The effects of fasting and diabetes mellitus on myocardial metabolism in man

Goodale, Walter T.; Olson, Robert E.; Hackel, Donald B.

doi:10.1016/0002-9343(59)90341-9

Cited by 73 publications

(23 citation statements)

References 25 publications

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“…The isotopic lactate extraction increased from 0.24±0.12 to 0.45±0. 13 ,tmol/ml, respectively, (P < 0.01). Myocardial FFA extraction fell significantly during both levels I and II of the glucose clamp, 0.18±0.05 umol/ml for control and 0.08±0.04 and 0.04±0.04 Mmol/ml for levels I and II, respectively, (P < 0.01).…”

Section: Resultsmentioning

confidence: 83%

“…Previous studies have concluded that glucose contributes 15-55% of the energy needed for oxidative metabolism during fasting conditions and that this percentage increases to 65-100% during acute hyperglycemia (7)(8)(9)(10)(11)(12)(13)(14)(15). These conclusions were based on OER data which were calculated from the A -CS glucose difference with the assumption that the entire A -CS difference was oxidized immediately.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have measured the arterial (A)' and coronary sinus (CS) difference for glucose and have calculated an oxygen extraction ratio (OER); the OER is based on the assumption that the entire A -CS difference is oxidized. These calculations suggest that glucose contributes from 15 to 55% of oxidative metabolism under fasting conditions (7)(8)(9)(10)(11)(12)(13)(14)(15). During acute hyperglycemia, the myocardial extraction ofglucose significantly increases; OER data obtained during hyperglycemia imply that glucose becomes the major substrate for oxidative metabolism under this condition (7-9, 12-13, 15).…”

Section: Introductionmentioning

confidence: 97%

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Effects of acute hyperglycemia on myocardial glycolytic activity in humans.

Wisneski¹,

Stanley²,

Neese³

et al. 1990

J. Clin. Invest.

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The effects of hyperglycemia on myocardial glucose metabolism were investigated in seven healthy male subjects (age 24±4 yr). I6-C4qGlucose and IU-'3Cilactate were infused as tracers. Circulating glucose was elevated to two hyperglycemic levels using a clamp technique for 1 h at each level. The mean arterial glucose concentration was 4.95±0.29 (control), 8.33±0.31 and 10.84±0.60 jumol/ml, respectively. Glucose extraction increased significantly from control (0.15±0.13 gsmol/ ml) during each level of the glucose clamp (0.28±0.12, P < 0.02, and 0.54±0.14 ;tmol/ml, P < 0.005, respectively). Myocardial production of '4CO2 showed that during control 9±10% of exogenous glucose was oxidized immediately upon extraction. Despite a significant increase in the amount of exogenous glucose oxidized with level II hyperglycemia, it represented only 32±10% of the glucose extracted.[I3C]Lactate analysis showed that the myocardium was releasing lactate; during control 40±30% of this lactate was derived from exogenous glucose and during hyperglycemia this value increased to 97±37% (P < 0.005). Thus, these data show that during short-term hyperglycemia, myocardial glucose extraction is enhanced. However, despite increases in exogenous glucose oxidation and the contribution of exogenous glucose to lactate release, the majority of the extracted glucose (i.e., 57%) is probably stored as glycogen. (J. Clin. Invest. 1990Invest. . 85:1648Invest. -1656.) myocardial metabolism * glucose oxidation * lactate release * glycogen * free fatty acids

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Section: Resultsmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

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Effects of acute hyperglycemia on myocardial glycolytic activity in humans.

Wisneski¹,

Stanley²,

Neese³

et al. 1990

J. Clin. Invest.

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“…Utilization of lactate has usually been expressed as an extraction ratio, i.e., uptake relative to arterial level. Extraction ratios for lactate and pyruvate have been shown to be decreased in a variety of human disease states (10)(11)(12)(14)(15)(16) and animal experiments (4)(5)(6)(7)(31)(32)(33)(34). In the current study, no differences were found in mean extraction of lactate and pyruvate between patients in failure and other patient groups at rest.…”

Section: Discussionmentioning

confidence: 99%

“…Excess lactate has not been found in normal or diseased human subjects (10)(11)(12)(13)(14)(15) at rest except in a few patients with progressive muscular dystrophy (16). None has been subjected to exercise.…”

mentioning

confidence: 99%

Myocardial Lactate and Pyruvate Metabolism*

Krasnow¹,

Neill²,

Messer³

et al. 1962

J. Clin. Invest.

128

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Although the heart has been considered primarily an aerobic organ, recent work (1) has reemphasized the possibility that measurement of oxygen consumption alone may not 1)e adequate to define the total energy utilization under all conditions. The role of anaerobic metabolism must be reviewed.Methods of defining as well as quantifying anaerobiosis are currently in dispute. When oxidation and glycolysis proceed at the same rate, carbohydrate is oxidized to CO2 and H20. Lactate arises whenever the rate of glycolysis exceeds the rate of oxidation. Net production of lactate by an organ, as evidenced for example by venous concentration greater than arterial, has been considered to represent anaerobic metabolism due to cellular hypoxia (2). More recent work (3) has demonstrated that large changes in lactate production can occur unassociated with hypoxia, but related instead to increased pyruvate production. Huckabee introduced the concept of "excess lactate" in order to distinguish between pyruvateinduced changes in lactate and those related solely to a shift in DPN: DPNH redox potential. This was inferred from alterations in arterial lactatepyruvate ratio and the relative arteriovenous differences of the two substrates. "Excess lactate," so defined, was considered an indicator of cellular oxygenation and was used quantitatively as a measure of anaerobic metabolic rate.Anaerobic metabolism in cardiac muscle has been considered to occur only under extreme conditions. Whereas earlier work (4-9) showed lactate production only sporadically with stresses of hypoxia, shock, or myocardial emboli, Huckabee (1) found that in dogs the stress of either 10 per cent oxygen breathing or leg exercise would result in myocardial excess lactate despite positive

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Induction of lipid droplet accumulation in cardiac muscle cells of guinea pigs and mice: An analysis of the effects of reserpine and fasting

Iacovitti

Gershon

1978

Anat. Rec.

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Reserpine has been demonstrated in previous studies to induce the accumulation of lipid droplets in ventricular cardiac muscle cells of bats and this effect has been attributed to mediation by the sympathetic nervous system. The present study was done to evaluate the species specificity of this action of the drug. Reserpine caused lipid droplet accumulation in cardiocytes of guinea pigs and mice. However, in contrast to the action of the drug in bats, this action of reserpine in guinea pigs and mice could not be antagonized by chemical sympathectomy with 6-hydroxydopamine or by treatment of animals with phenoxybenzamine, atropine or hexamethonium. Like reserpine, fasting for as little as 24 hours induced lipid droplet accumulation in cardiocytes of guinea pigs and mice. This effect also could not be prevented by treatment with 6-hydroxydopamine indicating that the sympathetic nervous system was not involved in its mediation. Force-feeding guinea pigs given reserpine prevented the accumulation of lipid droplets normally induced by this drug. It is concluded that the lipid droplet accumulation in the hearts of guinea pigs that follows administration of reserpine is not due to a direct cardiotoxicity of the drug but is secondary to the failure of drug-treated animals to eat. Since the autonomic nervous system appears to mediate reserpine's cardiotoxicity in bats, the species difference revealed by these experiments probably results from an underlying physiological difference in the nervous systems of these animals.Reserpine has been shown to induce lipid droplet accumulation (LDA) in cardiocytes of bats (Hagopian e t al., '72). This change is antagonized by pretreatment of bats with 6-hydroxydopamine (6-HD1, phenoxybenzamine, or atropine (Hagopian e t al., '73; Hagopian e t al., '75). The change is also seen during the first 1-4 hours following arousal of bats from hibernation (Hagopian e t al., '73b). Moreover, lipid droplets accumulate in the heart when bats are injected with exogenous norepinephrine (NE) or the tryptophan hydroxylase inhibitor parachlorophenylalanine (PCPA) (Nunez e t al., '75; Hagopian e t al., '73b). A hypothesis has been put forward ascribing LDA to sympathetic neural activity (Nunez e t al., '75).The present experiments were done t o determine if LDA of the kind induced in bats by reserpine is a species-specific phenomenon, or whether other mammals also develop the change. Guinea pigs and mice were used as experimental animals and LDA was assessed histochemically and biochemically. Although reserpine does induce LDA in these other animals, the change does not seem to be a primary one and the data derived from the guinea pigs and mice is not comparable to that from bats. In guinea pigs and mice starvation for as little as 24 hours causes LDA and it is likely that LDA following administration of reserpine is secondary to these animals' failure to eat. MATERIALS A N D METHODS AnimalsAdult male Hartley guinea pigs (300-350 gm) and Swiss white mice (10-35 gm) were used in this study. All...

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The effects of fasting and diabetes mellitus on myocardial metabolism in man

Cited by 73 publications

References 25 publications

Effects of acute hyperglycemia on myocardial glycolytic activity in humans.

Effects of acute hyperglycemia on myocardial glycolytic activity in humans.

Myocardial Lactate and Pyruvate Metabolism*

Induction of lipid droplet accumulation in cardiac muscle cells of guinea pigs and mice: An analysis of the effects of reserpine and fasting

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