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 effects of somatostatin (SRIF) on glucagon release have been studied in the monolayer culture of newborn rat pancreas. It was found that SRIF inhibited glucagon release rapidly and in a dose dependent manner at concentrations of 1-1000 ng/ml. SRIF inhibited glucagon release under basal conditions and after stimulation by arginine, 3-isobutyl-1-methylxanthine (IBMX), high Ca++ concentrations, ionophore A23187 and Ca++, and Ba++. SRIF inhibited ionophore-induced glucagon release over 60 min when a low concentration of A23187 was used (0.1 microgram/ml) but not when a high concentraion (10 microgram/ml) was used. The stimulant effect of 10 microgram/ml A23187 was, however, inhibited by SRIF during short periods of incubation. The per cent inhibition of arginine-stimulated glucagon release due to SRIF remained unchanged when the Ca++ concentration in the medium was varied from 1-10 mM. It is concluded that SRIF promptly inhibits glucagon release under basal conditions or when stimulated by a variety of agents. Thus, the action of SRIF appears to be basic to the granule release process and not specifically antagonisitc to any particular stimulants. Further, as SRIF inhibits release due to raised cytosol Ca++ (e.g., ionophore-Ca++ or high Ca++ experiments) the action is probably at a late point in the release mechanism.
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PMID:Somatostatin inhibition of pancreatic glucagon release from monolayer cultures and interactions with calcium. 33 Jan 54

Thirty-nine patients (14 non-diabetics, 8 chemical diabetics, and 17 overt diabetics) with circulating islet cell antibodies (ICA) were studied. Insulin and glucagon secretion after oral (100 g) and intravenous glucose loading (200 mg/kg bolus injection followed by an infusion of 20 mg/min over 60 min) and arginine infusion (25 g over 30 minutes) were evaluated in these patients and in non diabetic and diabetic ICA-negative controls. In the non-diabetic groups with or without ICA, insulin and glucagon responses to glucose were similar. Moreover, in ICA positive patients the response of these hormones to arginine infusion was reduced. Similar alterations in insulin and glucagon secretion were observed in the CIA positive and negative patients with chemical or overt diabetes. In particular, fasting hyperglucagonaemia and glucagon hyperresponse to arginine are associated with a lack of insulin secretion in the patients with overt diabetes. Hormonal differences between diabetics with and without ICA could not be detected.
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PMID:Insulin and glucagon secretion in diabetic and non-diabetic patients with circulating islet cell antibodies. 33 69

Investigation of glucagon secretion in isolated Wistar rat islets was carried out to elucidate further the regulatory function of glucose and arginine on pancreatic A-cells. The suppressive effect of D-glucose could also be demonstrated with L-glucose, D-mannose, D-fructose, D-galactose, D-glyceraldehyde and DL-dihydroxyacetone, but not in the presence of 3-O-methylglucose or mannitol. Sugars other than D-glucose inhibited glucagon secretion only at much higher concentrations than those at which D-glucose was effective. Furthermore, although 7.5 mM D-glucose up to 80% inhibition, the effects of other sugars appeared to level off at only 50--60% inhibition. The inhibitory action of D-glucose or D-glyceraldedyde on glucagon secretion could not be overcome by L-arginine, but 3-O-methylglucose, mannoheptulose, 2-deoxy-D-glucose, iodoacetamide, theophylline, epinephrine and acetylcholine were effective. The insulin secretion in response to glucose was inhibited by the metabolic inhibitors used, whereas the B-cell response in the presence of glyceraldehyde was diminished by iodoacetamide only. Like D-glucose, a variety of other sugars markedly reduced the stimulatory effect of L-arginine in glucagon release. The results show that the suppression of glucagon secretion is not specific for D-glucose and not strongly connected on a stimulated insulin secretion.
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PMID:Investigations on isolated islets of langerhans in vitro. 16.Modification of the glucose-dependent inhibition of glucagon secretion. 33 69

This study was performed in order to evaluate the effects of somatostatin on insulin releasing mechanisms and on glucose uptake in peripheral tissues using isolated pancreatic islets, isolated rat diaphragms and epididymal fat pads. Insulin release by various concentrations of glucose were examined, and it was found that 100 ng/ml of somatostatin significantly inhibited insulin release at the glucose concentration of 200 mg/dl. Somatostatin also significantly inhibted insulin release by the administration of 5microgram/ml of glucagon with 200 mg/dl of glucose concentration and 20 mM of orginine with 200mg/dl of glucose concentrations. But at the glucose concentration of 50mg/dl, no significant inhibition of somatostatin on insulin release was observed even when various concentrations of glucagon or arginine were added. The influence of somatostatin on peripheral tissues was examined in vitro, and no significant change on glucose uptake compared with the control group was shown in either tissues. The results indicated that somatostatin directly inhibited insulin release from rat pancreatic islets but had no effect on glucose uptake in peripheral tissues. The inhibitory effect of somatostatin on insulin release may act through the common mechanism of both glucose and other substances in leading to insulin release.
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PMID:[Effects of somatostatin on pancreatic isolated islets and peripheral tissues of rats]. 33 84

An animal model for testing the in vivo potency of somatostatin analogs in inhibiting the release of insulin and glucagon is described. The secretion of these pancreatic hormones was stimulated in rat by infusion of arginine. The plasma insulin level increased almost to a maximum after an infusion of 10 min, while plasma glucagon rose more slowly, reaching its maximum only after a 30 min infusion. Concomitant infusion of graded doses of somatostatin (2.5, 10, 40 and 160 microgram/100 g BW) for 30 min inhibited both insulin and glucagon release in a dose-dependent manner, enabling us to test somatostatin analogs for insulin and glucagon-suppressive activity in a semi-quantitative manner. Using this animal model, 3 analogs of somatostatin [D-Cys14]-, [Ala2, D-Cys14]- and [D-Trp8, D-Cys14]somatostatin were tested in a 4-point assay. They all showed dissociated activity in inhibiting the secretion of glucagon more than that of insulin.
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PMID:An in vivo model for testing inhibition of arginine-induced insulin and glucagon release by somatostatin analogs. 33 62

In this work we have investigated the effect of serotonin on glucagon release in mouse pancreatic islets isolated by the collagenase technique. Incubation of the islets with serotonin (4 X10(-3)mol/l) was associated with an inhibition of glucagon output both in the basal medium (3.3 mmol/l glucose) and in the presence of arginine (10 mmol/l). The inhibitory effect of serotonin on basal glucagon release was also apparent at concentrations of 2 X10(-3) mol/l, 10(-3)mol/l and 5 X 10(-4) mol/l. Addition of 5-hydroxytrypophan (4 X10(-3) mol/l) to the incubation medium was without effect on basal glucagon output while it significantly reduced arginine-induced glucagon release. In contrast, tryptophan (4 X10(-3) mol/l) provoked glucagon secretion. As inferred from our previous human studies, the present data indicate that serotonin is able to inhibit glucagon secretion. These findings provide further support for the participation of a serotoninergic mechanism in the control of A-cell function.
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PMID:Inhibition of glucagon release by serotonin in mouse pancreatic islets. 33 6

In order to investigate the action of caerulein upon insulin and glucagon secretion, experimental studies were carried out using anesthetized dogs, in which graded doses of caerulein were infused into the pancreatic artery, and insulin and glucagon were measured in the blood obtained from the pancreatic vein. When caerulein was administered at a rate of 15 ng/min, neigher changes of blood glucose in the femoral artery nor plasma levels of insulin or glucagon in the pancreatic vein were prominent. Caerulein infusion at a rate of 120, 240 or 480 ng/min caused a prompt rise of plasma insulin and a delayed increase of plasma glucagon in the pancreatin vein. Blood glucose in the femoral artery increased only with caerulein doses of 240 ng/min or more. A significant increase in pancreatic vein blood flow rate was demonstrated after the infusion of caerulein at a rate of 240 ng/min or more. Neither caerulein-induced insulin secretion nor glucagon secretion was influenced by a simultaneous infusion of glucose. In contrast, caerulein-induced glucagon secretion was exaggreated by a simultaneous arginine infusion. It was concluded from the present experiments that caerulein infusion into the pancreatic artery resulted in increased secretion of insulin and glucagon from the pancreas.
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PMID:Effect of caerulein upon insulin and glucagon secretion in dogs. 34 81

Insulin and glucagon have been studied in 20 subjects (both of the subjects' parents were diabetic or in case of only one diabetic parent, the other showed a first degree familiarity of diabetes): 10 showed normal glucose tolerance ('true prediabetics') and 10 impaired glucose tolerance ('genetic chemical diabetes'). Mean insulin response to oral (100 g) and i.v. glucose load (200 mg/kg followed by 20 mg/kg/min for 60 min) and to arginine infusion (25 g in 30 min) was normal in the prediabetics and delayed and higher in the subjects with chemical diabetes as compared to the control group. Glucagon response to arginine was higher, but not significantly, in prediabetics and in subjects with chemical diabetes. In both of these groups glucagon suppression by glucose was not observed. The insulin/glucagon molar ratio was significantly reduced after glucose infusion in these two groups. No correlation was found between insulin and glucagon secretion after arginine or glucose. A possible alteration in the mechanism controlling glucagon secretion even in the earliest phases of diabetes is suggested.
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PMID:Glucagon and insulin secretion in potential diabetes. 36 Jul 48

Functional alteration of the islet cells was investigated in dogs after the resection of different parts of the small intestine. Three weeks after jejunal or ileal resection, when the dogs might still have been in a catabolic state, insulin and pancreatic glucagon release in response to intravenously infused glucose and arginine was reduced. Three months after jejunal resection, both intravenous glucose tolerance and insulinogenic index in the intravenous glucose tolerance test were significantly below the preoperative values (P less than 0.001, P less than 0.05), while pancreatic glucagon release in response to arginine infusion release. This functional alteration three months after jejunal resection was similar to that seen in diabetes mellitus. On the other hand, three months after ileal resection, insulin and pancreatic glucagon release was almost normal. We conclude that the jejunum plays a more important role in the enteroinsular system than the ileum and that prolonged interruption of this enteroinsular axis can cause insular disorder and what could hypothetically be called enterogenic chemical diabetes, in view of the altered glucose tolerance test and the alteration in insulin secretory response.
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PMID:Functional alteration of islet cells after jejunal or ileal resection in dogs. 36 91

The release of glucagon from pancreatic and extrapancreatic sources was studied in normal rats and in rats carrying transplants of a MtT-W-15 tumor which secretes large quantities of growth hormone and prolactin. The tumor-bearing rats had high serum levels of A cell immunoreactive glucagon (IRGa), total immunoreactive glucagon (IRGT) and immunoreactive insulin (IRI) and an increased total glucagon and insulin content of the pancreas. Pancreatic islets isolated from tumor-bearing rats secreted more glucagon under basal conditions but did not respond significantly to low glucose stimulation. However, they contained more insulin per islet and secreted more insulin under basal and stimulated conditions. The serum IRGa response to arginine infusion in vivo was lower in the tumor-bearing than in the normal rats. The introduction of a 5% glucose solution into the small intestine caused similar increases in the level of serum IRGT in the two groups of rats. Thus, the tumor increased the total pancreatic glucagon content and basal secretion, blunted the A cell response to stimulation, but did not significantly alter the secretion of glucagon by the intestine. We attribute these responses to tumor-induced hypersomatotropinism although we cannot rule out an effect of the large amounts of circulating prolactin.
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PMID:Glucagon secretion in rats bearing a growth hormone producing tumor (MtT-W-15). 36 50


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