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)

Glucagon-like peptide-1(7-36)amide [GLP-1(7-36)amide], a new important incretin candidate, binds to specific high-affinity receptors on rat insulinoma-derived beta-cells (RINm5F). In the present study, the effect of somatostatin-14 on the GLP-1(7-36)amide-induced insulin release and cAMP generation in this cell line was investigated. Somatostatin did not decrease basal insulin release of RINm5F cells. The GLP-1(7-36)amide-induced insulin release was decreased concentration dependently by somatostatin. Somatostatin, 1 microM reduced the maximally GLP-1(7-36)amide-stimulated (0.1 microM) insulin release to basal insulin levels. The GLP-1(7-36)amide-induced cAMP production was significantly decreased by somatostatin in a concentration-dependent manner. The GLP-1(7-36)amide concentration causing half-maximal cAMP production was 2.98 +/- 1.56 nM. Somatostatin left the EC50 unaltered but decreased the maximal GLP-1(7-36)amide effect for 32% in the presence of 1 nM somatostatin and for 50% at 1 microM. In additional experiments, the interaction of both hormones was evaluated in the perfused pancreas as a nontumor model. Somatostatin (1 nM, 1 microM) inhibited the glucose-induced (6.7 mM) and GLP-1(7-36)amide-potentiated (0.05, 0.5, and 5 nM) insulin release dose dependently. The biphasic pattern of insulin release remained preserved. The GLP-1(7-36)amide-induced insulin release is potently inhibited by somatostatin-14. This effect was demonstrated in different model systems for beta-cell function studies. The present data allow the conclusion that the somatostatin action upon GLP-1(7-36)amide effects is at least partly related to regulation of intracellular cyclic nucleotides.
Pancreas 1989
PMID:Interaction of glucagon-like peptide-1(7-36)amide and somatostatin-14 in RINm5F cells and in the perfused rat pancreas. 257 56

We studied the intrapancreatic localization of peptide YY (PYY) and the effects of PYY on insulin and glucagon secretion in the mouse. Immunofluorescence staining of mouse pancreatic tissue showed that PYY occurred within islet cells. These cells were located preferentially at the periphery of the islets. Sequential and simultaneous double immunostaining revealed that most PYY cells also displayed glucagon immunoreactivity; some PYY cells contained immunoreactive pancreatic polypeptide (PP). At the electromicroscopic level, PYY immunoreactivity was demonstrated within the secretory granules of both glucagon cells and of a small granular cell type, which showed structural similarities to PP cells. In in vivo experiments, PYY at dose levels between 0.53 and 8.5 nmol/kg had no influence on basal plasma levels of insulin, glucagon, or glucose. In contrast, insulin secretion stimulated by glucose or the cholinergic agonist carbachol was inhibited by PYY (by 33 and 26%, respectively, at 4.25 nmol/kg). Similarly, carbachol-induced glucagon secretion was inhibited by PYY (by 47% at 4.25 nmol/kg). We conclude that PYY occurs in islet cells of the mouse pancreas, most of which are glucagon cells, and that PYY inhibits stimulated insulin and glucagon secretion in vivo in the mouse.
Pancreas 1989
PMID:Peptide YY: intrapancreatic localization and effects on insulin and glucagon secretion in the mouse. 266 Jan 31

Protein-rich meals stimulate secretion of insulin, glucagon, and pancreatic polypeptide (PP) from the endocrine pancreas. On the one hand, this is due to increased levels of circulating amino acids, and, on the other, neural and/or endocrine factors can contribute to activation of islet cell function. The present study was designed to determine, first, pancreatic endocrine function and postprandial amino acid levels after a protein and a protein-carbohydrate meal and second, insulin, glucagon, and PP levels during infusion of amino acid mixtures that imitate the postprandial amino acid pattern. In healthy volunteers the ingestion of a protein-rich meal (300 g tenderloin steak) elicited within 1 h an increase of virtually all amino acids by 20-400 mumol/L above basal values. The infusion of two different amino acid solutions available for use in humans showed that Aminosteril-N-Hepa (AS) was better for the imitation of the so-called "insulinogenic" amino acids while Aminoplasmal L-10 (AP) gave more comparable plasma levels of the "glucagonogenic" amino acids. Both solutions were not able to imitate the postprandial amino acid pattern completely. With regard to insulin levels, both solutions gave a comparable increase, while AP but not AS stimulated glucagon and PP levels. This suggests that circulating amino acids may be responsible for 60% of the postprandial insulin response after a protein meal, while their contribution to glucagon release can only be roughly estimated at 30-60%. The contribution of circulating nutrients to the greater insulin response after the protein-carbohydrate meal was comparable (60%), while the attenuated glucagon response can be ascribed almost completely to the effect of circulating nutrients. In conclusion, the present data demonstrate that the composition of amino acid mixtures is as yet not ideal for a complete imitation of the postprandial amino acid pattern. The insulin, glucagon, and PP response depends on the amino acid mixtures and accordingly the respective plasma amino acid concentrations obtained during infusion studies. The adequate imitation of plasma amino acid levels is of critical importance for the evaluation of absorbed and circulating amino acid effects in the postprandial state.
Pancreas 1989
PMID:Role of amino acids in stimulation of postprandial insulin, glucagon, and pancreatic polypeptide in humans. 266 Jan 33

Using cultured islet cells from both splenic lobe (SL) and uncinate process (UP) of the dog pancreas, we have measured responses of insulin, glucagon, and pancreatic polypeptide (PP) to glucose, carbamylcholine (carbachol), and exogenous PP. The results show that both insulin and PP cells of the two developmentally distinct lobes of the pancreas respond differentially to secretagogues. The results suggest that PP may play a role in regulation of islet cell secretion. Secretion of insulin by SL and UP cultures in response to 28 mM glucose in a 2h incubation was significantly greater, 2.9- (p less than 0.01) and 1.5-fold (p less than 0.01), respectively, than secretion by respective control cultures at 2.8 mM glucose. The difference in degree of stimulation between SL and UP was also significant (p less than 0.02). At 2.8 mM glucose, SL and UP cultures secreted 10% and 8.8%, respectively, of immunoreactive insulin (IRI) contents of the cultured cells (NS). Dose-response curves showed that for up to 8.5 mM glucose the degree of stimulation of SL was no greater than UP, but the UP response had nearly plateaued; whereas, the SL response continued to increase, such that SL was greater than UP at 16.7 mM glucose (p less than 0.01). Secretion of PP by SL and UP cultures in response to 5 microM carbachol and 2.8 mM glucose in a 2-h incubation was significantly greater, 2.2- (p less than 0.002) and 3.9-fold (p less than 0.002), respectively, than secretion by respective control cultures without carbachol. The difference in degree of stimulation between SL and UP was also significant (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Pancreas 1989
PMID:Lobe-specific responses of cultured islet cells of canine pancreas to carbamylcholine, glucose, and pancreatic polypeptide. 266 82

As insulin is a regulator of cartilage and bone growth, plasma levels of pancreatic hormones were determined in 41 lame male turkeys with long bone distortion and 42 control toms without leg deformities. Blood samples were collected 3.5 h following the removal of feed and then 1 h after the return of feed. The day following blood collection, toms, 119 days of age, were slaughtered to obtain leg measurements. Body weight, width, and length of the tarsometatarsus, presence of tibial dyschondroplasia (TD) lesions, pancreas weight, and plasma glucose did not differ between lame and control turkeys. A significantly greater proportion of growth plates of the tarsometatarsus was closed in the control as compared to the lame turkeys. Pancreas weight relative to BW was significantly greater for lame as compared to control turkeys. Plasma insulin was undetectable in both fasted lame and control turkeys. When feed was returned to the turkeys, plasma insulin concentrations were significantly lower in lame compared to control turkeys. The return of feed had no effect on plasma glucagon levels in controls, but concentrations were decreased significantly in lame birds. These data suggest that the regulation of plasma insulin and glucagon may be altered in lame turkeys perhaps contributing to the cause of long bone distortion.
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PMID:Plasma insulin and glucagon levels and leg measurements of lame turkeys. 268 88

The present study was designed to determine the effect of low doses of cholecystokinin (CCK) on insulin, glucagon, and pancreatic polypeptide (PP) secretion in the basal state and during prestimulation with amino acids and glucose alone or in combination. Two different amino acid solutions available for use in humans were employed. Aminosteril-N-Hepa was better for the imitation of the so-called "insulinogenic" amino acids while Aminoplasmal L-10 gave more comparable plasma levels of the "glucagonogenic" amino acids as observed after a protein-rich meal. In healthy volunteers, low-dose CCK infusion [Thr28,Nle31-CCK 25-33 (CCK-9)] in stepwise increasing doses of 5, 10, and 20 pmol/kg/h had no effect on basal, glucose-, or amino acid-stimulated insulin release. During the combination of Aminoplasmal + glucose, there was a small and only transient increase of plasma insulin levels that did not occur during Aminosteril + glucose. CCK did not alter glucagon levels either during i.v. amino acids alone or during combination of amino acids with glucose. CCK-stimulated PP levels in the basal state in a dose-dependent manner. This effect was enhanced during i.v. Aminosteril but not i.v. Aminoplasmal infusion. During i.v. glucose, the effect of CCK on PP levels was abolished. In conclusion, the present data demonstrate that CCK is unlikely to be a stimulus of insulin and glucagon secretion in the basal state and also during prestimulation by fairly physiological quantities of amino acid mixtures. On the other hand, the present data support a physiological role of CCK in the regulation of PP secretion.
Pancreas 1989
PMID:Effect of CCK on insulin, glucagon, and pancreatic polypeptide levels in humans. 268 4

Surgical fragments of healthy and tumor-bearing pancreas from a patient with pancreatic tumor were studied by electron or light microscopy, histochemistry, and immunocytochemistry (human insulin, glucagon, somatostatin, gastrin, and bovine pancreatic polypeptide). Histological results were compared to those obtained by radioimmunoassay, both in tumor and serum. The tumor was identified as a glucagonoma because reactions for Grimelius' silver impregnation and immunoreaction with an antiserum against glucagon were positive and because a very high level of glucagon in the tumor was observed. Insulin, somatostatin, and gastrin levels remained normal, both in tumor and serum, but the glucagon level was normal in serum. Associated with this silent glucagonoma, an uncommon nesidioblastosis was also diagnosed with many A cells irregularly mixed with acinar cells, isolated or clustered in small groups. Acinar "intermediate" cells of "A" type were also observed. Such associative histopathological processes evoked possible development of an endocrine tumor from nesidioblastic-like tissue. Its embryogenic origin remained uncertain.
Pancreas 1988
PMID:Silent human pancreatic glucagonoma and "A" nesidioblastosis. 285 84

The amounts of insulin, glucagon and somatostatin in the pancreas of NOD mice were determined and the results were compared with those of normal ICR-strain mice, and plasma antibodies to Coxsackie B-3 and reovirus types 1, 2 and 3 were measured. In the pancreas of NOD mice with fasting plasma glucose (FPG) less than 140 mg/100 ml, the insulin content of the male mice was similar to that of the normal controls, ranging to 3.55 +/- 0.31 U/g wet weight of pancreas, but it was already significantly decreased to 0.85 +/- 0.52 U/g in the female mice. In the NOD mice with FPG more than 201 mg/100 ml, it was 0.002 +/- 0.001 U/g. The glucagon content of the pancreas was 7.76 +/- 0.89 micrograms/g in the normal controls and it was decreased slightly in the NOD mice, but the values among the NOD mice were not significantly different. Pancreas somatostatin showed a tendency to be higher in the NOD mice with FPG more than 201 mg/100 ml. Histologically cell infiltration into the pancreatic islets was conspicuous in the hyperglycemic NOD mice, but it was found even in the normoglycemic NOD. Plasma antibodies to Coxsackie B-3 Virus and reovirus types 1, 2 and 3 were not detected at any stage of FPG.
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PMID:Insulin, glucagon and somatostatin content of the non-obese diabetic (NOD) mouse pancreas and plasma virus antibodies to Coxsackie B- and reoviruses. 286 17

A 41-year-old woman with metastatic glucagonoma and the characteristic disabling rash, necrolytic migratory erythema, was treated with a synthetic somatostatin analog while waiting to undergo curative surgical resection. Plasma glucagon concentration (1,500-3,300 pg/ml, normal less than 200) remained elevated during analog therapy as the rash cleared. Only with surgical resection (partial pancreatectomy and partial hepatectomy) did glucagon levels return to normal. The therapeutic benefit caused by the analog in this syndrome differs from that in other endocrine tumor syndromes such as pancreatic cholera, carcinoid, or gastrinoma where circulating levels of tumor-produced agents are suppressed in conjunction with control of symptoms.
Pancreas 1986
PMID:Somatostatin analog-induced remission of necrolytic migratory erythema without changes in plasma glucagon concentration. 288 3

The pathophysiological, biochemical, histological, ultrastructural, and immunohistochemical characters of a case of malignant pancreatic islet cell tumor with watery diarrhea syndrome were carefully investigated. Four hormones or mediators--somatostatin (SST), vasoactive intestinal peptide (VIP), serotonin, and prostaglandin E--were markedly elevated in the circulation. The diagnosis was further confirmed by exploratory laparotomy and autopsy. The contents of SST and VIP in tumor tissues were very high. Gel chromatography of tumor extract revealed single peaks for both SST and VIP. Immunohistochemical studies of tumor tissues showed numerous immunoreactive cells to anti-SST, moderate amount of VIP-positive cells, and a few hCG-, insulin-, and glucagon-positive cells. In conclusion, this is an unusual case of Verner-Morrison syndrome in which three kinds of bioactive hormones or mediators were simultaneously secreted; peptides, amine, and prostaglandin.
Pancreas 1986
PMID:Watery diarrhea syndrome caused by multihormonal malignant pancreatic islet cell tumor secreting somatostatin, vasoactive intestinal peptide, serotonin, and prostaglandin E--a clinicopathological, biochemical, immunohistochemical, and ultrastructural study. 288 47


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