Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2004-10-26
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1472-4472
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
929-35
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Mechanisms of vascular dysfunctionin insulin resistance.
pubmed:affiliation
Wake Forest University Health Sciences, Department of Physiology and Pharmacology, Winston-Salem, NC 27157-1023, USA. dbusija@wfubmc.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't