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)

Intravenous glucose tolerance tests were carried out in 61 chronic alcoholic patients, divided into two groups, and in a third group consisting of healthy, nonalcoholic volunteers. Members of one experimental group were drinking alcohol throughout the study. The patients of the other experimental group received no alcohol and were in withdrawal from alcohol. The glucose tolerance tests were carried out on each patient on admission to the hospital and 1 wk later. During the test, blood was drawn at 10 min intervals for glucose, immunoreactive insulin, and glucagon determinations. The results indicated that there was transient carbohydrate intolerance in the great majority of both patient groups, and it became evident that the carbohydrate intolerance was the result of continuous alcohol consumption and was not part of the withdrawal syndrome. Significant decrease in insulin secretion was found in the early part of the glucose tolerance tests in the majority of the patients in both alcohol and withdrawal groups. Based on results of this study and evidence from the literature, it is suggested that chronic alcoholism is dabetogenic in susceptible individuals and that the transient carbohydrate intolerance found in our study represents and early step in the development of adult-onset diabetes eventually developing in a significant number of chronic alcoholics.
Metabolism 1978 Sep
PMID:Mechanism and significance of carbohydrate intolerance in chronic alcoholism. 68 69

The glucose response to arginine infusion in normal rats was studied during insulin and glucagon deficiency (somatostatin infusion, 1 mg/kg/hr) or selective glucagon deficiency ([D-Cys14]-somatostain infusion, 1 mg/kg/hr). In control studies, plasma glucose levels rose 14 mg/dl in response to arginine and returned to basal levels at the termination of the infusion. Insulin levels increased 136 +/- 12 muU/ml and glucagon increased 76 +/- 12 pg/ml during the infusion. Infusion of somatostatin resulted in supression of both arginine-induced insulin and arginine-induced glucagon release, and marked hyperglycemia ensued. The administration of [D-Cys14]-somatostatin during arginine infusion produced no associated hyperglycemia. It resulted in suppression of glucagon secretion and a modest rise in insulin release. These results demonstrate that the hyperglycemic effects of somatostatin in arginine-treated animals do not arise in animals treated with glucagon-specific somatostatin analogs.
Metabolism 1978 Sep
PMID:Effect of somatostatin and a glucagon-specific analog on glucose homeostasis during arginine infusion. 68 72

Spontaneous fasting hypoglycemia developed in four nondiabetic patients with end-stage renal failure. All were undergoing long-term maintenance hemodialysis and three patients were anephric. Hypoglycemia was generally accompanied by severe metabolic acidosis and, in three patients, lactic acidemia. Abnormalities of hepatic structure and/or function were present in three patients. In one patient, hypoglycemia was refractory to exogenous glucagon, failed to respond to alanine, glycerol, or galactose, and was associated with suppressed plasma insulin and elevated plasma glucagon levels. Fasting hypoglycemia appeared to result from several mechanisms. In at least two patients, fasting hypoglycemia and lactic acidosis resulted from impaired hepatic gluconeogenesis in association with impaired or absent renal glucose production. Additionally, substrate limitation probably contributed to hypoglycemia in several patients.
Arch Intern Med 1978 Sep
PMID:Spontaneous hypoglycemia in chronic renal failure. 68 26

Using a single-isotope and immune precipitation technique the half-life (t 1/2) of hepatic phenylalanine:pyruvate transaminase (aminotransferase, EC 2.6.1.--, Number not yet assigned) from glucagon-treated rats was determined to be 2.8 days, similar to that of the control rats (t 1/2 = 3.3 days). The half-life of rat liver total soluble proteins also remained unchanged after glucagon treatment (t 1/2 = 2.7 days in glucagon-treated rats; t 1/2 = 2.8 days in normal). Thus, glucagon has no effect on the degradation of phenylalanine:pyruvate transaminase. Furthermore, the degradation rates are similar for both the holoenzyme and the apoenzyme of phenylalanine:pyruvate transaminase.
Biochim Biophys Acta 1978 Sep 11
PMID:Degradation of phenylalanine:pyruvate transaminase after glucagon treatment. 68 44

The electrocardiogram was monitored in 100 patients undergoing oesphago-gastro-duodenoscopy. Premedication differed: 25 patients each were given either (Group I) atropine 0.5 mg, hyoscine-N-butylbromide 20 mg, and diazepam 5 mg, or (Group II) hyoscine-N-butyl-bromide 20 mg and diazepam 5 mg, or (Group II) diazepam 5 mg and glucagon 0.2 mg, or (Group IV) only diazepam 5 mg intravenously. After injection of the parasympatholytic drugs (Groups I and II) there was a significantly higher heart rate duringthe entire length of the examination than in groups III and IV. Nine of the ten cases of ascending S-T depression were found in Groups I and II, while descending (ischaemic) S-T changes occurred equally frequently in patients of all four groups. Two of the three more serious arrhythmias were registered after atropine. Since parasympatholytic drugs fail to inhibit arrhythmias and ST-T changes, while accentuating the rise in heart rate, it is recommended that premedication for oesophago-gastro-duodenoscopy should not include such drugs.
Dtsch Med Wochenschr 1978 Sep 29
PMID:[Cardiac side-effects of oesophago-gastro-duodenoscopy in relation to premedication (author's transl)]. 68 92

The aim of the present experiments was to determine the effects of basal glucagon on glucose production after induction of prolonged insulin lack in normal conscious dogs fasted overnight. A selective deficiency of insulin or a combined deficiency of both pancreatic hormones was created by infusing somatostatin alone or in combination with an intraportal replacement infusion of glucagon. Glucose production (GP) was measured by a primed constant infusion of [3H-3]glucose, and gluconeogenesis (GNG) was assessed by determining the conversion rate of circulating [14C]alanine and [14C]lactate into [14C]glucose. When insulin deficiency was induced in the presence of basal glucagon the latter hormone caused GP to double and then to decline so that after 4 h it had returned to the conrol rate. The conversion of alanine and lactate into glucose, on the other hand, increased throughout the period of insulin lack. Withdrawal of glucagon after GP had normalized resulted in a 40% fall in GP, a 37% decrease in GNG, and a marked decrease in the plasma glucose concentration. Induction of insulin deficiency in the absence of basal glucagon resulted in an initial (30%) drop in GP followed by a restoration of normal GP after 2--3 h and moderately enhanced glucose formation from alanine and lactate. It can be concluded that (a) the effect of relative hyperglucagonemia on GP is short-lived; (b) the waning of the effect of glucagon is attributable solely to a diminution of glycogenolysis because GNG remains stimulated; (c) basal glucagon markedly enhances the GNG stimulation apparent after induction of insulin deficiency; and (d) basal glucagon worsens the hyperglycemia pursuant on the induction of insulin deficiency both by triggering an initial overproduction of glucose and by maintaining the basal production rate thereafter.
J Clin Invest 1978 Sep
PMID:Effect of glucagon on glucose production during insulin deficiency in the dog. 69 Jan 90

Conscious dogs were infused with 1) glucagon (3 ng/kg.min) alone for 120 min followed by glucagon plus epinephrine (0.1 microgram/kg.min) for 60 min and 2) epinephrine alone (150 min) followed by epinephrine plus glucagon for 90 min. Glucagon alone caused a 10--15 mg/dl rise in plasma glucose and a 45% increase in glucose production that returned to baseline by 75--120 min. After addition of epinephrine, glucose production rose again by 80%. Infusion of epinephrine alone resulted in unchanged plasma glucagon levels, a 60--70 mg/dl rise in plasma glucose, and an 80--100% rise in glucose production that returned to baseline by 60--120 min. When glucagon was added, glucose output promptly rose again by 85%. When glucagon was infused alone, there was a rise in glucose uptake, whereas, with epinephrine, glucose uptake failed to rise and glucose clearance fell by 35--50%. We conclude that 1) hepatic refractoriness to persistent elevations of glucagon or epinephrine is specific for the hormone infused; 2) epinephrine stimulates glucose production in the conscious dog in the absence of a rise in plasma glucagon; 3) the hyperglycemic response to glucagon or epinephrine is determined in part by accompanying changes in glucose utilization.
Am J Physiol 1978 Sep
PMID:Effect of sequential infusions of glucagon and epinephrine on glucose turnover in the dog. 69 23

The possible role of the hepatic fructose-6-phosphate substrate cycle (phosphofructokinase, fructose-1,6-diphosphatase) in the rapid hormonal regulation of gluconeogenesis was investigated in vivo in fasted normal and adrenalectomized rats after administration of [3-3H, U-14C]- or [3-3H, 6-14C]glucose. The plasma glucose 3H/14C ratio was used as an index of substrate cycling because the amount of 3H loss from liver hexose phosphates is determined by the extent of cycling. PFK and FDPase activities limit 3H loss during gluconeogenesis and glycolysis, respectively. Glucagon-stimulated hepatic glucose production is always accompanied by increased substrate cycling, i.e., increased FDPase and PFK activities. The high PFK activity may be a secondary event due possibly to elevated cellular fructose-6-phosphate levels. Decreased substrate cycling, i.e., lowered FDPase activity, always accompanies the depressed hepatic glucose production that occurs during hyperglycemia. Glucagon has no effect on substrate cycling in adrenalectomized rats that are insensitive to the hormone. The in vivo experiments presented provide evidence, although indirect, that glucagon administration results in changes in the fructose-6-phosphate substrate cycle in a living animal. Whether these changes are primary regulatory events or occur secondarily to hormone actions elsewhere is not known.
Am J Physiol 1978 Sep
PMID:Fructose-6-phosphate substrate cycling and hormonal regulation of gluconeogenesis in vivo. 69 24

1 The relaxant action of glucagon has been studied in strips of rabbit renal arteries partially contracted by a low concentration (1 ng/ml) of noradrenaline.2 The preparation was relaxed in a dose-dependent manner by concentrations of glucagon varying between 25 ng/ml and 420 ng/ml.3 The relaxant effect of glucagon (0.1 mug/ml approximately ED(60)) on this preparation was not affected by propranolol (5.0 mug/ml), cimetidine (10 mug/ml), diphenhydramine (10 mug/ml), indomethacin (5.0 mug/ml), phentolamine (1.2 mug/ml), atropine (10 mug/ml) and 8-Leu-AT(II) (1.0 mug/ml) but was slightly potentiated by Des-Arg(9) Leu-OMe(8)-Bk (25 mug/ml) and indomethacin (50 mug/ml).4 The dose-response curve to glucagon remained parallel in the presence of papaverine (2.5 mug/ml) but was shifted to the left by a factor of 2.5 to 2.8. Theophylline (250 mug/ml) also potentiated the vascular relaxation induced by glucagon.5 Insulin (10 mug/ml) did not influence the relaxant effect of glucagon.6 The removal of the N-terminal amino acid (His) of glucagon reduced by 89% the biological activity of this fragment on the vascular preparation. The removal of the C-terminal amino acids Met-27, Asn-28 and Thr-29 of glucagon resulted in a fragment which was inactive either as an agonist or as an antagonist when tested at concentrations as high as 925 ng/ml.7 It is concluded that the relaxation of partially contracted strips of rabbit renal arteries by glucagon constitutes a simple, sensitive, relatively specific and reliable bioassay which may be useful for the determination of glucagon in biological materials and for structure-activity relationship studies with this hormone.
Br J Pharmacol 1978 Sep
PMID:A new bioassay for glucagon. 69 87

At least four types of endocrine-like cells have been detected histochemically in the mucosa of the human colon and rectum, i.e. argentaffin cells storing 5-hydroxytryptamine (5HT) and non-argentaffin cells reacting with glucagon, somatostatin and bovine pancreatic peptide (BPP) antibodies. Ultrastructurally, four main types and three rare types of endocrine-like cells have been identified. Among the former cells were: (1) argentaffin EC1 cells, known to store 5HT and substance P, (2) poorly argyrophil L cells, corresponding to the glucagon-immunoreactive cells storing enteroglucagon or glucagon-like immunoreactivity (GLl), (3) inconstantly argyrophil F-like cells, possibly corresponding to BPP-immunoreactive cells, and (4) fairly argyrophil H cells of unknown function. Rare D cells, corresponding to somatostatin cells, N cells, corresponding to neurotensin cells, and P cells, of unknown function, have been also found.
Cell Tissue Res 1978 Sep 05
PMID:Types of endocrine cells in the human colon and rectum. 69 14


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