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)

In ten patients with a femoral shaft fracture, arterial plasma amino acids and glucagon, blood glucose, and serum insulin were measured after an overnight fast on the third, fifth, and seventh days following injury. Ten normal subjects were controls. On all days, concentrations of the key glucogenic amino acid, alanine, were the same in both groups, but levels of another glucogenic amino acid, glycine, were significantly less in the fracture patients. Other amino acid changes following injury were maximal at 7 days, with significant elevations of phenylalanine, methionine, tyrosine, ornithine, lysine, arginine, valine, isoleucine, and leucine. Increased levels of insulin, glucose, valine, isoleucine, and leucine on the fifth and seventh days after injury implied insulin resistance. Plasma glucagon was elevated on the third (p less than 0.05) and seventh (p less than 0.01) days after injury, but the concentrations measured are insufficient to explain the impaired carbohydrate tolerance following a fracture.
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PMID:Arterial plasma amino acids during the first week following femoral shaft fracture. 43 79

Somatostatin (SRIF) has been tested for its actions on the central nervous system to affect glucoregulation. In doses ineffective when given systemically , SRIF and SRIF analogs given intracisternally (ic) reduce hyperglycemia and hyperglucagonemia after ic bombesin administration. The SRIF analog, des-AA1, 2, 4, 5, 12, 13-[D-Trp8]SRIF, decreases plasma insulin and elevates plasma glucose and glucagon when given systemically. However, when given ic, this peptide prevents the rise in glucose and glucagon after ic bombesin administration and is 10 times more potent than SRIF in reducing bombesin-induced hyperglycemia. Other analogs of SRIF and various unrelated peptides were found to be ineffective in reducing bombesin-induced hyperglycemia. des-AA1, 2, 4, 5, 12, 13-[D-Trp]SRIF prevented the hyperglycemia induced by surgical stress or by ic administration of beta-endorphin or carbacol. des-AA1, 2, 4, 5, 12, 13-[D-Trp]SRIF given ic did not prevent hyperglycemia induced by systemic administration of epinephrine, arginine, or glucagon. These studies suggest that SRIF and its analogs may act within the brain to affect glucoregulation.
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PMID:Somatostatin: central nervous system actions on glucoregulation. 44 91

Glucogon immunoreactivity (IRG) was measured in plasma of duodenopancreatectomized subjects with a nonspecific (K-4023) and a specific (30-K) glucagon antiserum. After an overnight fast, plasma IRG (K-4023) was significantly (P < 0.05) higher in the subjects without pancreas, averaging 782+/-79 (SEM) pgeq/ml, than in the controls (482+/-80 pgeq/ml). IRG (30-K) of 162+/-68 pg/ml did not change during an infusion of arginine (450 mg/kg per 40 min). Insulin deprivation during 3 d in one patient did not restore the IRG response to arginine as reported in depancreatized dogs.Bio-Gel P-30 column chromatography revealed that virtually all IRG (30-K) measured in whole plasma was of different molecular weight than glucagon, and primarily of a mol wt >/= 40,000. Intravenous arginine did not significantly alter the chromatographic pattern of these plasmas. Thus, as postulated by others, duodeno-pancreatectomized humans have virtually no circulating 3,500-dalton glucagon. Hence, the presence of 3,500-dalton glucagon in plasma is not a condition for the diabetic state. It might, nevertheless, when present in normal or excessive amounts, worsen the metabolic state of diabetic patients. Among 14 amino acids measured in plasma of these patients, the concentrations of alanine, serine, ornithine, and arginine were significantly (P < 0.05) elevated to approximately twice that of normal: alanine and serine are both substrates for gluconeogenesis, whereas ornithine and arginine are involved in the formation of urea, the second product of hepatic gluconeogenesis. As the concentrations of branched chain amino acids were not grossly altered, it is hypothesized that this amino acid pattern is a consequence of glucagon deficiency rather than secondary to the diabetic state of these patients.
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PMID:Glucagon immunoreactivities and amino acid profile in plasma of duodenopancreatectomized patients. 44 30

The effects of somatostatin and a long acting, glucagon selective somatostatin analog (des-Ala1Gly2[His4,5-D-TrP8]-somatostatin) used studied during arginine tolerance tests in normal anaesthetized rats. Arginine infusion in control animals resulted in a rapid increase in plasma insulin and glucagon, and an increase of 15 +/- 5 mg/dl in plasma glucose. Somatostatin infusion (1 mg/kg/h) resulted in suppression of basal insulin secretion and a decrease in arginine-induced insulin and glucagon release. Glucose levels increased rapidly during the combined arginine-somatostatin infusion reaching a peak of 72 +/- 10 mg/dl above basal levels. Similar results were obtained when somatostatin was injected SC (1 mg/kg) at times 0, 15, 30, and 45 minutes (arginine infused from 30-60 minutes). A single injection (1 mg/kg) of the long-acting somatostatin analogue resulted in significant inhibition of basal insulin and glucagon release; during arginine infusion glucagon levels rose only slightly, the insulin response was, however, nearly normal, and only a small arginine-induced increase in glucose levels was observed. Carbohydrate absorption was not influenced by either somatostatin or the analogue.
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PMID:Effect of a long acting glucagon selective somatostatin analogue on plasma glucose, insulin and glucagon levels in the anaesthetized rat during arginine infusion. 46 54

To determine whether glucose intolerance in patients with chronic renal failure could improve by hemodialysis, the effects of arginine infusion on the concentration of blood sugar, insulin, glucagon, growth hormone were examined in healthy volunteers, undialyzed and dialyzed patients with chronic renal failure. Plasma concentrations of sugar and hormones in undialyzed and dialyzed patients responded similarly to arginine infusion. While blood samples were collected at 30, 45, 60, 90, 120 and 180 min after beginning infusion of arginine, the concentrations of sugar and hormones in both patients had no statistically significant differences. However, plasma concentrations of growth hormone in both patients 180 min after beginning of arginine infusion gave statistically significant differences. In the present study, the results suggest that hemodialysis might not improve the glucose tolerance in the patients with chronic renal failure.
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PMID:Response of insulin, glucagon and growth hormone to arginine infusion in patients with chronic renal failure. 49 15

In order to investigate secretion of extrapancreatic glucagon in dogs, plasma glucagon and total immunoreactive glucagon (IRG) in response to arginine were determined with antisera specific and non-specific for pancreatic glucagon, respectively. Only a tiny rise of plasma glucagon was observed in the portal vein following arginine infusion performed immediately after total pancreatectomy in a group of 5 normal dogs. In contrast, total IRG in the portal vein increased significantly after arginine infusion even after pancreatectomy. In alloxan diabetic dogs, arginine infusion after total pancreatectomy caused a rise in plasma glucagon in the portal vein, although not significantly. The response of total IRG to arginine in the portal vein was exaggerated in alloxan diabetic dogs. In a group of one-week post-pancreatectomized animals, plasma glucagon and total IRG increased significantly in response to arginine infusion. Furthermore, in these dogs, response of plasma glucagon and plasma total IRG to arginine infusion was abolished after gastrectomy. From the present results it is concluded that secretion of extrapancreatic glucagon increased in response to arginine infusion in the diabetic state, both alloxan diabetic dogs and one-week post-pancreatectomized dogs. In addition, a rise in extrapancreatic glucagon following arginine infusion in the chronically pancreatectomized dogs almost certainly derived from the stomach, as the rise was abolished by gastrectomy.
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PMID:Response of extrapancreatic glucagon to arginine in dogs. 49 57

The influence of calcium on basal and acetylcholine-stimulated pancreatic polypeptide (PP) secretion was investigated in an isolated pancreatico-duodenal preparation and compared to the secretion of glucagon and insulin. The stimulatory effect of 5 mmol/liter calcium on PP release was of the same magnitude as that obtained by 5 mmol/liter arginine or 10 nmol/liter isoproterenol but only one fifth of the PP response to acetycholine (1 mumol/liter). All stimuli were equipotent with respect to insulin and glucagon release. The acetylcholine (1 mumol/liter)-stimulated PP release was almost identical at calcium concentrations of 1.3 and 6.3 mmol/liter, whereas glucagon release was calcium dependent, with higher responses at high (6.3 mmol/liter) than at normal (1.3 mmol/liter) calcium concentrations. In a calcium-depleted medium, acetylcholine induced a prompt, short-lived, but repeatable PP response, whereas no increase in glucagon or insulin was found. Further, when calcium influx into cells was blocked by excess magnesium (5.0 mmol/liter), the basal and acetylcholine (1 mumol/liter)-stimulated PP secretion was only inhibited by 12% (P = NS) and 42% (2P less than 0.05), respectively, whereas glucagon release was inhibited 56% (2P less than 0.001) and 76% (2P less than 0.01), respectively. It is concluded that the secretion of PP is influenced by calcium ions; however, the PP release is much less dependent on extracellular calcium ions than are insulin and glucagon secretions.
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PMID:The influence of calcium on the basal and acetylcholine-stimulated secretion of pancreatic polypeptide. 49 84

We have demonstrated previously that cyclic somatostatin (GH-RIH) exerts a diabetogenic action in healthy subjects. To further examine the impact of this phenomenon studies of blood glucose (BG), immunoreactive insulin (IRI), glucagon (IRG) and growth hormone (GH) were performed in insulin requiring diabetics (n = 6) receiving i.v. arginine (0.5 g/kg) both in the absence and presence of i.v. GH-RIH (500 microgram/h). The infusion of GH-RIH-resulted in a persistent diminution in plasma IRI, IRG and GH. BG fell during i.v. GH-RIH during the initial 30 min and was below control values up to 45 min after initiation of i.v. arginine, but subsequently exceeded control levels (p less than 0.05 - less than 0.025). The excess rise in BG occurred in spite of suppression by somatostatin of the ariginine induced release of IRG, IRI and GH. A fall in BG was seen following cessation of i.v. GH-RIH and during a rebound of insulin release with glucagon levels remaining in the basal range. These findings indicate a diabetogenic action of somatostatin also in insulin requiring diabetics as long as some residual capacity for insulin release is retained.
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PMID:Increase by somatostatin of the arginine induced rise in blood glucose in untreated insulin requiring diabetics. 49

Acute oral administration of ethanol (150 and 750 mg/100g) to fasted rats produced dose-related inhibition of arginine-induced insulin (IRI) release, an elevation of plasma glucagon (IRG) levels and minor effects on blood glucose. In contrast, chronic consumption of ethanol for 10 weeks augmented arginine-induced hyperglycemia and hperinsulinemia. Thus, acute ethanol administration decreased plasma IRI levels at both doses, presumably by suppressing beta cell function; whereas, function of the alpha cell and plasma IRG levels were increased, but only by the high dose of ethanol. In these experiments the effects exerted by ethanol on the pancreatic endocrine responses to arginine infusion varied according to: dose of ethanol administered; duration of exposure to ethanol; and state of nourishment of the subjects.
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PMID:Alterations in arginine-induced pancreatic hormone release: influence of acute and chronic exposure to ethanol. 50 86

Four patients with glucagon-producing tumours of the pancreas were investigated. Fasting plasma glucagon concentrations ranged from 209--625 pmol/l. Plasma insulin concentrations were normal except in one patient, where the tumour also produced insulin (558 pmol/l). Intravenous glucose (25 g/m2) depressed the glucagon concentration in two patients, while no change was noted in the others. Intravenous arginine stimulated glucagon secretion in three patients, but not in the fourth. Intravenous somatostatin suppressed glucagon secretion in all three patients investigated. All patients had abnormally low plasma levels of individual amino acids; glucogenic and branched-chain amino acids were equally depressed. Surgical removal of the tumours led to complete recovery from dermatosis and the glucagon levels were normalized. Postoperative tests were performed in three patients. The alpha-cell responsiveness to iv glucose was restored. Glucose tolerance (Kg-value) was improved in one patient (0.73 to 1.65), persistently low in one patient (0.75 to 0.72) and impaired in the third patient (1.35 to 1.09). It is concluded that none of these functional tests will be of diagnostic value in cases suspected of glucagonomas. The results also show that glucose homeostasis is remarkably unaffected by the extreme hyperglucagonaemia of these patients and that hypoaminoacidaemia is an important consequence of chronic hyperglucagonaemia.
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PMID:Functional studies in patients with the glucagonoma syndrome. 51 Aug 30


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