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)

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

The role of catecholamines in shock metabolism in dogs was studied by comparing the metabolism of shock due to cardiac tamponade, shock with catecholamine depletion from prior reserpine adminstration and metabolism in the normal dog with continuous epinephrine infusion. It was concluded that the high serum concentrations of catecholamines in shock probably cause the increased blood lactate, initial hyperglycemia and, possibly, the poor free fatty acid oxidation seen in shock, but do not cause the increased protein catabolism of shock. With the simultaneous infusion of glucagon, cortisol and epinephrine in physiologic dosages, catabolic metabolism similar to that observed in shock was established in the normal dog. Lactacidemia, hyperglycemia, poor ability to oxidize free fatty acid and massive protein breakdown were observed. The decreased metabolic rate and diminished fatty acid mobilization of shock were not duplicated in those in the normal group and are probably a function of hypoperfusion. The importance of these observations is that impaired use of fat and increased protein breakdown, as seen in shock and trauma, are mediated by hormonal changes. It follows that there may be the opportunity to reverse or modify this catabolism by hormonal manipulation in the surgical patient.
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PMID:The role of stress hormones in the catabolic metabolism of shock. 50 56

In order to study the response of pancreatic alpha cells to the change blood glucose, plasma pancreatic glucagon levels were measured after glucose loading given orally (50g) or intravenously (25g) in twenty-two normal controls and eighty untreated diabetics. Basal plasma pancreatic glucagon levels did not differ significantly in the two groups. However, oral or intravenous glucose administration caused a decrease in plasma pancreatic glucagon in normal subjects but not in diabetics. In "moderate" or "severe" diabetics, plasma pancreatic glucagon tended to increase paradoxically following oral glucose loading. To evaluate the sensitivity of pancreatic alpha cells to glucose, we calculated the index, -sigma delta IRG/sigma delta BS, after oral glucose loading. It was 1.96 +/- 0.57 in normal subjects, and significantly higher than in "mild" (0.11 +/- 0.05), "moderate" (-0.002 +/- 0.06) and "severe" (-0.09 +/- 0.07) diabetics. These results demonstrate the insensitivity of alpha cells to hyperglycemia in patients with diabetes mellitus as compared with normal subjects.
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PMID:Insuppressibility of plasma glucagon by orally or intravenously administered glucose in diabetes mellitus. 59 Jan 99

Depancreatized dogs have plasma immunoreactive glucagon (IRG), which is of gastric origin and is immunologically indistinguishable from pancreatic glucagon. The effects of extrapancreatic IRG on the tracer-determined rate of glucose production were examined to establish whether this hormone contributes to the hyperglycemia observed in six conscious, depancreatized dogs after insulin withdrawal. The dogs were initially maintained normoglycemic with an intraportal insulin infusion. Insulin withdrawal resulted in a 53 and 70% decrease of serum immunoreactive insulin (IRI) at 60 and 210 min, respectively. At 60 min, plasma glucose rose and Ra increased by 50%. A somatostatin-induced decrease in IRG prevented a further increase in Ra and glucose; after somatostatin withdrawal, IRG, Ra, and plasma glucose increased. Arginine given 1 or 3 h after insulin withdrawal increased IRG by 100 pg/ml, and mean Ra rose by 8.9 mg/kg-min. Thus, in depancreatized dogs with low but detectable serum IRI, IRG suppression is associated with inhibition of Ra and further rise in plasma glucose is prevented. Stimulation of IRG release increases Ra and results in marked hyperglycemia. It is concluded that extrapancreatic glucagon has a diabetogenic effect during acute insulin defiency.
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PMID:Extrapancreatic glucagon in control of glucose turnover in depancreatized dogs. 62 97

Carbohydrate intolerance is a common abnormality in patients with chronic renal failure. In this group of patients we investigated the interrelation among glucose, insulin, and growth hormone and confirmed the presence of carbohydrate intolerance and hyperinsulinemia. In addition we demonstrated alterations in growth hormone regulation, characterized by (1) the lack of suppression of growth hormone by orally induced hyperglycemia and paradoxical increase in serum levels of growth hormone after the administration of intravenous glucose or glucagon; (2) lack of release of growth hormone with induced hypoglycemia and an exaggerated response to levodopa administration. Furthermore, thyrotrophin-releasing hormone stimulated growth hormone release, a phenomenon not observed in the control population. Our studies show an impaired hypothalamic regulation of growth hormones secretion in patients with renal failure undergoing long-term hemodialysis.
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PMID:Abnormalities in the regulation of growth hormone in chronic renal failure. 62 54

The concentrations of both GH and prolactin in the circulation of the domestic fowl have been determined after various treatments known to affect carbohydrate metabolism. Fasting decreased the level of glucose, stimulated the secretion of GH and inhibited the secretion of prolactin. Administration of insulin significantly depressed the level of GH in the plasma of normal or fasted birds and also in chickens which had received simultaneous injections of glucose or 2-deoxy-D-glucose. No consistent effect of insulin on the secretion of prolactin was observed. Hyperglycaemia subsequent to administration of glucose had no effect on the levels of either GH or prolactin. Glucagon-induced hyperglycaemia suppressed the level of GH in the plasma and stimulated that of prolactin.
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PMID:Influence of fasting, glucose and insulin on the levels of growth hormone and prolactin in the plasma of the domestic fowl (Gallus domesticus). 63 22

Two kindreds affected by maturity-onset type of hyperglycemia in young people were studied. The postglucose-load hyperglycemia segregated as an autosomal dominant trait; it was always mild, never requiring insulin, and generally seemed to start in the first two decades of life. Glucose, insulin, glucagon, and growth hormone were measured during glucose-tolerance tests in patients, relatives, and control subjects. Most hyperglycemic patients were found to have insulin deficiency. There was no correlation between the age of the patients and insulin secretion. Plasma glucagon and growth hormone were normal. Maturity-onset type of hyperglycemia in young people may be a frequent type of hyperglycemia, and its identification will generally depend on the presence of a strong family history. The recognition of maturity-onset type of hyperglycemia in young people as a specific disease different from juvenile, insulin-dependent diabetes is important, especially to prevent unnecessary use of insulin in hyperglycemic children.
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PMID:Plasma glucose, insulin, glucagon, and growth hormone in kindreds with maturity-onset type of hyperglycemia in young people. 64 40

The insulin and glucose responses to glucagon infusions (27 microgram/hr) were determined in sheep before and after parenteral lead treatment (6 mg/kg intravenously). Glucose production was measured by primed continuous infusion of [6-3H]glucose. Glucagon and insulin concentrations before and during glucagon infusions were not significantly different between lead treatment and control experiments. Lead administration did not affect the concentration or production of glucose in the preinfusion period. However, depressed hyperglycemia during glucagon infusion in lead treated experiments tended to be associated with decreased glucose production. The reduced glucogenic response to glucagon may be the result of reduced function of pyruvate carboxylase, a key hepatic gluconeogenic enzyme in sheep, from lead induced impairment of mitochondrial function.
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PMID:Depression of hyperglycemic response to glucagon by parenteral lead administration in sheep. 64 58

The effect of elevated glucagon concentrations on insulin requirements and on blood glucose concentrations was studied in five insulin-requiring diabetic subjects during feedback control of hyperglycemia with an automated glucose-controlled insulin infusion system (artificial endocrine pancreas) for six to eight hours. Two levels of hyperglucagonemia were induced by means of constant intravenous infusion. Raising plasma glucagon concentrations to levels reported in poorly controlled diabetics (450 to 665 pg. per milliliter) did not alter total insulin requirements or blood glucose concentrations. Higher glucagon concentrations (850 to 1,050 pg. per milliliter) caused a modest (26 per cent) increase in insulin requirements and only a slight increase in mean blood glucose concentrations. These studies demonstrate that the degree of hyperglucagonemia found most frequently in insulin-requiring diabetics does not increase insulin requirements or decrease insulin effectiveness in patients given insulin in amounts appropriate to maintain euglycemia.
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PMID:The effect of hyperglucagonemia on blood glucose concentrations and on insulin requirements in insulin-requiring diabetes mellitus. 65 10

Plasma glucose, immunoreactive glucagon (IRG), and insulin were measured in hypophysectomized dogs receiving cortisol and thyroid replacement therapy. 4 wk after hypophysectomy mean fasting plasma glucose levels had declined from 90+/-2 mg/100 ml to 64+/-2; fasting and arginine-stimulated insulin and IRG levels were, respectively, approximately 50% lower and unchanged. 12 wk or more after hypophysectomy, despite lower plasma glucose levels, fasting and arginine-stimulated IRG levels were significantly below control dogs. Hypophysectomized and shamhypophysectomized dogs were subjected to total pancreatectomy. Postoperatively, in the sham-hypophysectomized, depancreatized dogs fasting glucose levels ranged from 300-500 mg/100 ml on 8-10 U/day of insulin; IRG levels averaged 215+/-29 pg/ml. The hypophysectomized, depancreatized dogs required 0-4 U/day and fasting glucose levels under 100 mg/100 ml were not uncommon, even without insulin; fasting IRG levels averaged 63+/-4 pg/ml (P < 0.001). During arginine infusion in sham-hypophysectomized, depancreatized dogs, IRG levels rose from 215+/-60 pg/ml to a peak of 404+/-112 pg/ml; in hypophysectomized, depancreatized dogs, the base line IRG averaged 44+/-8 and the peak 110+/-25 pg/ml (P < 0.05). IRG levels in the venous effluent of the gastric fundus, the major source of nonpancreatic glucagon, reached a peak of 4,898+/-959 pg/ml in the sham-hypophysectomized, depancreatized group during arginine infusion and only 219+/-128 pg/ml in the hypophysectomized, depancreatized group. In three hypophysectomized, depancreatized dogs, a replacement infusion with glucagon for 10 h promptly increased hyperglycemia by 80-180 mg/100 ml and worsened glycosuria, evidence of a hepatic response to glucagon replacement. It is concluded that hypophysectomy somehow decreased both the hypersecretion of gastric IRG and the severe hyperglycemia that otherwise follows pancreatectomy. The hypophysectomized, depancreatized animal, therefore, has combined insulin and glucagon deficiency, and the latter may contribute to reduced severity of its hyperglycemia.
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PMID:The role of glucagon deficiency in the Houssay phenomenon of dogs. 65 97


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