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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activity of phosphorylase a was measured in isolated hepatocytes from fed lean and ob/ob mice after addition of vasopressin, angiotensin, phenylephrine and glucagon. The binding of these hormones to purified liver plasma membranes was also determined. In hepatocytes of ob/ob mice, no increase in phosphorylase a was measured after addition of vasopressin, whereas the other hormones promoted an increase in the activity of the enzyme. No specific vasopressin receptors could be measured on purified liver plasma membrane of ob/ob mice. A decrease in the number of receptors for angiotensin and glucagon, without modification of the affinity, was also observed. No restoration of the number of vasopressin receptors was observed in liver of ob/ob mice starved for 3 days or in younger (5-6 weeks) animals. Vasopressin receptors and vasopressin-stimulated adenylate cyclase, measured on purified kidney medulla membranes, were similar in both lean and ob/ob mice. The data indicate a selective lack of vasopressin receptors and metabolic response in liver of the ob/ob mouse.
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PMID:Lack of vasopressin receptors in liver, but not in kidney, of ob/ob mice. 631 39

Exposure of 32P-prelabelled isolated hepatocytes to vasopressin affected the phosphorylation of nine of the 26 phosphoproteins resolved by sodium dodecyl sulphate gel electrophoresis. Glucagon (2 nM) or cyclic AMP elicited significant changes in the phosphorylation of only four phosphoproteins. A very high concentration of glucagon (1000 nM) affected additional phosphoproteins. Insulin alone significantly increased the phosphorylation of a single protein. Vasopressin, A23187, glucagon and cyclic AMP all induced the dephosphorylation of a single phosphoprotein of mol. wt 20,000. The significance of these results with respect to the short-term control of hepatic metabolism is discussed.
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PMID:The short term hormonal control of cytoplasmic protein phosphorylation in hepatocytes from fed rats. 635 57

A detailed study of the control of liver pyruvate dehydrogenase activity by various hormones was carried out with perfused liver and isolated hepatocytes. Vasopressin produced a significant increase in the enzyme activity in fed rats, and the time course and sensitivity of the response was similar to that of glycogen phosphorylase a. The enzyme from starved animals was resistant to hormonal activation. The possible factors involved in the above effects are discussed. Angiotensin and phenylephrine also increased pyruvate dehydrogenase activity, and the magnitude of the response was of the same order as that to vasopressin by the liver enzyme. The effects of these hormones on pyruvate dehydrogenase activity were critically dependent on extracellular Ca2+, thus suggesting a role for this ion in the mechanism of action of the hormones. Insulin did not appear to have a role in the control of the enzyme activity, as shown by its lack of effect on the enzyme. Glucagon, in contrast with previous reports, produced a rapid, transient and significant increase in pyruvate dehydrogenase activity. The physiological importance of the above effects is discussed.
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PMID:Hormonal control of pyruvate dehydrogenase activity in rat liver. 639 71

Vasopressin, angiotensin and phenylephrine stimulate glycogenolysis in postnatal rat liver by a Ca2+-mediated mechanism not involving cyclic AMP. To determine whether these hormones promote glycogenolysis in foetal liver, we have examined their effects, and those of the Ca2+ ionophore A23187, on glycogen metabolism in cultured foetal-rat hepatocytes. Vasopressin and angiotensin (0.1 nM-0.1 microM) had no effects on either glycogen synthesis (as assessed by [14C]glucose incorporation into glycogen) or phosphorylase a activity. However, A23187 at 1 and 10 microM inhibited glycogen synthesis by 31.3 and 89.1% respectively (both P less than 0.001) and stimulated phosphorylase a activity by 66.9 and 184.1% respectively (both P less than 0.01). Incubation of cells in Ca2+-deficient medium attenuated the effects of 10 microM-A23187 on glycogen synthesis and abolished the effects of 1 microM-A23187. As in postnatal liver, glucagon (1 and 20 nM) and isoprenaline (1 and 10 microM), which activate adenylate cyclase, inhibited glycogen synthesis and stimulated phosphorylase a activity in foetal hepatocytes. The minimal effective concentration of phenylephrine was 10 times that of isoprenaline. These results indicate striking differences in the ontogeny of cyclic AMP-mediated and Ca2+-mediated processes which regulate hepatic glycogenolysis. Since increases in cytosolic Ca2+ induce glycogenolysis in foetal-rat liver, the weak or absent responses to vasopressin, angiotensin and the alpha-adrenergic agonists may result from defects in hormone-receptor binding or in post-receptor events leading to the mobilization of intracellular Ca2+ stores.
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PMID:Glycogenolytic effects of the calcium ionophore A23187, but not of vasopressin or angiotensin, in foetal-rat hepatocytes. 643 Feb 82

The effects of (1-desamino-8-D-arginine) vasopressin (dDAVP) on water and electrolyte transport in the distal tubule were investigated by micropuncture. Since, in addition to antidiuretic hormone, parathyroid hormone, calcitonin and glucagon stimulate the adenylate-cyclase system in this nephron segment, experiments were performed on hormone-deprived rats, i.e. homozygous DI Brattleboro rats with reduced levels of endogenous parathyroid hormone, calcitonin and glucagon. Along the distal tubule, dDAVP enhanced water, Cl, Na and Ca reabsorption and sharply increased net K secretion. Phosphate transport was left unchanged and Mg reabsorption was not significantly altered by dDAVP between the early and late distal tubule. Antidiuretic hormone also slightly increased water filtration rate in the superficial nephron, which rose in proportion to whole kidney glomerular filtration rate. It is concluded that, in rats: antidiuretic hormone stimulates water, NaCl and Ca absorption and enhances K secretion along the distal tubule and the tubular effects of dDAVP on electrolyte transport in the loop and distal tubule are responsible for decreasing Mg and Ca urinary excretion.
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PMID:Effects of antidiuretic hormone on electrolyte reabsorption and secretion in distal tubules of rat kidney. 647 69

Vasopressin induced a transient increase of 50% in the total concentration of diacylglycerols (determined by g.l.c.) in isolated hepatocytes. The increase was maximal at 0.25 min, and the concentration of diacylglycerols in cells treated with vasopressin had returned to the basal value by 4 min. No change in the concentration of diacylglycerols was observed after the treatment of cells with glucagon. The dependency of this effect on the concentration of vasopressin was similar to that of the effect of the hormone on 45Ca2+ efflux measured at 0.1 mM extracellular Ca2+. Vasopressin increased the proportion of arachidonic acid and stearic acid and decreased the proportion of oleic acid present in the diacylglycerols. In hepatocytes prelabelled with [14C]arachidonic acid, vasopressin increased the amount of [14C]diacylglycerol. The effects of vasopressin on the total concentration of diacylglycerols and [14C]diacylglycerol were mimicked by an exogenous phospholipid phosphodiesterase (phospholipase C) from Clostridium perfringens. The results are consistent with the conclusion that the transient increase in diacylglycerols induced by vasopressin is caused by the rapid hydrolysis of both the phosphoinositides and one or more other phospholipids.
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PMID:A transient increase in diacylglycerols is associated with the action of vasopressin on hepatocytes. 647 30

The hormonal regulation of L-type pyruvate kinase in hepatocytes from phosphorylase b kinase-deficient (gsd/gsd) rats was investigated. Adrenaline (10 microM) and glucagon (10 nM) each led to an inactivation and phosphorylation of pyruvate kinase. Dose-response curves for adrenaline-mediated inactivation of pyruvate kinase, phosphorylation of pyruvate kinase and the stimulation of gluconeogenesis from 1.8 mM-lactate were similar for hepatocytes from control and gsd/gsd rats. Time-course studies indicated that adrenaline-mediated inactivation and phosphorylation of pyruvate kinase proceeded more slowly in phosphorylase kinase-deficient hepatocytes than in control hepatocytes. The age-dependent change in the adrenergic control of pyruvate kinase was similar between control and phosphorylase kinase-deficient hepatocytes. Adrenaline, glucagon and noradrenaline activated the cyclic AMP-dependent protein kinase and inhibited pyruvate kinase in phosphorylase kinase-deficient hepatocytes. Vasopressin (0.2-2 nM), angiotensin (10nM) and A23187 (10 microM) had no effect on the activity ratio of the cyclic AMP-dependent protein kinase or pyruvate kinase in these cells. It is concluded that phosphorylase kinase plays no significant role in the hormonal control of pyruvate kinase and that phosphorylation and inactivation of this enzyme results predominantly from the action of the cyclic AMP-dependent protein kinase.
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PMID:Hormonal regulation of L-type pyruvate kinase in hepatocytes from phosphorylase kinase-deficient (gsd/gsd) rats. 652 78

The effects of the peptide hormones glucagon, vasoactive intestinal peptide, and vasopressin on the microcirculation of single jejunal villi were studied in anesthetized rats. By means of a recently developed in vivo video-microscopy technique, the red blood cell velocity (pretreatment value: 2.1 +/- 0.1 mm X s-1) and the diameter of the red blood cell column (5.5 +/- 0.2 micron) were measured in the villous arcade vessels. From these parameters, an index of blood flow was calculated in order to determine changes in response to intravenous infusions of the peptides. During the infusions of glucagon and vasopressin, simultaneous measurements were made of superior mesenteric artery blood flow and villous arcade flow. Glucagon (1 microgram X kg-1 X min-1) increased villous arcade flow markedly to 150.1 +/- 13.7% of control, while superior mesenteric artery flow remained unchanged. Vasoactive intestinal peptide (1 microgram X kg-1 X min-1) produced a dilation of the arcade vessel with a commensurate reduction of red cell velocity, leaving the flow index unaltered. Vasopressin (14.3 mU X kg-1 X min-1) was found to be a potent vasoconstrictor at the mucosal level, and since red cell velocity also decreased, villous flow was reduced substantially, paralleling a reduction of superior mesenteric artery flow. After the vasopressin infusion, a reactive hyperemia occurred in the villous arcades. No such increase in blood flow was observed in the superior mesenteric artery. From these findings, we conclude that the villous microvasculature is influenced by various hormones and, therefore, must occupy a prominent position in control of the circulation of the small intestine.
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PMID:Effects of glucagon, vasoactive intestinal peptide, and vasopressin on villous microcirculation and superior mesenteric artery blood flow of the rat. 661 98

Vasopressin, phenylephrine, and A23187 cause an accumulation of fructose 2,6-bisphosphate in hepatocytes from fed rats, but not in Ca2+-depleted hepatocytes from fed rats or in phosphorylase kinase-deficient hepatocytes from (gsd/gsd) rats. The effect of vasopressin and phenylephrine is not found in hepatocytes from overnight-starved rats. Thus, the accumulation of fructose 2,6-bisphosphate by these agents may depend on the stimulation of glycogenolysis and on the resulting accumulation of hexose 6-phosphate. In support of this hypothesis, conditions are described for the enzymatic synthesis of fructose 2,6-bisphosphate from fructose 6-phosphate and Mg-ATP in liver extracts. Half-maximal activity (0.8 nmol/min.g) is obtained with about 60 microM fructose 6-phosphate, and the activity can be separated fom phosphofructokinase by ammonium sulfate fractionation. Treatment of rats or isolated hepatocytes with glucagon results in a 4-5-fold decrease in the maximal activity of this enzyme.
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PMID:Fructose 2,6-bisphosphate. Hormonal regulation and mechanism of its formation in liver. 679 May 47

Intravenously administered oxytocin was found to increase plasma insulin and glucagon levels. To explore if the same effects could be obtained by nonparenteral routes of administration, oxytocin was given by nasal instillation in normal conscious dogs. Plasma glucose, insulin, and glucagon levels all increased to levels which previously were shown to cause increased glucose production and utilization. Vasopressin infusion had no effect on these measurements. This is the first report of the effectiveness of oxytocin to evoke insulin and glucagon secretion by the nasal route of administration.
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PMID:Intranasal instillation of oxytocin increases insulin and glucagon secretion. 703 64


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