Linked Life Data

18981538

Source:http://linkedlifedata.com/resource/pubmed/id/18981538

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-11-4
pubmed:abstractText
In order to test the potential role of inhibitory G-proteins in mechanisms of insulin resistance in adipose tissue of obese animals we determined the content of Galpha(i1) and Galpha(i2) proteins and an extent of protein tyrosine phosphorylation in epididymal fat tissue cell membranes using immunoblot. Monosodium glutamate-induced obese rats displayed adipose tissue hypertrophy, elevated levels of insulin, leptin and slightly elevated serum glucose. We found significantly decreased protein content of Galpha(i2) in adipose tissue plasma membranes of obese rats. This was in accordance with lower protein tyrosine phosphorylation noticed in adipose tissue cell homogenate of glutamate-treated animals. Our results confirm the role of Galpha(i2) in development of insulin resistance by crosstalk between the reduced level of inhibitory G-protein and insulin receptor mediated most likely by activation of phosphotyrosine protein dephosphorylation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0231-5882
pubmed:author
pubmed:issnType
Print
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
222-6
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Rats with monosodium glutamate-induced obesity and insulin resistance exhibit low expression of Galpha(i2) G-protein.
pubmed:affiliation
Institute of Experimental Endocrinology, Slovak Academy of Sciences, Vlárska 3, Bratislava, Slovakia. miroslava.baculikova@savba.sk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't