Document Detail


Functional effects of glucose transporters in human ventricular myocardium.
MedLine Citation:
PMID:  20083620     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
AIMS: Insulin-dependent positive inotropic effects (PIE) are partially Ca(2+) independent. This mechanism is potentially glucose dependent. In contrast to most animal species, human myocardium expresses high levels of sodium-glucose-transporter-1 (SGLT-1) mRNA besides the common glucose-transporters-1 and -4 (GLUT1, GLUT4).
METHODS AND RESULTS: We used ventricular myocardium from 61 end-stage failing human hearts (ischaemic cardiomyopathy, ICM and dilated cardiomyopathy, DCM) and 13 non-failing donor hearts. The effect of insulin on isometric twitch force was examined with or without blocking of PI3-kinase, GLUT4-translocation, or SGLT-1. Substrate-dependent (glucose vs. pyruvate vs. palmitoyl-carnitine) effects were tested in atrial myocardium. mRNA expression of glucose transporters was analysed. Insulin increased developed force by 122 + or - 7.4, 121.7 + or - 2.5, and 134.1 + or - 5.7% in non-failing, DCM, and ICM (P < 0.05 vs. DCM), respectively. Positive inotropic effect was partially blunted by inhibition of PI-3-kinase, GLUT4, or SGLT1. Combined inhibition of PI3-kinase and glucose-transport completely abolished PIE. Positive inotropic effect was significantly stronger in glucose-containing solution compared with pyruvate or palmitoyl-carnitine containing. mRNA expression showed only a tendency towards elevated GLUT4-expression in ICM.
CONCLUSIONS: Positive inotropic effect of insulin is pronounced in ICM, but underlying mechanisms are unaltered. The Ca(2+)-independent PIE of insulin is mediated via glucose-transporters. Together with the Ca(2+)-dependent PI-3-kinase mediated pathway, it is responsible for the entire PIE. Substrate-dependency affirms a glucose-dependent part of the PIE.
Authors:
Dirk von Lewinski; Robert Gasser; Peter P Rainer; Marie-Sophie Huber; Bastian Wilhelm; Ulrich Roessl; Tobias Haas; Andrae Wasler; Michael Grimm; Egbert Bisping; Burkert Pieske
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European journal of heart failure     Volume:  12     ISSN:  1879-0844     ISO Abbreviation:  Eur. J. Heart Fail.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-01-19     Completed Date:  2011-01-20     Revised Date:  2011-06-08    
Medline Journal Info:
Nlm Unique ID:  100887595     Medline TA:  Eur J Heart Fail     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  106-13     Citation Subset:  IM    
Affiliation:
Department of Cardiology, Working Group Metabolism and Energetics, Medical University Graz, Graz, Austria. dirk.von-lewinski@medunigraz.at
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MeSH Terms
Descriptor/Qualifier:
Aged
Carbonates / pharmacology
Cardiomyopathy, Dilated / physiopathology
Dose-Response Relationship, Drug
Female
Gene Expression Regulation
Glucose Transporter Type 1 / genetics,  metabolism*
Glucose Transporter Type 4 / genetics,  metabolism*
Glucosides / pharmacology
Heart Failure / physiopathology*
Heart Ventricles
Humans
Inhibitory Concentration 50
Insulin / pharmacology
Male
Middle Aged
Myocardial Contraction / drug effects,  physiology*
Myocardial Ischemia / physiopathology
Myocardium / metabolism*
Phosphatidylinositol 3-Kinases / antagonists & inhibitors
RNA, Messenger / metabolism
Sodium-Glucose Transporter 1 / antagonists & inhibitors,  genetics,  metabolism*
Sodium-Glucose Transporter 2 / antagonists & inhibitors,  genetics,  metabolism
Chemical
Reg. No./Substance:
0/Carbonates; 0/Glucose Transporter Type 1; 0/Glucose Transporter Type 4; 0/Glucosides; 0/RNA, Messenger; 0/Sodium-Glucose Transporter 1; 0/Sodium-Glucose Transporter 2; 0/T 1095; 11061-68-0/Insulin; EC 2.7.1.-/Phosphatidylinositol 3-Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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