Effect of Glucagon on Gluconeogenesis by the Isolated Perfused Rat Liver

Sokal, Joseph E.; Schiller, Carol M.; Dobbins, Ann

doi:10.1210/endo-78-3-538

Cited by 48 publications

(11 citation statements)

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“…Urea production rates could not be determined accurately over so short a time period. However, previous studies in this laboratory 15 showed that the stimulation of urea production induced by glucagon persists for at least one hour after addition of this hormone. Thus, despite the fact that glucagon concentrations were probably very low during the final thirty minutes of the experimental period, it seemed reasonable to evaluate effects on urea production over this time period.…”

Section: Experimental Designmentioning

confidence: 81%

Antagonism Between the Effects of Insulin and Glucagon on the Isolated Liver

1969

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Antagonism was demonstrated between the effects of insulin and glucagon, added simultaneously to the perfusing blood, on phosphorylase activity, glucose output and urea production of the isolated rat liver. However, the degree of antagonism varied greatly, according to the action under study, and there appeared to be a clear-cut hierarchy in the effects of each hormone. For glucagon, this was (stimulation of): (1) phosphorylase activity, (2) glycogenolysis and glucose release, (3) urea production. For insulin, it was (inhibition of): (1) urea production, (2) glycogenolysis, (3) phosphorylase activation. Thus, high concentrations of insulin completely failed to inhibit the phosphorylase activation induced by 1.4 m/jg./ml. of glucagon, while modest concentrations of insulin totally suppressed the stimulation of urea production induced by sustained glucagon concentrations at least ten times greater, and well above the biologic range. Our findings argue against a single common primary site of action of these two hormones. DIABETES iS: 724-32, November, 1969.

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Section: Experimental Designmentioning

confidence: 81%

Antagonism Between the Effects of Insulin and Glucagon on the Isolated Liver

1969

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“…A direct protein catabolic effect of glucagon is well-documented [7, 18--20,221. At least part of the carbon arising from endogenous liver protein can be accounted for by increased glucose formation which is observed in the absence of gluconeogenic substrate following glucagon addition [6,9,18,19,20]. That glucagon has an additional catabolic effect on liver fat metabolism is supported by several lines of evidence.…”

Section: Effects Of Insulin and Buado-3' :5'-p On Endogenous Liver Mmentioning

confidence: 96%

“…Evidence for a direct effect of glucagon on endogenous liver constituents can be found in work from various laboratories . I n particular, an accelerated breakdown of endogenous liver protein, as indicated by an increased urea production is observed following glucagon addition to perfusion [7,[18][19][20]22,23].…”

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confidence: 99%

Interactions of Glucagon and Insulin on the Metabolism of Perfused Livers from Fasted Rats

Menahan

Wieland²

1969

European Journal of Biochemistry

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Glucagon (28 nM) stimulated gluconeogenesis, urea production and ketogenesis in perfused livers from fasted rats. Since the livers were perfused without added substrate, liver protein is the source of carbon of the glucose synthesis. Addition of N6, O2′‐dibutyryl cyclic adenosine 3′:5′‐monophosphate in concentrations of 100 and 10 μM to the perfusion medium resulted in a response similar to that of glucagon. It is suggested that cyclic adenosine 3′:5′‐monophosphate is the mediator of glucagon action in liver. Preperfusion of the isolated livers with insulin diminished the glucagon effects. The glucagon‐stimulation of glucose and urea production was completely suppressed, while the increased ketogenesis was inhibited by 60% in the presence of insulin. Since all three glucagon responses were inhibited, this supports the concept that insulin lowers, in some way, the elevation of cyclic adenosine 3′:5′‐phosphate which occurs following glucagon administration. That insulin does not exert its effect subsequent to cyclic adenosine 3′:5′‐phosphate is suggested by the observation that insulin, under the same conditions which inhibited the response of liver to glucagon, had little or no effect on the increases in gluconeogenesis, ureogenesis, and ketogenesis following, dibutyryl cyclic adenosine‐3′:5′‐phosphate. Since an effect of insulin on cyclic adenosine 3′:5′‐phosphate phosphodiesterase seems unlikely, it is suggested that the inhibition of glucagon responses by insulin is the result of an interaction at the adenyl cyclase or one of the step(s) between binding of the hormone and the enzyme.

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“…Once in circulation it exerts its endocrine effects on the liver through activation of the glucagon receptor (GCGR), a G protein-coupled receptor (GPCR), and engagement of the Gα s and β-arrestin pathways. Glucagon ultimately stimulates an increase in the export of glucose from the liver-the result of enhanced glycogenolysis and gluconeogenesis [9][10][11][12].…”

Section: Glucagon: Hormonal Mediator Of Hepatic Metabolismmentioning

confidence: 99%

“…Early studies defined the primary physiological actions of glucagon as acute increases in both glycogenolysis and gluconeogenesis, occurring in the time frame of seconds to minutes [9][10][11][12], but a deep understanding of the metabolic phenomena awaited a pioneering set of work performed at Vanderbilt University by Exton and Park [15][16][17]. This work, published in a series of papers in the Journal of Biological Chemistry, used enzymatic methods to quantify intracellular metabolites in livers perfused with increasing concentrations of lactate and pyruvate.…”

Section: Glucagon: Hormonal Mediator Of Hepatic Metabolismmentioning

confidence: 99%

Glucagon: acute actions on hepatic metabolism

Miller

Birnbaum

2016

Diabetologia

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Type 2 diabetes mellitus is the result of impaired systemic control of glucose homeostasis, in part through the dysregulation of the hormone glucagon. Glucagon acts on the liver to increase glucose production through alterations in hepatic metabolism, and reducing the elevated glucagon signalling in diabetic patients is an attractive strategy for the treatment of hyperglycaemia. Here we review the actions of the hormone in the liver, focusing on the acute alterations of metabolic pathways. This review summarises

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Effect of Glucagon on Gluconeogenesis by the Isolated Perfused Rat Liver

Cited by 48 publications

References 0 publications

Antagonism Between the Effects of Insulin and Glucagon on the Isolated Liver

Antagonism Between the Effects of Insulin and Glucagon on the Isolated Liver

Interactions of Glucagon and Insulin on the Metabolism of Perfused Livers from Fasted Rats

Glucagon: acute actions on hepatic metabolism

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