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)

The concentrations of insulin and glucagon were measured in the portal and hepatic vein, the abdominal aorta and caval vein in the rat during a normal 24-h feeding cycle. Portal insulin levels showed little diurnal variation while hepatovenous and peripheral values were clearly increased during the eating phase. Conversely, portal glucagon levels were maximal during the fasting period while hepatovenous and peripheral concentrations showed little diurnal variation. The removal of insulin and glucagon by the liver was not constant, but independently regulated. During meals the liver increased the high portal insulin/glucagon ratio further to an even higher peripheral ratio favouring glucose utilization, e.g. by muscle and adipose tissue. During a short fast the liver decreased the low portal insulin/glucagon ratio further to an even lower peripheral ratio leading to glucose saving, e.g. by muscle and adipose tissue in favour of the brain and erythrocytes. The results indicate that the liver has an important role in the regulation of peripheral insulin/glucagon levels.
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PMID:Regulation of peripheral insulin/glucagon levels by rat liver. 637 34

Effects of electrical stimulation to the posterior (P-S) and celiac (C-S) branches of the abdominal vagus on the secretion of pancreatic glucagon (GI), insulin (IRI), gastrin (IRG) and secretion (IRS) were studied in anesthetized mongrel dogs. Following P-S and C-S, plasma concentration of GI and IRI increased without any changes of blood flow in the cranial pancreaticoduodenal vein. The similar responses shown in their magnitudes and timing would indicate that the output of the hormones were accelerated by both branches to the same extent and subsequently the effect of the posterior branch was caused via the celiac one. Plasma concentration of GI and IRI in the portal vein increased was elevated following P-S, but remained unchanged following C-S. these data would account for that an increase in portal blood flow exceeded relatively that of the output of the hormones following C-S. Portal plasma concentration of IRG increased following P-S and this would be due to the accelerated production of antral gastrin via the posterior antral branches. No response shown following C-S would reveal that an increase of portal blood flow exceeded over the production of extragastric gastrin via the celiac branch. Portal plasma concentration of IRS remained unchanged following P-S, but decreased following C-S. However, as these results were strongly influenced by changes of portal blood flow, the effect of both branches on pancreatic secretion needed further investigation with blood flow measurement.
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PMID:[An experimental study of the effect of the posterior and celiac branches on the secretion of pancreatic glucagon, insulin, gastrin and secretin]. 638 87

To clarify the impact of hypothermia on the hormonal control of glucose metabolism, rats were rendered hypothermic (25 C) after catheterization of the portal vein. Glucose, insulin, glucagon, and catecholamine concentrations were serially monitored, and the regional blood flows were measured, allowing the estimation of hormone outputs. Hypothermia reduced the portal blood flow by 50% without changing arterial blood pressure, blood gases, or pH. Portal plasma insulin secretion dropped (0.05 +/- 0.01 vs. 0.23 +/- 0.04 mU/min), and glucagon secretion increased (0.81 +/- 0.18 vs. 0.38 +/- 0.10 ng/min). The B cell responses to glucose, arginine, and glucagon were abolished, while the A cell response to arginine was not significantly affected. Glucose intolerance was apparent after iv glucose or arginine loads. Haloperidol and to a lesser extent phentolamine suppressed the cold-induced glucagon rise. Phentolamine and to a lesser extent haloperidol alleviated the cold-induced suppression of insulin release. Propranolol, naloxone, and atropine were relatively inactive. The cold-induced glucose intolerance was not corrected by phentolamine treatment. A marked resistance to iv insulin was apparent in these rats, which is in contrast to a normal sensitivity to iv glucagon.
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PMID:Glucagon and insulin secretion and their biological activities in hypothermic rats. 643 6

Pancreas isotransplantation was performed on streptozotocin-diabetic Wistar rats. To study the influence of the graft on diabetic hyperglucagonemia, immunoreactive glucagon (IRG) and its response to alanine (peak IRG) were determined in peripheral blood at intervals for up to 8 months after the transplantation. Concentrations of IRG and immunoreactive insulin (IRI) in effluent blood from host pancreas (portal vein) and graft (caval vein) were measured 4 months after the transplantation to estimate the hormone release from both organs. Following transplantation, caval IRI increased sixfold. Portal IRI increased 180% and reached 65% of the concentration observed in control rats. Peripheral basal and peak IRG were initially restored to normal, but were later increased to levels equal to those of diabetic rats. Also portal and caval IRG concentrations were similar in recipients and diabetic rats. The results show that relatively small amounts of glucagon are released from the graft, and that the exaggerated glucagon release from the host pancreas is only transiently normalized following pancreas transplantation.
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PMID:Long-term effect of pancreas transplantation on diabetic hyperglucagonemia. 674 10

To compare the effect of parenteral with enteral nutrition on gastroentero-pancreatic hormones, hypercaloric and hypocaloric nutrient preparations, commonly used clinically, were administered to rats either through cannulae in the jugular vein or gastrostomies. Control rats were fed orally ad libitum. Portal and aortic plasma was collected for radioimmunoassay with antibodies to C-terminal regions of gastrin and glucagon and to N-terminal-to-central regions of glucagon and VIP. Levels of all immunoreactivities were significantly lower in aortic than portal plasma. Apparent clearance of glucagon and gastrin by liver or lung both was enhanced by administration of the hypercaloric nutrient intravenously. Only intragastric hypercaloric nutrition maintained levels of VIP immunoreactivity close to those of control rats. Intragastric administration of either preparation appeared to maintain adequate levels of gastrin. Differences in the levels of glucagon immunoreactivities may be related to the stimulatory effects of metabolites in the lower gut and pancreas.
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PMID:The effect of parenteral and enteral nutrition on portal and systemic immunoreactivities of gastrin, glucagon and vasoactive intestinal polypeptide (VIP). 681 13

In adult rats, proteins fed as a meal apart from the remainder of the diet induce alterations of protein metabolism characterized by the simultaneous stimulation of protein synthesis and breakdown. These alterations occur in parallel with an acceleration of glycogenolysis. The purpose of this work was to investigate whether these metabolic changes are related to variations in portal insulin and glucagon levels or to insulin-glucagon balance. Portal hormone concentrations, aortic glycemia and aminoacidemia, liver glycogen contents were followed over a day-night cycle in rats adapted either to mixed feeding (10% protein) or to separate feeding (protein meal given 2 hours after the onset of the light phase). Insulin and glucagon were assayed by radioimmunoassay, glucagon with antibody K 964 specific for 3500 MW glucagon. During the 3 hours following the protein meal, the portal ratio of insulin to glucagon decreased; liver glycogenolysis and glucogenic amino acid catabolism were enhanced. This glucagonotropic and glucogenic response to a protein meal administered during daytime is consistent with the increase in protein turnover previously observed. Separate feeding did not alter the overall circadian pattern of portal insulinemia which rose at night but it did alter the overall circadian pattern of portal insulinemia which rose at night but it did alter that of portal glucagonemia by maintaining it at a low level during the nightly prandial period. No correlation could be evidenced between portal insulin concentrations and the aortic levels of any amino acid in either mixed-fed or separately-fed animals. Portal glucagonemia appeared to be weakly correlated with the aortic level of arginine in both experimental groups. In the separately fed group, highly significant correlation could be evidenced between portal insulin concentrations and the aortic levels of any amino acid in either mixed-fed or separately-fed animals. Portal glucagonemia appeared to be weakly correlated with the aortic level of arginine in both experimental groups. In the separately fed group, highly significant correlations were found between portal glucagonemia and aortic concentrations of the three branched and the two aromatic amino acids.
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PMID:Portal insulin and glucagon in rats fed proteins as a meal: immediate variations and circadian modulations. 699 44

Five morbidity obese subjects with fasting normoglycemia underwent catheterization of portal and peripheral veins immediately prior to jejunoileal bypass surgery. Levels of immunoreactive insulin (IRI), immunoreactive glucagon (IRG), and glucose were determined in simultaneously obtained serum samples before and after infusion of arginine. Portal levels exceeded peripheral levels by at least 50% with IRI and by 30%-40% with IRG. These results were similar to those reported in nonobese subjects and show that in morbid obesity as well as in nonobese states, peripheral insulin to glucagon molar ratios (I/G) underestimate portal I/G. Although hepatic extraction was not specifically measured, the data suggest that the peripheral levels of insulin and glucagon reported in morbid obesity result from alterations in secretion and not altered extraction.
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PMID:Portal and peripheral vein concentrations of insulin and glucagon after arginine infusion in morbidly obese subjects. 700 Nov 74

Basal portal and systemic venous hyperinsulinemia and hyperglucagonemia were present in fasted rats at 24 h after experimental liver injury by partial (67%) hepatectomy, carbon tetrachloride gavage, and intravenous D-galactosamine administration. Both enhanced pancreatic hormone secretion and depressed hepatic hormone extraction were likely responsible for the insulin and glucagon oversupply. Endogenous gut-derived endotoxin is proposed as the causative factor for the exaggerated hormonal response because intravenous exogenous endotoxin elicited an identical elevation of insulin and glucagon. Systemic endotoxemia at 24 h after liver injury was indicated by marked (78-100%) lethality in lead-sensitized rats and positive Limulus lysate gelation tests of plasma samples. Furthermore, antiendotoxin treatments, including endotoxin tolerance, polymyxin B, and gut sterilization, significantly reduced both lead-sensitized lethality and hyperinsulinemic and hyperglucagonemic responses at 24 h in most liver-injury groups. Portal versus systemic venous administration of endotoxin at a low dose implied that normal endotoxin phagocytosis by the liver suppressed the pancreatic endocrine response. A physiological negative-feedback control system involving gut-derived systemic endotoxemia after liver damage with insulin and glucagon hypersecretion by the pancreas for stimulation of hepatic regeneration is hypothesized.
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PMID:Endotoxin-induced hyperinsulinemia and hyperglucagonemia after experimental liver injury. 703 47

Acute hepatic ischaemia was induced in pigs by means of a portacaval shunt with hepatic artery ligation after 24 hours. Despite significant elevation in blood ammonia, fatty acids, aspartate aminotransferase, cerebrospinal fluid glutamine and ammonia, and brain tissue glutamine, ammonia and tryptophan, the experimental animals remained awake and alert and indistinguishable from sham-operated controls. The molar ratio of branched-chain to aromatic amino acids fell sharply in the arterial blood, but showed a terminal attempt at compensation in muscle venous samples. Portal and muscle venous insulin levels were elevated, and glucagon values rose in all circulation segments in the experimental group. The failure to induce coma in these pigs, despite the presence of many of the classical biochemical features, suggests that the syndrome of encephalopathy comprises several stages, and that the pig may be an important model in which to define these.
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PMID:Acute hepatic ischaemia in the pig- the changes in plasma hormones, amino acids and brain biochemistry. 725 Aug 93

The suppression of food intake elicited in rats by injection of pancreatic glucagon and the accompanying changes in energy metabolite flux were investigated. Glucagon injections, 120-360 micrograms ip, were made as rats began the first meal of the dark phase after food deprivation during the light phase. Glucagon-injected rats terminated their meals sooner and ate smaller meals than vehicle-injected rats. For metabolic assays, rats were identically treated and killed just at meal onset or 15 min later. Portal vein blood glucose increased similarly in all rats allowed to feed, whereas plasma nonesterified fatty acid and D-(-)-3-hydroxybutyrate levels decreased during feeding. In contrast, hepatic vein and aorta blood glucose levels increased more after glucagon than after vehicle injections. Liver glycogen content decreased after glucagon injections. The highest glucagon dose only had slight lipolytic and ketogenic effects. It was concluded the glycogenolytic and hyperglycemic action of glucagon may generate a satiety signal sufficient to cause premature termination of meals. Changes in ketone and lipid fluxes do not appear necessary for this behavioral effect.
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PMID:Metabolic concomitants of glucagon-induced suppression of feeding in the rat. 730 77


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