Linked Life Data

18407031

Source:http://linkedlifedata.com/resource/pubmed/id/18407031

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2008-4-14
pubmed:abstractText
Recent data suggest that diabetes in general, and particularly diabetes in association with insulin resistance, obesity, and hyperglycemia, results in inflammatory changes including the production of cytokines, adhesion molecules, and reactive oxygen species that are toxic to the endothelium and could lead to vascular damage. Insulin suppresses these effects, either indirectly by decreasing glucose levels or directly by stimulating nitric oxide production and inhibiting important pathways in the inflammatory cascade. In addition, insulin directly reduces plasma concentrations of adhesion molecule production in endothelial cells and thus may decrease vascular inflammation. Some of these effects of insulin may be attenuated in patients with insulin resistance, and this finding may provide a mechanistic link for the increase in vascular disease seen in patients with insulin resistance. Doses of insulin adequate to restore normoglycemia may help overcome these abnormalities, although some patients may require insulin sensitization with lifestyle changes or pharmacologic therapy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0889-8529
pubmed:author
pubmed:issnType
Print
pubmed:volume
36 Suppl 2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
20-6
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
The effects of insulin on the endothelium.
pubmed:affiliation
Tullis Tulane Alumni Chair in Diabetes, Chief, Section of Endocrinology, Tulane University Health Sciences Center, New Orleans, Louisiana 70112, USA. vfonseca@tulane.edu
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural