Alterations in myocardial metabolism in the diabetic myocardium.
Free fatty acids are the preferred substrate for the myocardium. However, under conditions of ischemia, glucose becomes the primary myocardial energy source. Its metabolism avoids the toxic end-products of free fatty acids, which include oxygen free radicals. Patients with diabetes mellitus have impaired uptake of glucose. As a consequence the diabetic myocardium relies heavily on free fatty acid metabolism as its energy source. The results of these alterations in myocardial metabolism ultimately contribute to changes in endothelial function, inflammation, and oxidative stress. This review describes the defects in diabetic myocardial metabolism and how they contribute to cardiovascular dysfunction. The mechanisms by which intravenous insulin infusions can be used to modulate these changes in myocardial metabolism to improve clinical outcomes are discussed.
Lazar
Harold L
HL
Boston University School of Medicine, Department of Cardiothoracic Surgery, Boston Medical Center, Boston, MA 02118, USA. harold.lazar@bmc.org
D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D003920:Diabetes Mellitus / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D006801:Humans; D006943:Hyperglycemia / Q000378:metabolism; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007262:Infusions, Intravenous; D007328:Insulin / Q000627:therapeutic use; D017202:Myocardial Ischemia / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects
D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007004:Hypoglycemic Agents; D007328:Insulin