Regulation of carbohydrate metabolism in ischemia and reperfusion.
Administration of L-carnitine reduces ischemic myocardial injury in a number of experimental model systems and may improve the clinical outcomes of patients with acute myocardial infarction. The efficacy of carnitine in this setting is probably not attributable to an increase in fatty acid oxidation, which can be detrimental to myocardial recovery during reperfusion. Instead, recent research suggests that carnitine is also crucial in the regulation of carbohydrate metabolism in addition to its role in the oxidation of fatty acids. In isolated rat hearts, administration of carnitine increases the oxidation of glucose while decreasing the oxidation of palmitate. This increase in carbohydrate metabolism is accompanied by a significant improvement of contractile function during reperfusion of ischemic hearts. The beneficial effects of carnitine seen in patients after an acute MI may be attributable to an improvement in myocardial energy metabolism. Controlled clinical trials will be useful in confirming the results from these experimental studies.
Lopaschuk
G
G
University of Alberta, Edmonton, Canada. gary.lopaschuk@ualberta.ca
D000818:Animals; D050260:Carbohydrate Metabolism; D002331:Carnitine / Q000378:metabolism / Q000627:therapeutic use; D004734:Energy Metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006801:Humans; D008929:Mitochondria, Heart / Q000378:metabolism; D009200:Myocardial Contraction / Q000187:drug effects; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000503:physiopathology / Q000517:prevention & control; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology / Q000517:prevention & control; D009206:Myocardium / Q000378:metabolism*; D010084:Oxidation-Reduction
D005230:Fatty Acids, Nonesterified; D005947:Glucose; D002331:Carnitine