Linked Life Data

16565309

Source:http://linkedlifedata.com/resource/pubmed/id/16565309

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-7-14
pubmed:abstractText
To investigate the association between hyperinsulinemia and cardiac hypertrophy, we treated rats with insulin for 7 wk and assessed effects on myocardial growth, vascularization, and fibrosis in relation to the expression of angiotensin II receptors (AT-R). We also characterized insulin signaling pathways believed to promote myocyte growth and interact with proliferative responses mediated by G protein-coupled receptors, and we assessed myocardial insulin receptor substrate-1 (IRS-1) and p110 alpha catalytic and p85 regulatory subunits of phospatidylinositol 3 kinase (PI3K), Akt, MEK, ERK1/2, and S6 kinase-1 (S6K1). Left ventricular (LV) geometry and performance were evaluated echocardiographically. Insulin decreased AT1a-R mRNA expression but increased protein levels and increased AT2-R mRNA and protein levels and phosphorylation of IRS-1 (Ser374/Tyr989), MEK1/2 (Ser218/Ser222), ERK1/2 (Thr202/Tyr204), S6K1 (Thr421/Ser424/Thr389), Akt (Thr308/Thr308), and PI3K p110 alpha but not of p85 (Tyr508). Insulin increased LV mass and relative wall thickness and reduced stroke volume and cardiac output. Histochemical examination demonstrated myocyte hypertrophy and increases in interstitial fibrosis. Metoprolol plus insulin prevented the increase in relative wall thickness, decreased fibrosis, increased LV mass, and improved function seen with insulin alone. Thus our data demonstrate that chronic hyperinsulinemia decreases AT1a-to-AT2 ratio and increases MEK-ERK1/2 and S6K1 pathway activity related to hypertrophy. These changes might be crucial for increased cardiovascular growth and fibrosis and signs of impaired LV function.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
291
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H787-96
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:16565309-Animals, pubmed-meshheading:16565309-Blood Glucose, pubmed-meshheading:16565309-Blotting, Western, pubmed-meshheading:16565309-Body Weight, pubmed-meshheading:16565309-Electrocardiography, pubmed-meshheading:16565309-Female, pubmed-meshheading:16565309-Fibrosis, pubmed-meshheading:16565309-Gene Expression Regulation, Enzymologic, pubmed-meshheading:16565309-Heart, pubmed-meshheading:16565309-Hemodynamics, pubmed-meshheading:16565309-Hyperinsulinism, pubmed-meshheading:16565309-Immunohistochemistry, pubmed-meshheading:16565309-Insulin, pubmed-meshheading:16565309-Mitogen-Activated Protein Kinases, pubmed-meshheading:16565309-Organ Size, pubmed-meshheading:16565309-Phosphatidylinositol 3-Kinases, pubmed-meshheading:16565309-Proto-Oncogene Proteins c-akt, pubmed-meshheading:16565309-Rats, pubmed-meshheading:16565309-Rats, Sprague-Dawley, pubmed-meshheading:16565309-Receptors, Angiotensin, pubmed-meshheading:16565309-Receptors, G-Protein-Coupled, pubmed-meshheading:16565309-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:16565309-Signal Transduction, pubmed-meshheading:16565309-Ventricular Function, Left
pubmed:year
2006
pubmed:articleTitle
Hyperinsulinemia: effect on cardiac mass/function, angiotensin II receptor expression, and insulin signaling pathways.
pubmed:affiliation
Cardiovascular Institute, The Wallenberg Laboratory, Sahlgrenska Univ. Hospital, Göteborg University, S-413 45 Göteborg, Sweden. anne-maj.samuelsson@wlab.gu.se
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't