Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6568
pubmed:dateCreated
1996-3-25
pubmed:abstractText
Integration of information between tyrosine kinase and G-protein-mediated pathways is necessary, but remains poorly understood. Here we use cells from transgenic mice harbouring inducible expression of RNA antisense to the gene encoding G ialpha2 to show that G ialpha2 is critical for insulin action. G ialpha2 deficiency in adipose tissue and liver produces hyperinsulinaemia, impaired glucose tolerance and resistance to insulin in vivo. Insulin resistance affects glucose-transporter activity and recruitment, counterregulation of lipolysis, and activation of glycogen synthase, all of which are cardinal responses to insulin. G ialpha2 deficiency increases protein-tyrosine phosphatase activity and attenuates insulin-stimulated tyrosine phosphorylation of IRS (insulin-receptor substrate 1) in vivo. G ialpha2 deficiency creates a model for insulin resistance characteristic of noninsulin-dependent diabetes mellitus (NIDDM), implicating G ialpha2 as a positive regulator of insulin action.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Blood Glucose, http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Glucose Transporter Type 4, http://linkedlifedata.com/resource/pubmed/chemical/Glycogen Synthase, http://linkedlifedata.com/resource/pubmed/chemical/Insulin, http://linkedlifedata.com/resource/pubmed/chemical/Insulin Receptor Substrate Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Irs1 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Monosaccharide Transport Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Muscle Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Phosphoproteins, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Antisense, http://linkedlifedata.com/resource/pubmed/chemical/Slc2a4 protein, mouse
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0028-0836
pubmed:author
pubmed:issnType
Print
pubmed:day
29
pubmed:volume
379
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
840-4
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:8587610-Adipose Tissue, pubmed-meshheading:8587610-Animals, pubmed-meshheading:8587610-Biological Transport, pubmed-meshheading:8587610-Blood Glucose, pubmed-meshheading:8587610-Diabetes Mellitus, Type 2, pubmed-meshheading:8587610-Disease Models, Animal, pubmed-meshheading:8587610-GTP-Binding Proteins, pubmed-meshheading:8587610-Glucose Transporter Type 4, pubmed-meshheading:8587610-Glycogen Synthase, pubmed-meshheading:8587610-Hyperinsulinism, pubmed-meshheading:8587610-Insulin, pubmed-meshheading:8587610-Insulin Receptor Substrate Proteins, pubmed-meshheading:8587610-Insulin Resistance, pubmed-meshheading:8587610-Lipolysis, pubmed-meshheading:8587610-Liver, pubmed-meshheading:8587610-Mice, pubmed-meshheading:8587610-Mice, Transgenic, pubmed-meshheading:8587610-Monosaccharide Transport Proteins, pubmed-meshheading:8587610-Muscle Proteins, pubmed-meshheading:8587610-Phosphoproteins, pubmed-meshheading:8587610-RNA, Antisense
pubmed:year
1996
pubmed:articleTitle
Insulin action impaired by deficiency of the G-protein subunit G ialpha2.
pubmed:affiliation
Department of Molecular Pharmacology, Diabetes and Metabolic Diseases Research Program, University Medical Center, SUNY/Stony Brook, New York 11794-8651, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't