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)

Concentrations of regulatory peptides in an extract of the intestine of the cyclostome, Myxine glutinosa (Atlantic hagfish), were measured by radioimmunoassay using 12 antisera of defined regional specificity that were raised against mammalian gastrointestinal peptides. The hagfish gut contained somatostatin-, cholecystokinin/gastrin-, C-terminal substance P-, and neurokinin A-like immunoreactivity in concentrations that were 10 to 100 times less than the corresponding concentrations in the rat intestine. The hagfish gut also contained glucagon-like immunoreactivity, measured with both C- and N-terminally directed antisera, but the immunoreactivity did not dilute in parallel with the porcine glucagon standard in radio-immunoassay. No immunoreactivity was detected using antisera to calcitonin gene-related peptide, gastrin-releasing peptide, neuromedin U, neurotensin, N-terminal substance P, and vasoactive intestinal polypeptide. The somatostatin-like immunoreactivity in the hagfish gut was resolved by HPLC into components with the retention times of somatostatin-34 and somatostatin-14, previously isolated from the hagfish islet organ (relative abundance 2:1). The retention times of hagfish glucagon and of the multiple molecular forms of the tachykinin-like peptides were appreciably different from the retention times of the corresponding mammalian peptides.
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PMID:Neurohormonal peptides in the gut of the Atlantic hagfish (Myxine glutinosa) detected using antisera raised against mammalian regulatory peptides. 248 Feb 67

We previously reported that sulfonylurea treatment reduces insulin (IRI), glucagon (IRG) and somatostatin (SRIF) release following metabolic stimuli from the isolated perfused pancreas of normal rats and that a reduction in IRI, IRG and SRIF pancreatic content was also observed. The present work was undertaken to investigate the effects of long-term glibenclamide treatment on the gastrointestinal content of gut hormones in normal rats. Moreover, the effects of sulfonylurea treatment on IRI, IRG, and SRIF pancreatic content were also analyzed and compared to the peripheral hormone plasma levels. Two groups of male Sprague-Dawley rats received glibenclamide (1 mg/kg/day per os; n = 14) or placebo (distilled water; n = 10) for 5 months, respectively. Tissue contents of IRI, IRG and SRIF in acid-ethanol extracts of pancreas and of gastric inhibitory peptide (GIP), vasoactive intestinal polypeptide (VIP), entero-glucagon (gut-GLI) and SRIF in acid-ethanol extracts of intestine were determined. Blood glucose and plasma pancreatic hormone levels were also measured. Glibenclamide treatment lowered the levels of IRI, IRG and SRIF in the pancreatic tissue; in the same way gut-GLI, SRIF and VIP intestinal concentrations were significantly reduced, whereas no significant inhibition was detected in intestinal GIP content. Blood glucose levels and IRI and SRIF plasma concentrations were similar in the two groups. IRG plasma levels were reduced in the sulfonylurea group. These findings might suggest that sulfonylurea suppresses hormone biosynthesis in a non-specific manner.
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PMID:Effects of long-term glibenclamide administration on gastrointestinal and pancreatic hormones in normal fasting rats. 249 27

A protein that inactivates the immunoreactivity of GnRH, TRH and angiotensin II has been isolated from human term placentae. Only in the presence of DTT, a sulphydryl agent, are OXY and SRIF also inactivated by this protein. However, it is without effect on CRF, hCS, or hCG. It also inhibits the biological activity of GnRH, i.e. its ability to stimulate pituitary LH and FSH. The ability of this protein to inactivate GnRH, TRH or angiotensin II can be inhibited by various peptidase inhibitors. Thus, we have postulated that it is a chorionic peptidase, specific for these peptides, and herein called chorionic peptidase-1 (C-ase-1). Isolation of this protein, C-ase-1, has been effected using permeation, ion exchange and affinity chromatography. As estimated by SDS-PAGE and HPLC analyses, C-ase-1 has an apparent molecular weight of 58,000. It is proposed that C-ase-1 may be an important chorionic regulator of GnRH, TRH and angiotensin II levels during pregnancy.
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PMID:Characterization and purification of a placental protein that inactivates GnRH, TRH and angiotensin II. 250 48

In vitro assessment was made of the hormone-release capability of splenic pancreatic tissue 16 days after adult chickens had 99% of the pancreatic mass surgically removed. The objective of this study was to evaluate if the enlargement of the splenic lobe remnant after 99% pancreatectomy was attended by alterations in the responsivity of hormone release and, if so, were such changes reflective of all pancreatic hormones. After a 24-hr fast, splenic lobe tissue was obtained from young adult chickens on Postoperative Day 16, diced into 18-22 mg cubes, and incubated in vitro in media containing varying amounts of glucose with or without added somatostatin (SRIF). At 15-min intervals, the tissue cubes were transferred to fresh media and samples of each medium measured for insulin, glucagon, and APP. Viability of the tissue after 75 min was tested by tissue response to added 5 mM phenylalanine. The results obtained indicated that while total content of all four hormones (including SRIF) increased with tissue enlargement, the concentration of each decreased significantly except for SRIF, which remained at control levels. Further, the sensitivity of the B-cell in releasing insulin when confronted by a glucose challenge was not altered by previous pancreatectomy, while that of glucagon release from the A-cell was depressed. A-cell responsivity to SRIF does not appear to be adversely affected by previous 99% pancreatectomy. APP release was least affected by SRIF addition to the media, although depression by high glucose occurred. It is concluded that differential alterations occur in chicken pancreatic hormone-releasing cells as a result of 99% pancreatectomy. The efficacy in maintaining low, but still adequate, plasma I/G molar ratios (reported earlier) by the splenic remnant tissue either reflects a remarkable functional readjustment to surgical removal of 99% of the pancreatic mass in chickens or, alternatively, suggests the existence of extrapancreatic sources of insulin and glucagon, but not APP.
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PMID:In vitro release of pancreatic hormones following 99% pancreatectomy in the chicken. 256 76

The potential use of somatostatin-14 and its long lasting analogue Sandostatin as antiulcer agents led us to study the functional properties of these peptides on the histamine H2-receptor H2R adenylate cyclase system in gastric glands isolated from the rat fundus. The action of the two peptides has also been compared on membrane receptors sensitive to isoproterenol and the truncated glucagon-like peptide TGLP-1. The data indicate that somatostatins inhibit selectively H2R and TGLP-1 receptor activity with similar potencies and kinetics, suggesting that the two peptides share the same receptor pool coupled with the Gi subunits of adenylate cyclase. Somatostatin-14 and Sandostatin have no evident action on the beta 2-type adrenergic receptor beta 2R. Therefore, the higher potency of Sandostatin compared to somatostatin-14 in inhibiting acid secretion is probably related to an increased stability of the analogue in vivo.
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PMID:Differential regulation of membrane receptors sensitive to histamine (H2-type), isoproterenol (beta 2-type) and glucagon-like peptides by the somatostatin analogue Sandostatin in rat gastric glands. 256 37

Islet A and B cells were purified from the rat pancreas and examined for their respective sensitivity to somatostatin. Both somatostatin-14 (S14) and -28 (S28) inhibited glucagon and insulin release through direct interactions with the corresponding cell types. A dose-dependent suppression of the secretory activities was paralleled by a reduction in cellular cyclic AMP formation with similar ED50 values for both actions. The somatostatin effects on pancreatic hormone release may thus be mediated via an inhibition of adenylate cyclase activity. In pancreatic A cells, S14 and S28 were equally potent inhibitors with ED50 values ranging from 2 x 10(-12) to 2 x 10(-11) mol/l. Pancreatic B cells exhibited a similar sensitivity to S28 as the A cells (ED50 of 2 to 5 x 10(-11) mol/l), but not to S14 (ED50 of 2 x 10(-9) mol/l). Extrapolation of these in vitro sensitivities of islet A and B cells to the in vivo situation suggests that both cell types can respond to circulating S28 levels and that A cells are sensitive to both locally and distally released S14. Islet B cells appear insensitive to the normal peripheral S14 levels but could respond to locally released somatostatin. The marked difference in the sensitivities of islet A and B cells to S14 suggest that these cell types are equipped with different somatostatin receptors. This notion was further supported by the cell-selective actions of the synthetic S14 analogues [D-Trp8, D-Cys14]S14 and desAsn5[D-Trp8, D-Ser13]S14.
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PMID:Sensitivity of rat pancreatic A and B cells to somatostatin. 256 61

The effects of the islet cell hormones glucagon, somatostatin-28 and pancreatic polypeptide on insulin secretion from cultured cloned pancreatic B cells (HIT-T15 and RINm5F) have been investigated. Glucagon stimulates the secretion of insulin from HIT-T15 cells in the absence and presence of glucose and from RINm5F cells in the absence and presence of glyceraldehyde. HIT-T15 cells were more sensitive to the stimulatory effect of glucagon than RINm5F cells. Somatostatin-28 and pancreatic polypeptide, both alone and in combination, reduced glucose- and glucagon-stimulated insulin release from HIT-T15 cells and glyceraldehyde- and glucagon-stimulated insulin release from RINm5F cells. HIT-T15 cells were more sensitive to the inhibitory actions of somatostatin-28 and pancreatic polypeptide than RINm5F cells. This study supports the hypothesis that insulin release from normal B cells may be modified by the paracrine activity of islet hormones, glucagon, somatostatin and pancreatic polypeptide and probably occurs before any fine tuning imposed by subsequently released insulin.
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PMID:Effects of islet hormones on insulin secretion from cloned B cell lines, HIT-T15 and RINm5F. 256 24

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.
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PMID:Interaction of glucagon-like peptide-1(7-36)amide and somatostatin-14 in RINm5F cells and in the perfused rat pancreas. 257 56

High circulating levels of somatostatin (SRIF) were detected in a patient with a metastatic tumour after development of diabetic ketoacidosis (DKA). Fasting insulin and C-peptide levels were markedly suppressed, but plasma glucagon was not suppressed below normal. Progressive cachexia ensued; at autopsy a poorly differentiated non-small cell neuroendocrine carcinoma metastatic to liver was found. Small gallstones were noted. Electron microscopy of tumour tissue showed neurosecretory granules and tonofilament bundles. Immunohistochemical staining of tumour cells was diffusely positive for carcinoembryonic antigen, bombesin-like immunoreactivity, and calcitonin with focal immunoreactivity for SRIF, serotonin, neuron-specific enolase, chromogranin, and epithelial membrane antigen. Column chromatography of plasma and tumour extract revealed five or more peaks of material with SRIF-like immunoreactivity (SRIF-LI): predominantly SRIF-28 and intermediates in tumour extract, and SRIF-14 and an intermediate between SRIF-28 and SRIF-14 in plasma, DKA in this case of somatostatinoma syndrome may reflect differential effects of tumour production of larger molecular weight SRIF forms on insulin and glucagon secretion.
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PMID:Malignant somatostatinoma presenting with diabetic ketoacidosis. 282 97

GHRH receptors in pituitary adenoma cell membranes from five patients with acromegaly were characterized using [125I] [His1,Nle27]GHRH-(1-32)NH2 ([125I]GHRHa) as a ligand. Specific binding of [125I]GHRHa to adenoma cell membranes was maximal within 20 min at 24 C, remained stable for 60 min, and was reversible in the presence of 500 nmol/L human GHRH-(1-44)NH2 (hGHRH). The specific binding increased linearly with 10-160 micrograms cell membrane protein. This binding was inhibited by 10(-11)-10(-6) mol/L hGHRH in a dose-dependent manner, with an ID50 of 0.20 nmol/L, but not by 10(-7) mol/L vasoactive intestinal peptide, glucagon, somatostatin-14, somatostatin-28, TRH, LHRH, and CRH. The specific binding of [125I]GHRHa to the membranes was saturable, and Scatchard analysis of the data revealed an apparent single class of high affinity GHRH receptors in five adenomas from acromegalic patients; the mean dissociation constant was 0.30 +/- 0.07 (+/- SE) nmol/L, and the mean maximal binding capacity was 26.7 +/- 7.0 (+/- SE) fmol/mg protein. In three nonfunctioning pituitary adenomas, GHRH receptors were not detected. The plasma GH response to hGHRH (100 micrograms) injection was studied in four acromegalic patients before surgery. Plasma GH levels increased variably in response to hGHRH injection in all four patients. However, there was no correlation between the characteristics of the tumor GHRH receptors and plasma GH responsiveness in these patients. We conclude that pituitary GH-secreting adenomas have specific GHRH receptors. Exogenously administered GHRH presumably acts via these receptors, but the variations in plasma GH responsiveness to hGHRH in these patients cannot be directly related to the variations in binding characteristics of the GHRH receptors on the GH-secreting adenoma cells.
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PMID:Characterization of growth hormone-releasing hormone receptors in pituitary adenomas from patients with acromegaly. 283 73


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