Document Detail


Mechanisms of vascular dysfunctionin insulin resistance.
MedLine Citation:
PMID:  15503646     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Insulin resistance (IR) has profound, negative effects on the function of arteries and arterioles throughout the body. In addition to the obvious link between IR and the development of type 2 diabetes, IR-associated dysfunction of resistance vessels is associated with arterial hypertension and vascular occlusive diseases, such as heart attacks and strokes. IR affects arteries and arterioles at both the endothelium and smooth muscle levels. For example, IR causes reduced responsiveness of vascular smooth muscle to dilator agents; predominantly due to impaired potassium channel function. The common, underlying mechanism of vascular dysfunction, at both endothelium and smooth muscle levels, appears to involve the augmented availability and subsequent actions of reactive oxygen species (ROS). However, in some circulations, other factors, such as increased production of, and actions by, constrictor agents also appear to restrict normal dilator responses. The underlying cause of augmented ROS availability is not completely understood, but vascular inflammatory processes appear to be involved. Furthermore, application of superoxide dismutase, a specific scavenger of superoxide anion, is able to immediately restore normal vascular responsiveness in IR arteries. Additional treatments involving behavioral and pharmacological approaches, such as dietary adjustments, weight loss, exercise and the use of statins or insulin-sensitizing agents also appear to offer some benefit against the detrimental effects of IR.
Authors:
David W Busija; Allison W Miller; Prasad Katakam; Steve Simandle; Benedek Erdös
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Current opinion in investigational drugs (London, England : 2000)     Volume:  5     ISSN:  1472-4472     ISO Abbreviation:  Curr Opin Investig Drugs     Publication Date:  2004 Sep 
Date Detail:
Created Date:  2004-10-26     Completed Date:  2005-01-25     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100965718     Medline TA:  Curr Opin Investig Drugs     Country:  England    
Other Details:
Languages:  eng     Pagination:  929-35     Citation Subset:  IM    
Affiliation:
Wake Forest University Health Sciences, Department of Physiology and Pharmacology, Winston-Salem, NC 27157-1023, USA. dbusija@wfubmc.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Brain / blood supply
Diabetes Mellitus, Type 2 / complications,  metabolism,  physiopathology
Diabetic Angiopathies / etiology,  physiopathology*
Endothelium-Dependent Relaxing Factors / physiology
Humans
Insulin Resistance / physiology*
Potassium Channels / physiology
Reactive Oxygen Species / metabolism
Grant Support
ID/Acronym/Agency:
DK-62372/DK/NIDDK NIH HHS; HL-30260/HL/NHLBI NIH HHS; HL-50587/HL/NHLBI NIH HHS; HL-65380/HL/NHLBI NIH HHS; HL-66074/HL/NHLBI NIH HHS; HL-77731/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Endothelium-Dependent Relaxing Factors; 0/Potassium Channels; 0/Reactive Oxygen Species

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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