Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reliable and specific radioimmunoassays have been developed for the gut hormones secretin, gastrin, cholecystokinin, pancreatic glucagon, VIP, GIP, motilin, and enteroglucagon. Using these assays, the relative pattern of distribution of the gut hormones has been determined using the same bowel extracts for all measurements. VIP occurred in high concentration in all regions of the bowel, whereas secretin, GIP, motilin, and CCK were predominantly localised in the proximal small intestine. Pancreatic glucagon was almost exclusively confined to the pancreas. Like VIP, enteroglucagon also exhibited a wide pattern of distribution but was maximal in the ileum. The acid ethanol extraction method that was used was found to be unsuitable for gastrin. On gel chromatography of the extracts, motilin and VIP eluted as single molecular species in identical position to the pure porcine peptides. CCK, pancreatic glucagon, enteroglucagon and GIP were all multiform.
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PMID:Distribution of the gut hormones in the primate intestinal tract. 11 57

A radioreceptor-assay for glucagon was developed employing pig liver plasma membranes isolated by means of an aqueous two-phase polymer system. The assay is simple, precise, and has a detection limit of 40 pg/ml. Acid-ethanol extracts of porcine intestinal mucosa and entero-glucagon purified by affinity chromatography interfered strongly with the binding of 125I-labelled glucagon. The affinity of enteroglucagon for the membranes was lower than that of glucagon, but even physiological concentrations of the former interfere with glucagon binding, indicating that enteroglucagon may compete with pancreatic glucagon for binding to the hepatocyte under physiological conditions.
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PMID:A radioreceptor-assay for glucagon: binding of enteroglucagon to liver plasma membranes. 16 10

Fasting cats anesthetized with chloralose were used for the experiments. DBcAMP infused at a rate of 340 nmol/kg/min increased the gastrointestinal and intrahepatic portal conductances whereas the hepatic arterial conductance was decreased. The hemodynamic responses to portal and systemic venous administration of DBcAMP were identical. In half of the experiments DBcAMP increased the splanchnic ethanol elimination rate and oxygen consumption and in all experiments there was a decrease in the plasma clearance and extraction ratio of Indocyanine Green. No change in bile flow was observed. DBcAMP infused at a rate of 85 nmol/kg/min was without significant effects on either splanchnic hemodynamics or liver metabolism. DBcAMP infused at a rate of 850 nmol/kg/min accentuated the decrease in hepatic arterial conductanc- but was found to decrease the splanchnic ethanol elimination rate and oxygen cownsumption. Infusion of cAMP, AMP and adenosine at a rate of 340 nmol/kg/min were without measurable effects. Based on these results it is concluded that like the metabolic effects also the vascular effects of glucagon are caused by stimulation of specific glucagon receptors which results in an intracellular release of cAMP.
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PMID:Imitation of glucagon effects on splanchnic hemodynamics and liver function by N6,2'-O-dibutyryl 3',5'-cyclic AMP (DBcAMP) in cats. 17 Jul 94

The hormonal control of [14C]glucose synthesis from [U-14C-A1dihydroxyacetone was studied in hepatocytes from fed and starved rats. In cells from fed rats, glucagon lowered the concentration of substrate giving half-half-maximal rates of incorporation while it had little or no effect on the maximal rate. Inhibitors of gluconeogenesis from pyruvate had no effect on the ability of the hormone to stimulate the synthesis of [14C]glucose from dihydroxyacetone. The concentrations of glucagon and epinephrine giving half-maximal stimulation from dihydroxacetone were 0.3 to 0.4 mM and 0.3 to 0.5 muM, respectively. The meaximal catecholamine stimulation was much less than the maximal stimulation by glucagon and was mediated largely by the alpha receptor. Insulin had no effect on the basal rate of [14C]clucose synthesis but inhibited the effect of submaximal concentration of glucagon or of any concentration of catecholamine. Glucagon had no effect on the uptake of dihydroxyacetone but suppressed its conversion to lactate and pyruvate. This suppression accounted for most of the increase in glucose synthesis. In cells from gasted rats, where lactate production is greatly reduced and the rate of glucose synthesis is elevated, glucagon did not stimulate gluconeogenesis from dihydroxyacetone. Findings with glycerol as substrate were similar to those with dihyroxyacetone. Ethanol also stimulated glucose production from dihydroxyacetone while reducing proportionately the production of lactate. Ethanol is known to generate reducing equivalents fro clyceraldehyde-3-phosphate dehydrogenase and presumably thereby inhibits carbon flux to lactate at this site. Its effect was additive with that of glucagon. Estimates of the steady state levels of intermediary metabolites and flux rates suggested that glucagon activated conversion of fructose diphosphate to fructose 6-phosphate and suppressed conversion of phosphoenolpyruvate to pyruvate. More direct evidence for an inhibition of pyruvate kinase was the observation that brief exposure of cells to glucagon caused up to 70% inhibition of the enzyme activity in homogenates of these cells. The inhibition was not seen when the enzyme was assayed with 20 muM fructose diphosphate. The effect of glucagon to lower fructose diphosphate levels in intact cells may promote the inhibition of pyruvate kinase. The inhibition of pyruvate kinase may reduce recycling in the pathway of gluconeogenesis from major physiological substrates and probably accounts fromsome but not all the stimulatory effect of glucagon.
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PMID:Hormonal control of [14C]glucose synthesis from [U-14C]dihydroxyacetone and glycerol in isolated rat hepatocytes. 18 97

The effect of a single large dose of ethanol (5 mg/kg body weight) on plasma glucagon (IRG) and insulin (IRI) concentrations was studied in rats fasting for 24 hr. Hepatic cAMP concentration and blood glucose were also estimated and correlated with hormonal changes. Plasma IRG concentrations had doubled by the first sampling time (2 hr) and remained at this level up to 16 hr after ethanol administration. Plasma IRI concentrations were not affected by ethanol. Hepatic cAMP concentrations reflected changes in the plasma insulin/glucagon ratio, which seems to be the major determining factor for hepatic cAMP even during ethanol oxidation. Hypoglycemia was not found in the ethanol group during the experimental period of 24 hr, and it was therefore concluded that ethanol may stimulate glucagon secretion in rats even without concurrent hypoglycemia. Possible mechanisms for the action of ethanol on the endocrine pancrease are discussed.
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PMID:Effect of acute ethanol load on plasma immunoreactive insulin and glucagon. 20 41

The effect of glucagon, dibutyrylic cyclic AMP and theophylline on bile production and liver metabolism was studied in fasting, chloralose anesthetized cats. After 45 min infusion of glucagon (0.1 mug/kg/min) total bile flow started to increase and finally reached a level 32% above control bile flow. The rise in flow was accompanied by a parallel increase in the biliary clearance of erythritol and the rate of biliary excretion of inorganic ions, whereas the bile acid excretion remained constant. Glucagon therefore appears to stimulate selectively the bile acid-independent canalicular production of bile. In contrast to the delayed action on bile production, glucagon caused an immediate change in liver metabolism as judged from the elimination rate of ethanol and the rise in plasma glucose concentration. Dibutyrylic cyclic AMP or theorphylline also caused similar immediate changes in liver metabolism but neither substance influenced bile production or the biliary excretion of electrolytes or bile acids. It thus appears that glucagon choleresis in the cat is either independent of cAMP release or that an increase in intracellular cAMP is not in itself sufficient to influence bile secretion. The results also seem to exclude that an increase in insulin production induced by hyperglycemia, or hemodynamic changes in the liver, can explain glucagon choleresis.
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PMID:The effect of glucagon, dibutyrylic cyclic AMP and theophylline on bile production in the cat. 22 77

The regulation of ornithine decarboxylase activity was studied in freshly isolated rat hepatocytes incubated in a chemically defined medium for 5 h. Glucagon, dibutyryl cyclic AMP, insulin and dexamethasone produced dramatic increases in ornithine decarboxylase activity, 6--100-times the basal activity. Actinomycin D inhibited completely the stimulatory action of these substances. With glucagon, dibutyryl cyclic AMP and insulin, the rise in ornithine decarboxylase activity was rapid but transient, peaking at 200 min and then declining rapidly. By contrast, the response to dexamethasone was gradual and sustained in the 5 h incubation. The transient nature of the response to glucagon was unaltered by repeated additions of optimally effective doses of glucagon suggesting the development of 'refractoriness' to the actions of this hormone. Ethanol oxidation inhibited by 50% the stimulation of ornithine decarboxylase by glucagon and dexamethasone and this effect was blocked by 4-methylpyrazole, an inhibitor of alcohol dehydrogenase. Acetate (2.5--20 mM), the metabolic product of hepatic ethanol oxidation, was also effective. The data indicate that glucagon, insulin and glucocorticoids are all effective in stimulating the activity of ornithine decarboxylase in isolated hepatocytes but they differ in their duration and time of peak of action. Additionally, the inhibitory effect of ethanol on the hormonal stimulation of ornithine decarboxylase is dependent on its oxidation and may be mediated by acetate.
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PMID:Hormonal control of ornithine decarboxylase in isolated liver cells and the effect of ethanol oxidation. 22 51

Prior studies indicated that acute ethanol feeding induced a decrease in adrenergic sensitivity as measured by the plasma cAMP response to isoproterenol. In this report we show that two hours after acute ethanol ingestion the plasma cyclic AMP levels were increased 8.5 fold 6 minutes after glucagon injection. Saline controls showed a 35 fold increase in plasma cAMP levels after glucagon injection. It is suggested that the decreased response caused by ethanol may be due to a decrease in the sensitivity of glucagon receptors.
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PMID:Effect of alcohol on the plasma cAMP response to glucagon. 22 31

Seven patients with clinical alcoholic hypoglycemia showed suppressed pretreatment plasma insulin levels and raised concentrations of somatotropin, hydrocortisone and pancreatic glucagon. A prolonged intravenous glucose infusion failed to elicit adequate insulin output and marked hyperglycemia supervened.
J Stud Alcohol 1975 May
PMID:Hormonal responses in ethanol-induced hypoglycemia. 23 77

1. A method for the preparation of hepatocytes from livers of 11-15-day old rats is described. These cells in general behave similarly to hepatocytes made from adult rats with respect to stimulation of gluconeogenesis by glucagon and adrenaline and the effects of added oleate. 2. Significant differences in the behaviour of hepatocytes from neonatal and adult rats were nevertheless seen in certain situations, e.g. with alanine as gluconeogenic substrate, and appeared to be related to the redox state of the cells. 3. The importance of redox state upon gluconeogenesis was examined in more detail by determining the effects of oleate, ethanol and DL-3-hydroxybutyrate alone and in combinations. Major differences between neonatal and adult hepatocytes were again observed with alanine as substrate. 4. A discussion concludes that, while some relevant differences in the enzyme complements of neonatal and adult rat livers are known, it is the high capacity of the neonatal liver to generate reducing power by oxidation of fatty acid that can explain the observed differences.
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PMID:A comparison of gluconeogenesis in hepatocytes from neonatal and adult rats. 31 86


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