GH replacement increases IGF-I levels and reduces CRP and large-artery stiffness. Reviews of rhGH in the somatopause have not been overtly favorable. Whereas reviews of rhGH/rhIGF-I combinations in GH resistance are more positive than those for rhGH alone, their combined use in the somatopause is limited. Senescent individuals may benefit from such a combination.",
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Changes in endothelial dysfunction and associated cardiovascular disease morbidity markers in GH-IGF axis pathology. / Graham, Michael R.; Evans, Peter; Thomas, Non-Eleri; Davies, Bruce; Baker, Julien S.

In: American Journal of Cardiovascular Drugs, Vol. 9, No. 6, 01.12.2009, p. 371-381.

Research output: Contribution to journalArticle

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