Decreased myocardial glucose uptake during ischemia in diabetic swine

William C. Stanley, Jennifer L. Hall, Timothy A. Hacker, Lisa A. Hernandez, Larry F. Whitesell

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33 Scopus citations

Abstract

The purpose of the study was to assess myocardial glucose uptake in nondiabetic (n = 5) and streptozotocin-diabetic (n = 6) Yucatan miniature swine under matched hyperglycemic and hypoinsulinemic conditions. Fasting conscious diabetic swine had significantly higher plasma glucose levels (20.9 ± 2.6 v 5.2 ± 0.3 mmol/L) and lower insulin levels (6 ± 1 v 14 ± 4 μU/mL) than nondiabetic animals. Myocardial glucose uptake was measured in open-chest anesthetized animals under aerobic and ischemic conditions 12 weeks after streptozotocin treatment. Coronary blood flow was controlled by an extracorporeal perfusion circuit. Ischemia was induced by reducing left anterior descending (LAD) coronary artery blood flow by 60% for 40 minutes. Animals were treated with somatostatin to suppress insulin secretion, and nondiabetic swine received intravenous (IV) glucose to match the hyperglycemia in the diabetic animals. The rate of glucose uptake by the myocardium was not statistically different under aerobic conditions, but was significantly lower in diabetic swine during ischemia (0.20 ± 0.08 v 0.63 ± 0.14 μmol · g-1 · min-1, p < .01). Myocardial glucose transporter (GLUT4) protein concentration was decreased by 31% in diabetic swine. In conclusion, 12 weeks of streptozotocin diabetes in swine caused a significant decrease in myocardial GLUT4 protein and a decrease in myocardial glucose uptake during ischemia.

Original languageEnglish (US)
Pages (from-to)168-172
Number of pages5
JournalMetabolism: clinical and experimental
Volume46
Issue number2
DOIs
StatePublished - 1997

Bibliographical note

Funding Information:
From the Section of Cardiovascular Pharmacology, Syntex Discovery Research, Palo Alto, CA; and the Section of Cardiology and the Biodynamics Laboratory, University of Wisconsin, Madison, WI. Submitted February 16, 1996; accepted August 7, 1996. Supported by grants from the Juvenile Diabetes Foundation International and the National Institutes of Health (HL-47094). Address reprint requests to William C. Stanley, PhD, Department of Physiology and Biostatistics, School of Medicine, Case Western Reserve University, 10900 Euclid Ave, Cleveland, OH 44106-4970. Copyright © 1997 by WB. Saunders Company 0026-0495/97/4602-0011503.00/0

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