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 cell line In-R1-G9 is one of the clones from the hamster insulinoma cell line, In-111-R1, and it produces glucagon. Phorbol esters markedly enhanced glucagon secretion and the stimulatory effect was found to be correlated to their biological activity as tumor promoters. At a concentration of 200 nM, 12-O-tetradecanoylphorbol 13-acetate (TPA) stimulated glucagon secretion 13-fold more than the control in 10 min. The effect of TPA was not influenced by actinomycin D, cycloheximide, colchicine or vincristine. Depletion of calcium from the incubation medium inhibited TPA-induced glucagon secretion by approximately 50% and dibucaine also suppressed glucagon secretion to 67.4%. An addition of A23187 to TPA induced 150% enhancement over the TPA-stimulated glucagon level, and the maximum secretory response was observed when the cells were stimulated with the simultaneous addition of TPA, A23187 and theophylline.
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PMID:Effect of phorbol esters on glucagon secretion from a glucagon-secreting clonal cell line. Synergistic effects of A23187 and theophylline. 301 54

The rapid growth (0.8 +/- 0.3 g/day) of a transplantable insulinoma, which also contained substance P (2.9 +/- 2.3 pmol/g) and gastrin-releasing peptide (3.2 +/- 2.1 pmol/g), resulted in the development of hyperphagia, hyperinsulinaemia and hypoglycaemia in rats (n = 8). After a 14-day growth period, the insulinoma-bearing rats showed an increase (49%; p less than 0.01) in the weight of the small intestine but no significant change in stomach weight compared with control animals. The content (pmol/organ) of somatostatin, substance P, neurokinin A and vasoactive intestinal peptide in the stomachs of the tumour rats was unchanged. A depletion in the content (53% p less than 0.01) and concentration (57%; p less than 0.01) of gastrin-releasing peptide, however, suggested either hypersecretion, possibly mediated through hypoglycaemia-induced vagal stimulation, or inhibition of synthesis. The concentration and content of glucagon-like immunoreactivity (enteroglucagon) in the small intestine of the insulinoma rats increased markedly (47%; p less than 0.01 and 120%; p less than 0.01). This increase is consistent with a proposed role of this peptide as a factor trophic to the intestinal mucosa. No significant changes in the concentrations of somatostatin, substance P, neurokinin A, vasoactive intestinal peptide and gastrin-releasing peptide in the small intestine were observed. However, the increase in gut weight resulted in a greater content of vasoactive intestinal peptide (40%; p less than 0.01) and substance P (37%; p less than 0.05) in the insulinoma rats.
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PMID:Effects of a transplantable insulinoma upon regulatory peptide concentrations in the gastrointestinal tract of the rat. 301 8

The aim of this retrospective study was to correlate the results of hormonal immunocytochemistry of 46 endocrine tumors to the corresponding clinical syndromes in 24 patients. They were divided as following: 14 cases of insulinoma, 3 cases of Zollinger-Ellison syndrome, 1 case of glucagonoma, 1 case of carcinoid syndrome and 5 cases without any obvious endocrine manifestations. Each tumor was tested with anti-insulin, anti-glucagon, anti-pancreatic polypeptide, anti-vasoactive intestinal peptide, anti-gastrin immune sera according to the peroxidase-antiperoxidase method. The presence of insulin was proved in 13 of 14 cases of insulinomas and the presence of gastrin in 2 of 3 cases of Zollinger-Ellison syndrome. Among the 5 asymptomatic cases, a somatostatinoma and a vipoma were individualized. More than 50 p. 100 of the tumors showed plurihormonal secretion with one predominantly secreted hormone responsible for the clinical syndrome. This study demonstrated the diversity of the hormonal secretion by some tumors and their metastasis in the same patient. Malignant insulinomas correspond either to poorly secreting tumors or to plurihormonal tumors secreting gastrin and glucagon as well.
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PMID:[Hormone immunocytochemical studies of 46 endocrine tumors of the pancreas in 24 patients]. 301 9

Monolayer cell cultures were obtained from a human insulinoma (HIN) after collagenase digestion. HIN cells were initially plated on extracellular matrix (ECM) secreted by bovine corneal endothelial cells. Capsular integrity from cell clusters quickly interrupted and cell began to migrate as adhesive sheets onto ECM. After 2 months on ECM cell attachment and proliferation occurred on plastic allowing cloning of cells by limiting dilution. 9 clones were successfully cultured for 7 months with 20 subsequent passages. Immunoreactivity for insulin by indirect immunofluorescence typical secretory granules by electron microscopy and stable amounts of immunoreactive insulin in culture media suggest that HIN cells are beta cell related. One clone HIN D8 when challenged for half an hour with either 30 mM glucose, 1 mM isobutyl Methylxanthine 4 mM Tolbutamide, 10(-6) M glucagon responded respectively with a 1.5, 2, 3 and 1.5 fold increase in insulin output. Population doubling time of HIN D8 was 42 hrs. Establishment of such insulin secreting cell lines provides a valuable tool for diabetes research.
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PMID:[Morphologic and functional study of a human insulin-secreting cell line]. 302 94

To define glucose flux in a state of chronic endogenous insulin excess, a patient with an insulinoma was studied. Plasma glucose, insulin (IRI), glucagon (IRG) and glucose turnover ([3-3H]glucose infusion) were measured before and after insulinoma resection in the postabsorptive state (PA), during a glucose infusion adjusted to attain euglycemia (before insulinoma resection only) and following an intravenous glucagon bolus (1 mg). Before insulinoma resection, plasma glucose was 55 mg/dl, glucose production (Ra) and disappearance (Rd) were equal (1.6 mg/kg/min) and glucose clearance was elevated (2.8 ml/kg/min) in PA. When glycemia was raised with a glucose infusion to 77 mg/dl, Rd did not change; in contrast Ra dropped to zero. Plasma IRI and IRG concentrations were 0.7 ng/ml and 110 pg/ml respectively before glucose infusion and remained constant throughout. After resection of the insulinoma, glycemia in PA was 103 mg/dl, Ra and Rd were increased slightly to 1.9 mg/kg/min while the metabolic clearance of glucose was decreased by 25% (2.1 ml/kg/min). Glucagon stimulation pre- and postinsulinoma resection resulted in significant increases in glycemia and IRI. We conclude that hypoglycemia with insulinoma is a consequence of decreased glucose production and increased glucose clearance. Hepatic sensitivity to small increments in glycemia is markedly enhanced so as to fully suppress endogenous glucose production at euglycemic levels in the absence of any change in IRI and IRG. The mechanisms controlling hepatic Ra in insulinoma appear different from normal.
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PMID:Glucose turnover in insulinoma--a case report. 303 48

Insulin secretion is controlled by a complex set of factors. Although blood glucose levels serve as the major stimulus of insulin secretion in mammals, insulin release is also modulated by amino acids, catecholamines, glucagon, and other, intestinal hormones. The identification of factors that modulate insulin production has engendered much interest because of their potential importance in the altered dynamics of insulin secretion in response to glucose characteristic of maturity-onset diabetes mellitus. Decoding of the glucagon gene has uncovered two additional glucagon-like peptides encoded in proglucagon, the polypeptide precursor of glucagon. One of these peptides, glucagon-like peptide I, is processed from proglucagon in two forms, of 31 and 37 amino acids. We report that the smaller of the two glucagon-like peptides potently increases cAMP levels, insulin mRNA transcripts, and insulin release in cultured rat insulinoma cells. These results indicate that glucagon-like peptide I may be a physiologic modulator of insulin gene expression.
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PMID:Glucagon-like peptide I stimulates insulin gene expression and increases cyclic AMP levels in a rat islet cell line. 303 47

A novel putative polypeptide hormone identified as islet amyloid polypeptide (IAPP) was recently purified from islet amyloid (IA) of diabetic humans and cats, and also from amyloid of a human insulinoma. Although the function of IAPP is yet unknown, its occurrence in pancreatic endocrine tissue and its partial amino acid sequence identity with calcitonin gene-related peptide (CGRP) suggests an endocrine regulatory effect. In the present investigation, the authors utilized antisera to insulin, glucagon, somatostatin, pancreatic polypeptide, synthetic human CGRP, and a synthetic human IAPP (7-17) undecapeptide to immunohistochemically (PAP technique) document the presence of IAPP immunoreactive cells in the islets of the cat, dog, mouse, and rat, but not in the islets of the horse or calf. In serial sections of islets from these species it was shown that IAPP immunoreactivity occurred in insulin-reactive beta cells. This observation was confirmed immunocytochemically in cat islets by means of protein A-gold probes. With protein A-gold labeling techniques, IAPP immunoreactivity was localized to the outer lucent compartment of the beta cell secretory granule, whereas insulin immunoreactivity was associated with the electron-dense core. These findings provide strong evidence that IAPP or an IAPP precursor is synthesized by beta cells and is stored in beta cell granules for subsequent co-secretion with insulin. The conservation of IAPP in humans and multiple animal species and the localization of IAPP to pancreatic beta cells provide further evidence that IAPP has an important endocrine regulatory function. The propensity of IAPP to polymerize and form IA fibrils in diabetes associated with aging may indicate that IAPP is in some way also linked to the development of Type 2 diabetes.
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PMID:Immunolocalization of islet amyloid polypeptide (IAPP) in pancreatic beta cells by means of peroxidase-antiperoxidase (PAP) and protein A-gold techniques. 327 6

The state of differentiation of various neoplastic cell lines is inversely correlated with the rate of cellular growth. To delineate the changes in hormone gene expression associated with an induced decrease in the growth rate of rat insulinoma cells, we studied the effects of sodium butyrate on the expression of the genes encoding insulin, glucagon, and angiotensinogen. Sodium butyrate inhibited cellular proliferation and decreased levels of c-myc mRNA. Concomitantly, steady-state levels of mRNAs encoding insulin and glucagon increased by 10- and 8.5-fold, respectively, as a result of a specific increase in the transcription of both genes. Sodium butyrate also inhibited angiotensinogen gene expression, which was ectopic in the insulinoma cells. These observations suggest that sodium butyrate induces a pattern of events leading to the differentiation of the rat insulinoma cells.
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PMID:Transcriptional regulation of genes encoding insulin, glucagon, and angiotensinogen by sodium butyrate in a rat islet cell line. 355 Apr 24

The capillary blood glucose response to lmg of intramuscular glucagon was determined in 13 patients with insulinoma and in 33 normal controls; the insulinoma patients showed a normal initial rise, but this was followed by an abnormally large fall, reaching hypoglycaemic levels between 90 and 180 minutes in every case. In 14 insulinoma patients the response of venous blood glucose and also plasma insulin to lmg of intravenous glucagon was compared with 10 normal controls; there was an abnormally large rise of plasma insulin in 10 of the 14 patients, and in the majority the venous blood glucose was below normal throughout the test. In these 14 patients the plasma insulin response was also determined after oral and intravenous glucose, after oral leucine, and after intravenous tolbutamide, and the value of these tests in the recognition and differential diagnosis of insulinoma was compared with that of the intravenous glucagon test.
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PMID:Glucagon test for insulinoma: a chemical study in 25 cases. 430 88

Glucagon-producing cell lines were established by fusing pancreatic islet cells of adult hamster and 6-thioguanine-resistant hamster insulinoma cells. Under phase-contrast microscopy, the morphology of cultured hybrid cells was intermediate between those of the parental cells. The hybrid cells contained A-like granules, though few in number, and were stained with anti-glucagon antibody. The mode of chromosome number decreased to 78 or 79 by 3 mo after hybridization in comparison with the expected chromosome number of the heterokaryon of 104, and showed a minute decrease in 4 of 6 cell lines after 6 mo. The population doubling time ranged from 24 to 38 h, while that of parental insulinoma cells was 22.8 h. There was no correlation between the expression of cellular function and the stability of chromosome number or the length of population doubling time. The capacity of glucagon secretion was between that of the parental cells. The glucagon secreted into the medium, as assayed by the glucagon-specific antibody, was 0.6-2.5 ng/10(6) cells for 2 h, which was about 40% of total glucagon-like immunoreactivity secreted. Secretion of glucagon was not affected by high concentration of glucose, was markedly increased by theophylline, and was suppressed by exogenous insulin. All of the hybrid cells produced tumors on transplantation 6 mo after hybridization. The tumor-bearing hamsters exhibited high levels of plasma glucagon and blood glucose as well as a high level of serum insulin.
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PMID:Establishment of glucagon-producing cells by cell hybridization. 608 32


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