Effect of epinephrine on myocardial triglyceride and free fatty acid utilization

Ra, Kreisberg

doi:10.1152/ajplegacy.1966.210.2.385

Cited by 51 publications

(13 citation statements)

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“…That the above mechanism may become more important under conditions of elevated tissue triglycerides, as in ketonic diabetic hearts (5, 20, 22), cannot be excluded. Kreisberg (16) found elevated rates of glycerol release from hearts of diabetic rats in comparison with control hearts. This may explain why diabetic hearts are more vulnerable to ischemia than normal hearts (8).…”

Section: Discussionmentioning

confidence: 97%

Relation between lipolysis and glycolysis during ischemia in the isolated rat heart

1986

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The relation between lipolysis and glycolysis during ischemia was investigated in isolated perfused rat hearts. In hearts perfused with 11 mM glucose, ischemia caused a marked increase of glycerol release from 10 to 33 nmol/g wt weight/min. Substrate-free perfusion induced an initial stimulation of glycerol release, but lipolysis was subsequently reduced to values comparable to normoxic conditions. Neither did perfusion in the presence of acetate (10 mM) and beta-hydroxybutyrate (10 mM) stimulate lipolysis. Inhibition of glycolysis by pyruvate prevented the increase of glycerol release during ischemia. These data suggest a tight link between glycolysis and lipolysis during ischemia which is probably mediated by the availability of glycolytically produced glycerol-3-phosphate for reesterification. In the absence of glycerol-3-phosphate, the lipolysis is regulated by product inhibition. As a consequence, the tissue triglyceride levels after perfusion remained fairly constant in all groups of hearts. The calculated energy loss by the reesterification cycle during ischemia was found to be approximately 2.5% of the total energy production. These data are inconsistent with the assumption that this energy loss contributes significantly to the negative energetic balance of the heart during ischemia. Removal of fatty acids by reesterification may constitute a protective mechanism in order to prevent excessive intracellular accumulation of fatty acids and derivative esters during ischemia.

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Section: Discussionmentioning

confidence: 97%

Relation between lipolysis and glycolysis during ischemia in the isolated rat heart

1986

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“…The evidence for activation of a lipase of heart by cAMP is that an increased release of glycerol occurs under the influence of adrenaline (WILLIAMSON, 1964;CHALLONER and STEINBERG, 1965;KREISBERG, 1966) or isopropylnoradrenaline (CHRISTIAN et aI., 1969). The increase in glycerol release coincides with the increase in phosphorylase a activity and both these responses follow the initial increase in cAMP concentration and in contractile force caused by isopropylnoradrenaline; the dose-response curves for these two responses are also very similar (CHRISTIAN et aI., 1969).…”

Section: A) Adenyl Cyclasementioning

confidence: 99%

Effects of Catecholamines on Metabolism

Himms‐Hagen¹

1972

Catecholamines

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“…This enzyme has previously been demonstrated in extracts of beef hearts [13,14], but without quantitation of total activity. It has been suggested that it might be involved also in utilization of endogenous triglyceride stores as well as in provision of fatty acids from plasma triglycerides [15].…”

Section: Nature Of Tgl Activity In Subcellular Fractionsmentioning

confidence: 99%