Regulation of glucose uptake by muscle. 3. The effects of insulin, anoxia, salicylate and 2:4-dinitrophenol on membrane transport and intracellular phosphorylation of glucose in the isolated rat heart

Morgan, Howard E.; Randle, P. J.; Regen, David M.

doi:10.1042/bj0730573

Cited by 244 publications

(163 citation statements)

References 10 publications

(4 reference statements)

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“…Since this is not observed, the inhibition of glycolysis by butyrate likely occurs before phosphorylation of glucose. These observations are in agreement with previous studies showing a decrease in the rate of glycolysis [1,2,4] and accumulation of free intracellular glucose [3] in the presence of butyrate. The results also suggest that the effects of iodoacetate on high-energy phosphate metabolism are reasonably specific.…”

Section: Resultssupporting

confidence: 83%

“…Although the exact mechanism by which the presence of fatty acids inhibits glucose utilization is somewhat uncertain, the observed accumulation of glucose [3] in the heart when both glucose and fatty acids are provided in the medium suggests that the inhibition of glucose utilization occurs after glucose uptake but before the first phosphorylation event. "P-NMR spectroscopy of the Langendorff perfused rat heart can be used to follow changes in the concentrations of major pools of phosphorus-containing metabolites in vivo [5].…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of glucose phosphorylation by fatty acids in the perfused rat heart

1988

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The flux of glucose entering the glycolytic pathway under various metabolic conditions has been indirectly monitored in the Langendorff perfused rat heart using 31P-NMR spectroscopy. By totally inhibiting (> 95%) glyceraldehyde-3-phosphate dehydrogenase with low concentrations of iodoacetic acid (0.2 mM) in the perfusion medium, active glycolysis results in the accumulation of sugar phosphate species (fructose 1,6_bisphosphate, dihydroxyacetone phosphate, and glyceraldehyde 3-phosphate) which can be observed in the slP-NMR spectrum. Using this technique, it has been shown that butyrate (10 mM) in the perfusion medium decreases the flux through the initial steps of the glycolytic pathway by at least 6-fold and that both glucose phosphorylation and glycogenolysis are inhibited. Upon total global ischemia in the presence of both glucose and butyrate, the glycolysis rate is stimulated approx. lOO-fold.31P-NMR; Glycolysis; Fatty acid; Iodoacetate; Glyceraldehyde-3-phosphate dehydrogenase

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Section: Resultssupporting

confidence: 83%

Section: Introductionmentioning

confidence: 99%

Inhibition of glucose phosphorylation by fatty acids in the perfused rat heart

1988

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“…Also Morgan, Henderson, Regen & Park (1961) (1967) found that material accumulated by uptake2 washed out very readily, though this finding may not be capable of strict application to the trachea in which there is some retention of isoprenaline (Foster, 1969).…”

Section: The Effect Of Substrate Concentration On Metabolism Of (-)-Fmentioning

confidence: 99%

Some evidence of the active uptake of noradrenaline in the guinea‐pig isolated trachea

Foster

O’Donnell

1972

British J Pharmacology

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Summary . Guinea‐pig isolated trachea immersed in a low concentration (50 nm) of (—)‐3H‐noradrenaline accumulates radioactive material against an apparent concentration gradient. . Compartmental analysis based on the decay curve of radioactive material content during washout and its comparison with that of 14C‐sorbitol shows that some extracellular noradrenaline is adsorbed. A considerable mass exists in a slowly exchanging compartment, i.e. is retained. This retention is inversely concentration dependent. . Over a 25‐fold range of concentration the entry of either total radioactive material or noradrenaline followed Michaelis‐Menten kinetics. . The uptake of radioactive material was sodium‐dependent and ouabainsensitive. . The uptake was susceptible to metabolic poisons which deprive the tissue of all available energy but it was not exclusively associated with either oxidative or glycolytic energy supply. . Although net uptake could not be distinguished from exchange with endogenous amine, other evidence has been obtained for an active noradrenaline transport system with properties similar to neuronal uptake.

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“…Hearts were excised rapidly, dropped into 0.9% NaCl (4°C), and mounted on a modified Langendorff perfusion apparatus. 18 For synthesis studies, preliminary perfusion was performed for 30 minutes with amino acid-rich "BGJ" solution (Grand Island Biological Co.) in Krebs-Henseleit buffer, containing 50 ;itg/ml bovine insulin (Sigma Chemical Co.), 15 nut glucose and 0.80 mM phenylalanine, and gassed with 95% O 2 + 5% CO 2 -The perfusion pressure was 65 mm Hg throughout the study, and beating rates were held constant at 350/min by atrial pacing. After the preliminary perfusion, the solution was changed to a similar one containing 0.80 mM [ 3 H]phenylalanine (1.3 X 10 6 dpm/ftmol).…”

Section: " 17mentioning

confidence: 99%

Synthesis and degradation of myocardial protein during the development and regression of thyroxine-induced cardiac hypertrophy in rats.

Sanford¹,

Griffin²,

Wildenthal³

1978

Circulation Research

111

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SUMMARY Cardiac hypertrophy was induced in rats by daily injections of L-thyroxine (1.0 mg/kg).Regression from hypertrophy was studied 4 days after discontinuing thyroxine. Isolated, Langendorffperfused hearts were perfused with Krebs-Henseleit buffer, glucose, insulin, and amino acids. To measure protein synthesis, left ventricular tissue was assayed for incorporation of tritiated phenylalanine into protein. Indices of rates of protein degradation were obtained by measuring the release of cold phenylalanine after blocking protein synthesis with cycloheximide. After 3 days of thyroxine (when cardiac growth was maximally increased), the rate of protein synthesis increased by 22% (P < 0.001). After 1 week, synthesis was 8% greater than control (P < 0.05), and by 2 weeks (when hypertrophy was stable and the rate of cardiac growth was similar to controls), synthesis had returned to control levels. In hearts regressing from hypertrophy, synthesis was reduced to 68% of control (P < 0.001). The rate of protein degradation was decreased by 12% ( P < 0.05) after 3 days of thyroxine, but was not different from control at 1 or 2 weeks. During regression, degradation was 12% below control (P < 0.05). Changes in the release of several amino acids that are synthesized or metabolized in heart (e.g., alanine, glycine, serine) were different from changes in phenylalanine release. In conclusion thyroxine-induced cardiac hypertrophy and regression are accompanied by changes in protein synthesis and degradation, and amino acid metabolism. The predominant change in hypertrophy is increased protein synthesis with a minor contribution from reduced degradation. Regression of hypertrophy is accompanied by decreased synthesis, not increased degradation.THEORETICALLY, cardiac hypertrophy may occur as a consequence of increased protein synthesis, reduced protein degradation, or both. Similarly, a decrease in heart size, as in regression of hypertrophy, might be brought about by accelerated protein degradation, a decreased rate of synthesis, or both.The relative importance of these factors is defined imprecisely. There is a general agreement that protein synthesis is accelerated during the development of hypertrophy, 1 " 5 but reports differ regarding whether rates of degradation are retarded 5 or not. 23 The type and magnitude of changes that occur may depend on the nature, intensity, and duration of the stress imposed on the heart, and on whether or not the hypertrophic process is accompanied by cellular damage and/or repair.To clarify the roles of altered synthesis and degradation of cardiac protein in one experimental model of hypertrophy and regression, we have measured their rates in vitro following induction and Received January 13, 1978; accepted for publication July 12, 1978. cessation of a well-defined stimulus to hypertrophy-daily injections of L-thyroxine in rats. The regimen employed produces rapid growth of the heart (over and above that observed in age-matched controls), predominantly involving myocardial cells and without...

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Regulation of glucose uptake by muscle. 3. The effects of insulin, anoxia, salicylate and 2:4-dinitrophenol on membrane transport and intracellular phosphorylation of glucose in the isolated rat heart

Cited by 244 publications

References 10 publications

Inhibition of glucose phosphorylation by fatty acids in the perfused rat heart

Inhibition of glucose phosphorylation by fatty acids in the perfused rat heart

Some evidence of the active uptake of noradrenaline in the guinea‐pig isolated trachea

Synthesis and degradation of myocardial protein during the development and regression of thyroxine-induced cardiac hypertrophy in rats.

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