Glycolysis and glucose oxidation in the rat heart under nonrecirculating perfusion conditions.
Isolated rat hearts were perfused according to Langendorff and as a working heart preparation with glucose as the only exogenous substrate under nonrecirculating conditions to avoid accumulation of heart metabolites and, thereby, changes in the composition of the perfusion medium. In the absence of insulin or at low work, oxidation of endogenous substrates as glycogen is of importance for myocardial energy metabolism. Accordingly, about 1/3 of the glucose oxidized by the heart was derived from myocardial glycogen. Lipolysis of endogenous triglycerides and oxidation of the fatty acids produced were, however, low in normal rat hearts. By contrast, in the presence of insulin or at high work load endogenous substrates play a minor role for energy provision. About 80% of the total oxygen consumption could be attributed to the oxidation of exogenous glucose. Furthermore, insulin exerted its major effect in accelerating glucose uptake and glycolysis, but had little influence on PDH-activity. Insulin increased lipolysis in control hearts, however, changes in the endogenous triglycerides were less than valves calculated from the rate of lipolysis. Thus, glycerol release can be taken as a measure for lipolysis, but not as a measure for fatty acid oxidation, since the produced fatty acids were partly reesterified to glycerides. On the basis of the metabolic data obtained, the oxygen and energy balance was calculated. We conclude that a sufficient energy provision is only warranted if the rat heart is perfused either in the presence of insulin or at higher--more physiological--work load.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D004734:Energy Metabolism; D005990:Glycerol / Q000378:metabolism; D006019:Glycolysis; D007328:Insulin / Q000502:physiology; D008297:Male; D009200:Myocardial Contraction; D009206:Myocardium / Q000201:enzymology*; D010084:Oxidation-Reduction; D010101:Oxygen Consumption; D010477:Perfusion; D010725:Phosphocreatine / Q000378:metabolism; D011768:Pyruvate Dehydrogenase Complex / Q000378:metabolism; D011773:Pyruvates / Q000378:metabolism; D019289:Pyruvic Acid; D051381:Rats; D011919:Rats, Inbred Strains; D014280:Triglycerides / Q000378:metabolism
D001786:Blood Glucose; D007328:Insulin; D011768:Pyruvate Dehydrogenase Complex; D011773:Pyruvates; D014280:Triglycerides; D010725:Phosphocreatine; D019289:Pyruvic Acid; D000255:Adenosine Triphosphate; D005990:Glycerol