Nachweis des direkten Antagonismus zwischen Glucagon und Insulin in der Glykolysekette

Schimassek, H.; Mitzkat, H. J.

doi:10.1007/bf00261116

Cited by 5 publications

(12 citation statements)

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“…As shown in Table 2, glucagon (a gift of Dr Otto K. Behrens, Eli Lilly and Co., Indianapolis, Ind., U.S.A.), when added to the perfusion medium at 38min., greatly increased the rate of glucose formation from lactate, as has already been reported by Schimassek & Mitzkat (1963), Struck, Ashmore & Wieland (1965) and . There was also an effect with pyruvate, the absolute increase being 0.80,umole/g./min.…”

Section: Methodssupporting

confidence: 69%

“…it was one-ninth of the maximal value. Similar observations have been recorded by Schimassek (1963). The causes of the initial rise in the concentration of oc-glycerophosphate remain to be explored; it could not be correlated to the lactate/pyruvate ratio.…”

Section: Methodssupporting

confidence: 64%

“…One effect is concerned with glycogenolysis; it causes a conversion of liver glycogen into glucose and a depletion of the glycogen store of the liver (see Foa, 1964). The other, first observed by Schimassek & Mitzkat (1963), is concerned with the promotion of gluconeogenesis from lactate and pyruvate. The question arises whether these two effects have a common denominator.…”

Section: Discussionmentioning

confidence: 99%

“…In the experiments of Krebs & Bellamy (1960, Primary 8ite8 of action of glucagon. Recent work on the action of glucagon in the perfused liver (Schimassek & Mitzkat, 1963;Struck, Ashmore & Wieland, 1965;Sokal, 1966) indicates that glucagon may affect carbohydrate metabolism at two different sites of the metabolic chain. One effect is concerned with glycogenolysis; it causes a conversion of liver glycogen into glucose and a depletion of the glycogen store of the liver (see Foa, 1964).…”

Section: Discussionmentioning

confidence: 99%

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The rate of gluconeogenesis from various precursors in the perfused rat liver

Ross

Hems

Krebs

1967

Biochemical Journal

391

139

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1. The rates of gluconeogenesis from many precursors have been measured in the perfused rat liver and, for comparison, in rat liver slices. All livers were from rats starved for 48hr. Under optimum conditions the rates in perfused liver were three to five times those found under optimum conditions in slices. 2. Rapid gluconeogenesis (rates of above 0-5,.umole/g./min.) were found with lactate, pyruvate, alanine, serine, proline, fructose, dihydroxyacetone, sorbitol, xylitol. Unexpectedly other amino acids, notably glutamate and aspartate, and the intermediates of the tricarboxylic acid cycle (with the exception of oxaloacetate), reacted very slowly and were not readily removed from the perfusion medium, presumably because of permeability barriers which prevent the passage of highly charged negative ions. Glutamine and asparagine formed glucose more readily than the corresponding amino acids. 3. Glucagon increased the rate of gluconeogenesis from lactate and pyruvate but not from any other precursor tested. This occurred when the liver was virtually completely depleted ofglycogen. Two sites of action of glucagon must therefore be postulated: one concerned with mobilization of liver glycogen, the other with the promotion of gluconeogenesis. Sliced liver did not respond to glucagon. 4. Pyruvate and oxaloacetate formed substantial quantities of lactate on perfusion, which indicates that the reducing power provided in the cytoplasm was in excess of the needs of gluconeogenesis. 5. Values for the content of intermediary metabolites of gluconeogenesis in the perfused liver are reported. The values for most intermediates rose on addition of lactate. 6. The rates of gluconeogenesis from lactate and pyruvate were not affected by wide variations of the lactate/pyruvate ratio in the perfusion medium.

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Section: Methodssupporting

confidence: 69%

Section: Methodssupporting

confidence: 64%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

The rate of gluconeogenesis from various precursors in the perfused rat liver

Ross

Hems

Krebs

1967

Biochemical Journal

391

139

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“…The identification of a glucagon-mediated site of regulation of hepatic gluconeogenesis between triose phosphate and glucose (1) supports earlier speculation from this laboratory (2)(3)(4) and others (5)(6)(7)(8)(9) that a control site occurs in this region. In addition, the identification of a control site at phosphofructokinase-fructose diphosphatase may explain observations by Haugaard and Haugaard (10), repeated and confirmed recently by Tepperman and Tepperman (11), that glucagon specifically acts to inhibit incorporation of carbon from glucose, but not fructose, into fatty acids in rat liver slices.…”

supporting

confidence: 78%

Glucose Inhibition of Epinephrine Stimulation of Hepatic Gluconeogenesis by Blockade of the α-Receptor Function

Kneer

Bosch

Clark

et al. 1974

Proc. Natl. Acad. Sci. U.S.A.

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For isolated rat hepatocytes, glucagon, The presence in liver of both phosphofructokinase (EC 2.7.1.11) and fructose diphosphatase (EC 3.1.3.11) provides for the possibility of a substrate cycle and the apparent futile hydrolysis of ATP. Until recently, it was considered that the reactions of glycolysis and gluconeogenesis were mutually exclusive and that minimal flux occurred through phosphofructokinase during periods of gluconeogenesis in liver. In recent studies in this laboratory significant rates of flux through phosphofructokinase were observed concomitant with gluconeogenesis (1) and these rates were directly proportional to the extracellular glucose concentration. Thus, at physiologically normal glucose concentrations (i.e., 5.5 mM), the rate of flux through phosphofructokinase varied from 4 to 36% of the flux rate through fructose diphosphatase, depending upon the nature and concentration of the gluconeogenic substrate.Furthermore, it was found that glucagon and cAMP stimulate glucose formation from galactose, dihydroxyacetone, xylitol, and fructose by influencing the rate of reactions involving fructose 6-phosphate (1). Both agents were found to inhibit flux through phosphofructokinase and simultaneously to enhance flux through fructose diphosphatase.The identification of a glucagon-mediated site of regulation of hepatic gluconeogenesis between triose phosphate and glucose (1) supports earlier speculation from this laboratory (2-4) and others (5-9) that a control site occurs in this region. In addition, the identification of a control site at phosphofructokinase-fructose diphosphatase may explain observations by Haugaard and Haugaard (10), repeated and confirmed recently by Tepperman and Tepperman (11), that glucagon specifically acts to inhibit incorporation of carbon from glucose, but not fructose, into fatty acids in rat liver slices.In the present work further regulatory control at the phosphofructokinase-fructose diphosphatase site is examined.Both epinephrine and cGMP are effective stimulants of gluconeogenesis and appear to act in a manner similar to that previously described for glucagon and cAMIP (1

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The Role of Futile Cycles in the Regulation of Carbohydrate Metabolism in the Liver

Hue¹

1981

Advances in Enzymology - And Related Areas of Molecular Biology

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Nachweis des direkten Antagonismus zwischen Glucagon und Insulin in der Glykolysekette

Cited by 5 publications

References 0 publications

The rate of gluconeogenesis from various precursors in the perfused rat liver

The rate of gluconeogenesis from various precursors in the perfused rat liver

Glucose Inhibition of Epinephrine Stimulation of Hepatic Gluconeogenesis by Blockade of the α-Receptor Function

The Role of Futile Cycles in the Regulation of Carbohydrate Metabolism in the Liver

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