Document Detail


Abnormal in vivo myocardial energy substrate uptake in diet-induced type 2 diabetic cardiomyopathy in rats.
MedLine Citation:
PMID:  20159856     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The purpose of this study was to determine in vivo myocardial energy metabolism and function in a nutritional model of type 2 diabetes. Wistar rats rendered insulin-resistant and mildly hyperglycemic, hyperinsulinemic, and hypertriglyceridemic with a high-fructose/high-fat diet over a 6-wk period with injection of a small dose of streptozotocin (HFHFS) and control rats were studied using micro-PET (microPET) without or with a euglycemic hyperinsulinemic clamp. During glucose clamp, myocardial metabolic rate of glucose measured with [(18)F]fluorodeoxyglucose ([(18)F]FDG) was reduced by approximately 81% (P < 0.05), whereas myocardial plasma nonesterified fatty acid (NEFA) uptake as determined by [(18)F]fluorothia-6-heptadecanoic acid ([(18)F]FTHA) was not significantly changed in HFHFS vs. control rats. Myocardial oxidative metabolism as assessed by [(11)C]acetate and myocardial perfusion index as assessed by [(13)N]ammonia were similar in both groups, whereas left ventricular ejection fraction as assessed by microPET was reduced by 26% in HFHFS rats (P < 0.05). Without glucose clamp, NEFA uptake was approximately 40% lower in HFHFS rats (P < 0.05). However, myocardial uptake of [(18)F]FTHA administered by gastric gavage was significantly higher in HFHFS rats (P < 0.05). These abnormalities were associated with reduced Glut4 mRNA expression and increased Cd36 mRNA expression and mitochondrial carnitine palmitoyltransferase 1 activity (P < 0.05). HFHFS rats display type 2 diabetes complicated by left ventricular contractile dysfunction with profound reduction in myocardial glucose utilization, activation of fatty acid metabolic pathways, and preserved myocardial oxidative metabolism, suggesting reduced myocardial metabolic efficiency. In this model, increased myocardial fatty acid exposure likely occurs from circulating triglyceride, but not from circulating plasma NEFA.
Authors:
S?bastien L M?nard; Etienne Croteau; Otman Sarrhini; Roselle G?linas; Pascal Brassard; Ren? Ouellet; M'hamed Bentourkia; Johannes E van Lier; Christine Des Rosiers; Roger Lecomte; Andr? C Carpentier
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-02-16
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  298     ISSN:  1522-1555     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-04-14     Completed Date:  2010-05-03     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E1049-57     Citation Subset:  IM    
Affiliation:
Division of Endocrinology, Department of Medicine, University de Sherbrooke, Sherbrooke, QC, Canada.
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Cardiomyopathies / etiology,  metabolism*,  radionuclide imaging
Diabetes Mellitus, Experimental / complications,  metabolism*,  radionuclide imaging
Energy Metabolism / physiology*
Enzyme-Linked Immunosorbent Assay
Fatty Acids, Nonesterified / blood
Glucose / metabolism*
Glucose Clamp Technique
Heart / radionuclide imaging
Heart Failure / etiology,  metabolism,  radionuclide imaging
Insulin / blood
Male
Myocardium / metabolism*
Rats
Rats, Wistar
Reverse Transcriptase Polymerase Chain Reaction
Triglycerides / blood
Grant Support
ID/Acronym/Agency:
MOP-53094//Canadian Institutes of Health Research; PRG-80137//Canadian Institutes of Health Research
Chemical
Reg. No./Substance:
0/Fatty Acids, Nonesterified; 0/Triglycerides; 11061-68-0/Insulin; 50-99-7/Glucose

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


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