Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
49-50
pubmed:dateCreated
2008-1-16
pubmed:abstractText
nitric oxide (NO) plays an important role in the regulation of cardiovascular and glucose homeostasis. Mice lacking the gene encoding the neuronal isoform of nitric oxide synthase (nNOS) are insulin-resistant, but the underlying mechanism is unknown. nNOS is expressed in skeletal muscle tissue where it may regulate glucose uptake. Alternatively, nNOS driven NO synthesis may facilitate skeletal muscle perfusion and substrate delivery. Finally, nNOS dependent NO in the central nervous system may facilitate glucose disposal by decreasing sympathetic nerve activity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1424-7860
pubmed:author
pubmed:issnType
Print
pubmed:day
22
pubmed:volume
137
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
700-4
pubmed:dateRevised
2011-2-15
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Insulin resistance in mice lacking neuronal nitric oxide synthase is related to an alpha-adrenergic mechanism.
pubmed:affiliation
Department of Internal Medicine and Botnar Center for Clinical Research, CHUV, Lausanne, Switzerland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't