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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Islets were isolated by mild collagenase digestion and microdissection from rat fetuses 2 days before term and pups 1 or 2 days after birth and their insulin and glucagon secretion studied in vitro. Fetal B cells were stimulated by 16.7 mmol/l glucose, 20 mmol/l leucine or 20 mmol/l arginine. Fetal A cells were not affected by glucose or leucine, but were significantly stimulated by arginine. Somatostatin abolished the effect or arginine on both IRI and IRG output. Neonatal islets proportionally released more insulin and glucagon than their fetal counterparts, but reacted to the tested agents in a similar fashion. During the perinatal period, pancreatic insulin storage increased at a higher rate than that of glucagon. It is concluded that fetal B cells are equipped with sensors to a variety of agents and able to modulate their secretory rate according to the concentration of these agents. A cells are reactive to arginine 2 days before term but do not become glucose reactive until several days after birth.
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PMID:Insulin and glucagon secretion by islets isolated from fetal and neonatal rats. 36 57

Previous studies have demonstrated that prostaglandins stimulate glucagon secretion in vitro and in vivo. The present work was aimed at investigating the influence of two inhibitors of prostaglandin synthesis, isopropyl-2 nicotinoyl-3 indole (L8027) and indomethacin, on basal and arginine- or noradrenaline-stimulated glucagon release from isolated guinea-pig islets incubated in the absence of glucose. L8027 (10(-4) and 10(-5) mol/l) did not alter basal glucagon release, blocked almost completely the glucagon response to arginine (10(-2) mol/l), had no effect on the glucagon release induced by noradrenaline (10(-4) mol/l), but reduced the stimulatory effect of a lower concentration of noradrenaline (5.10(-7) mol/l). The kinetic study of this inhibitory effect demonstrated that (1) it necessitates preincubation of the islets with L8027 for 30 minutes before the addition of arginine, (2) after a short preincubation period (30 minutes) in the presence of L8027, removal of the inhibitor at the time of arginine stimulation resulted in enhanced glucagon response, (3) on the contrary, after a prolonged incubation period (75 min) with arginine and L8027, the inhibitory effect remained transiently detectable after removal of L8027. Indomethacin similarly blocked arginine- and noradrenaline-induced glucagon secretion. These results suggest that an intra-insular synthesis of prostaglandins is involved in the A cell response to arginine and noradrenaline.
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PMID:Possible role of endogenous prostaglandins in glucagon secretion by isolated guinea-pig islets. 36 55

To determine the dynamics of insulin and of glucagon secretion in response to several sequential stimuli administered shortly after an arginine pulse (5 g), 20 nonobese, apparently healthy volunteers were given arginine (5 g), glucose (5 g), and tolbutamide (1 g) by rapid intravenous injection. The early insulin and glucagon area 0-8 min was studied. At the intervals and with the dosages used in this study, different stimuli with and without prestimulation with arginine did not lead to changes in early secretion of insulin. There was no exhaustion of the pool of insulin released after multiple sequential pulses. These results suggest a pattern in which stimulation induces a rapid release of insulin and activates the interchange between the stored and labile insulin pool; the 8-min interval is sufficient for the rapid return of the two compartments to a state of equilibrium. Also for glucagon, subsequent different stimuli did not exhaust glucagon release; nevertheless, glucagon is immediately suppressed by a submaximal glucose pulse.
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PMID:Early insulin and glucagon response to subsequent pulses of arginine, glucose, and tolbutamide in normal man. 36 91

The calcium dependency of glucagon release by the perfused rat pancreas was investigated in the presence of different nutrients: glucose, arginine, and a mixture of "fumarate + glutamate + pyruvate" (FGP, 5 mM of each salt). At a 3.3 mM glucose concentration, FGP-induced glucagon release was inhibited by the removal of calcium or addition of verapamil. At a higher glucose concentration (16.6 mM), the glucagonotropic action of FGP was again inhibited by verapamil, but the removal of extracellular calcium enhanced transiently glucagon release. Comparable results were obtained when arginine (10 mM) instead of FGP was used to stimulate the alpha cell. These findings suggest that the glucagonotropic effect of FGP or arginine depends on the availability and inward transport of calcium, whereas extracellular calcium per se may be required for glucose to be sensed by the alpha cell as an inhibitor of glucagon secretion. Thus, the nutritional environment offered to the alpha cell may condition the expression of the different mechanisms involved in the control of glucagon release by calcium.
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PMID:Calcium dependency of glucagon release: its modulation by nutritional factors. 36 92

The acute in vitro effect of alloxan on glucagon and insulin secretion from the isolated perfused rat pancreas was examined. Alloxan alone produced transient insulin secretion. Pretreatment with alloxan attenuated both the stimulatory effect of glucose on insulin secretion and the inhibitory effect of glucose on glucagon secretion. Exposure to alloxan in varying doses either partially or completely inhibited insulin secretion induced by arginine in the presence or absence of glucose. On the contrary, pretreatment with alloxan produced complex effects on arginine-induced glucagon secretion. In the absence of glucose, the response of glucagon to arginine infusion was lower in the pancreas exposed to alloxan than in the control experiment. In the presence of glucose, however, an apparently augmented response of glucagon to arginine was observed after exposure to higher doses of alloxan, suggesting an impaired inhibitory effect of glucose on arginine-induced glucagon secretion. These effects of pretreatment with alloxan on glucagon secretion can not be explained by earlier or simultaneous insulin secretion. Therefore, we conclude that alloxan acts not only on beta-cells, but also directly on alpha-cells, although the latter are less sensitive to this agent.
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PMID:Modulation by alloxan of glucagon and insulin secretion in the isolated perfused rat pancreas. 36 31

A tissue culture-perifusion system is described that allows for long-term culture of pancreatic islets and study of the dynamics of islet hormone secretion. Islets cultured in this system demonstrate brisk, reproducible biphasic insulin and glucagon release. Glucose-stimulated insulin release is similar after 1 or 14 days in culture. Freshly isolated islets are relatively insensitive to somatostatin, requiring 100 ng/ml to suppress partially the glucose-induced insulin secretion. After 24 h of culture, the same islets demonstrate a marked increase in sensitivity to this hormone. Glucagon secretion from islets maintained in this system occurred in a predictable fashion to arginine stimulation and glucose inhibition.
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PMID:Insulin and glucagon secretion from rat islets maintained in a tissue culture-perifusion system. 37 72

The effects of neurotensin on the release of insulin, glucagon, and somatostatin were investigated in isolated pancreatic islets prepared from 3- to 4-day-old rats and maintained in culture for 48 h before use. Islets were incubated for 20 and 60 min in the presence of 3 or 23 mM glucose with or without neurotensin. In 20-min incubations at 3 mM glucose, neurotensin (10-100 nM) increased the release of insulin, glucagon, and somatostatin by 60%, 90%, and 110%, respectively. These increases were not detected in 60-min incubations. Neurotensin (100 nM) inhibited the release of both insulin (by 60-90%) and somatostatin (by 100%) which was induced by 23 mM glucose in 60-min incubations; this inhibitory effect could be detected with neurotensin at a concentration of 1 nM. Neurotensin also significantly inhibited the elevations in glucagon, insulin, and somatostatin release induced by 20 mM arginine. It is concluded that neurotensin exerts a dual effect on the endocrine pancreas in vitro: 1) at low glucose concentration and over short term (20 min) incubations, the peptide stimulates insulin, glucagon, and somatostatin release; and 2) under stimulated conditions (high glucose or arginine), neurotensin inhibits insulin, glucagon, and somatostatin release.
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PMID:Effect of neurotensin on insulin, glucagon, and somatostatin release from isolated pancreatic islets. 37 97

The present status of knowledge about glucagon pathophysiology in diabetes is reviewed. 1) A-cells behave abnormally in all varieties of diabetes mellitus, spontaneous and experimental, except perhaps in case of pancreatectomized humans. These abnormalities are : hyperreactivity of A-cells to arginine, non suppressibility by glucose, and absence of stimulation following hypoglycemia. 2) These abnormalities appear as secondary in most instances : a) A-cells behave in a normal way in most studies with prediabetics ; b) plasma glucagon concentration is normalized by excellent control of diabetes or following prolonged insulin infusion. High doses of insulin are required most of the times to obtain a normalization of A-cell function : in insulin-dependent diabetics, the physiological portoperipheral insulin gradient no longer exists, and the high doses of insulin which are necessary may be the only mean to reconstitute the high insulin concentrations supposed to be present at the A-cell level. 3) Conflicting results have been collected about the role of this glucagon excess in aggravating the diabetic metabolic syndrome. Evanescent effects follow sustained glucagon infusions: but in diabetics, glucagon bursts rather than permanent hyperglucagonemia are observed and these appear deleterious to glucose tolerance. It seems clear however that insulin deprivation is required for the full expression of the consequences of glucagon excess.
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PMID:Glucagon and diabetes mellitus. 37 65

Obesity in the Zucker rat is accompanied by hyperlipemia, hyperinsulinism, insulin resistance, pancreatic hyperplasia, and islet hypertrophy. This study correlates the morphologic heterogeneity of isolated pancreatic islets with secretion of insulin and glucagon in the perifusion system. Islet size was arbitrarily defined as large (greater than 0.45 mm) or small (smaller than 0.12 mm). Protein content and volume (V = 4/3pir3) were calculated for groups and individual islets, respectively. Islets from obese rats secreted more insulin in response to glucose and aminophylline than islets from lean rats (peak 7.8 +/- 2.4 vs. 1.5 +/- 0.37 microU/islet/min, P less than 0.005). Insulin release was related directly to islet size and protein content. Small islets from lean and obese animals produced less insulin per islet than large islets (P less than 0.005). In terms of islet volume, however, large islets were inefficient insulin releasers as compared to small islets (P less than 0.005). Stimulation with Br-cAMP released glucagon from islets of lean but not from large islets of obese animals (peak 11 +/- 3.3 vs. 4.1 +/- 0.3 pg/microgram protein per minute, P less than 0.05). Arginine produced the same effect on glucagon release (P less than 0.05) as stimulation with Br-cAMP. The observed increased insulin release rates and the blunted glucagon response are related to islet size in the pancreas of the Zucker rat.
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PMID:Correlation between morphology and function in isolated islets of the Zucker rat. 37 79

Arginine infusion tests were carried out in seven patients with pheochromocytoma before and after extirpation of the tumors in order to evaluate pancreatic islet alpha- and beta-cell function during the state of endogenous catecholamine excess. Six of the patients had glucose intolerance; one did not. Preoperatively, the pancreatic glucagon response was suppressed, while the insulin response was comparable to that in normal control subjects. Plasma glucose levels decreased rapidly after the beginning of arginine infusion in all patients. Theses changes during the infusion were evident in the one patient without glucose intolerance. Postoperatively, the glucagon response and plasma glucose changes were normalized. In addition to the obvious suppression of pancreatic alpha-cell function in our patients with pheochromocytoma, it seems likely that pancreatic beta-cell function also was suppressed; there was no enhancement of the insulin response to arginine during the period of chronic hyperglycemia, a situation in which a synergistic effect between glucose and arginine might be expected.
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PMID:Pancreatic alpha- and beta-cell function in pheochromocytoma. 38 21


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