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)

Histological, immunocytochemical and immunofluorescence methods were employed to study the oesophagus and stomach of the elephant. The histological findings were in line with the situation in monogastric species like swine and man. In the mucosa of the stomach, endocrine cells were immunoreactive to gastrin, somatostatin, chromogranin A and serotonin. Nerve cells immunoreactive to somatostatin, bombesin, VIP, PHI and CGRP were detected in the submucosal and myenteric plexus of the stomach. In the stomach, the absence of glucagon cells and the presence of endocrine cells immunoreactive to PYY, are in contrast to the situation in mammals and need further investigation. Small gastric ulcers were observed in some of the specimens.
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PMID:The oesophagus and stomach of the African elephant: a histological, immunocytochemical and immunofluorescence study. 759 75

Several gastrointestinal peptides inhibit pancreatic secretion in intact animals, but fail to do so in isolated pancreas preparations. Using isolated perfused porcine pancreas with intact innervation, we studied the influence of such peptides (somatostatin, peptide YY, glucagon-like peptide-1, oxyntomodulin, neuropeptide Y, galanin, and calcitonin gene-related peptide) on vagally induced secretion and on release of vasoactive intestinal polypeptide (VIP), a neuropeptide involved in fluid and bicarbonate secretion. In control experiments electrical vagus stimulation increased flow of juice from 0.9 +/- 0.1 to 37.3 +/- 5.6 ml/h and protein output from 43 +/- 5 to 1,244 +/- 336 mg/h (mean +/- SD). With somatostatin-14 at 10(-10) mol/L, the fluid response was reduced to 64 +/- 11% of controls, protein concentration to 78 +/- 3.8%, and protein output to 50 +/- 5% (p < 0.05). At 10(-8) M the response was almost abolished. VIP release, which in control experiments increased from 0.2 +/- 0.05 to 2.1 +/- 0.4 pmol/min, was similarly reduced (p < 0.01). Galanin at 10(-8) M inhibited the fluid response to 54 +/- 7% of controls, protein output to 51.7 +/- 11%, and VIP release to 54 +/- 6% (p < 0.01). None of the other inhibitory peptides affected vagus responses. It is concluded that somatostatin and galanin inhibit pancreatic secretion through interaction with intrapancreatic ganglia. The other peptides act on extrapancreatic, possibly central sites.
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PMID:Effect of intestinal inhibitory peptides on vagally induced secretion from isolated perfused porcine pancreas. 767 28

Peptide YY is an insulinostatic peptide which is released into the circulation from the intestinal mucosa upon food intake. Peptide YY is also co-stored with glucagon in the secretory granules of the pancreatic alpha cells. We examined the mechanisms underlying the insulinostatic effect of peptide YY in isolated mouse pancreatic islets. We found that peptide YY (0.1 nmol/l-1 mumol/l) inhibited glucose (11.1 mmol/l)-stimulated insulin secretion from incubated isolated islets, with a maximal inhibition of approximately 70% observed at a dose of 1 nmol/l (p < 0.001). Also in perifused islets the peptide (1 nmol/l) inhibited insulin secretion in response to 11.1 mmol/l glucose (p < 0.001). Furthermore, peptide YY inhibited glucose-stimulated cyclic AMP formation (by 67%, p < 0.05), and insulin secretion stimulated by dibutyryl cyclic AMP (p < 0.01). In contrast, the peptide was without effect both on the cytoplasmic Ca2+ concentration in dispersed mouse islet-cell suspensions as measured by the FURA 2-AM technique, and on insulin release in isolated islets, when stimulated by the protein kinase C-activator 12-O-tetradecanoyl phorbol 13-acetate. Finally, in pre-labelled perifused islets, peptide YY caused a small and transient increase in the 86Rb+ efflux (p < 0.001), but only in the absence of extracellular Ca2+. We conclude that peptide YY inhibits glucose-stimulated insulin secretion from isolated mouse islets by inhibiting two different steps in the cyclic AMP cascade, that is, both the accumulation and the action of the cyclic nucleotide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms underlying the insulinostatic effect of peptide YY in mouse pancreatic islets. 780 16

In order to study the cellular mechanisms involved in peptide YY (PYY) and truncated glucagon-like peptide 1 (TGLP1) release, a model of rat intestinal cells dispersed with collagenase/EDTA and enriched for L-cells by counterflow elutriation was developed. Elutriation significantly increased in the harvested cells the concentration of PYY (828 +/- 97 vs 151 +/- 16 fmol/10(6) cells) and TGLP1 (1,094 +/- 109 vs 167 +/- 20 fmol/10(6) cells), and brought the contribution of L-cells to 4-5% of the total cell population. Forskolin (1-10 microM) and dibutyryl cyclic AMP (dbcAMP, 1-5 mM) increased over an 1-h period PYY and TGLP1 secretion, with a maximal rate at 5 microM forskolin (232% and 250% of basal, respectively) and at 5 mM dbcAMP (347% and 234% of basal, respectively). Furthermore, 3-isobutylmethyl xanthine (IBMX, 1 mM) increased PYY (226% of basal) and TGLP1 (198% of basal) secretion. A combination of both 10 microM forskolin and 1 mM IBMX stimulated in an additive manner PYY (389% of basal) and TGLP1 (393% of basal) secretion. TPA (12-0-tetradecanoylphorbol-13-acetate, 0.1-1 microM) dose-dependently increased the secretion of PYY and TGLP1 (maximal release at 328% and 326%, respectively), whereas 4 alpha-phorbol was ineffective. Ionomycin (1-5 microM) and thapsigargin (0.1-5 microM) produced a dose-dependent increase in PYY and TGLP1 release (272% and 337% of basal for 5 microM ionomycin; 342% and 339% of basal for 5 microM thapsigargin, respectively). At gel chromatography, the immunoreactive PYY and TGLP1 material in cell extracts and in release medium co-eluted with the respective synthetic peptides.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Secretion of peptide YY and truncated glucagon-like peptide 1 by isolated intestinal cells in rats]. 781 61

We have produced transgenic mice expressing fusion genes consisting of 1.6 kilobase pairs of the secretin gene 5' flanking region to direct the expression of human growth hormone (hGH) or simian virus 40 large T antigen to secretin-producing cells. Analysis of different mouse tissues for hGH transcripts revealed expression in each of the major secretin-producing tissues, namely the intestine and endocrine pancrease. Multiple label immunohistochemistry demonstrated that the transgene was correctly directed to secretin cells in the intestinal tract, including a previously unrecognized population of secretin cells in the colon of adult and developing mice. In the small intestine, subpopulations of hGH-containing cells frequently coexpressed substance P, serotonin, and cholecystokinin, whereas in the colon, cells expressing hGH frequently coexpressed glucagon, peptide YY, or neurotensin. Transgenic mice expressing large T antigen in secretin cells developed poorly differentiated neuroendocrine tumors of the small intestine, well differentiated colonic tumors containing glucagon-expressing cells, and insulin-producing tumors in pancreas. These studies indicate that the major cis-regulatory sequences necessary for secretin expression in enteroendocrine cells and fetal islets are localized with 1.6 kilobase pairs of the transcriptional start site. Coexpression of reporter transgenes with several gastrointestinal hormones suggests a potential relationships between secretin cells and other enteroendocrine cell types, as well as pancreatic beta cells.
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PMID:Studies in transgenic mice reveal potential relationships between secretin-producing cells and other endocrine cell types. 782 27

Enterocolitis (EC) remains the most serious complication of Hirschsprung's disease (HD). The aetiology of EC is uncertain. Ischemic and bacterial causes, and recently rotavirus infection, have been suggested to explain the occurrence of EC. The gut has an abundance of neuroendocrine (NE) cells which modulate gut function by endocrine, paracrine, or neurocrine routes. We studied NE cell populations in the bowel from 16 patients with HD (six of whom had clinical evidence of EC) and rectal tissue from 6 controls. Immunohistochemical studies were carried out using monoclonal and polyclonal antibodies against chromogranin A, synaptophysin (general markers of NE cells), 5-Hydroxytryptamine (5-HT), somatostatin, peptide YY (PYY), and glucagon/glicentin (neuropeptides). The six patients who had clinical evidence of EC prior to defunctioning colostomy showed histological evidence of EC in the defunctioned bowel. Using immunocytochemistry and serial tissue sectioning it was found that the number of NE cells in the aganglionic segment of colon in patients with HD was significantly (P < .05) increased compared with the numbers in the ganglionic segment. However, in the ganglionic colon, there was a significant (P < .05) reduction in NE cells in EC patients compared with non-EC patients. These results were seen both with the generic endocrine cell marker chromogranin A, which stains virtually all endocrine cells, and with specific markers for 5-HT, PYY, and glucagon/glicentin, which identify distinct subpopulations of endocrine cells. These differences may be partially responsible for previous conflicting reports of NE cell distribution in HD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional reduction in intestinal neuroendocrine cell populations in enterocolitis complicating Hirschsprung's disease. 790 60

This chapter has focused on many of the gut hormones that regulate gastric function. Gastrin remains the principal, and only, gastric hormone controlling gastric acid secretion during the cephalic, gastric and intestinal phases of secretion. Several other hormones, including cholecystokinin, peptide YY and secretin, released from intestinal endocrine cells in response to food substrates, have significant inhibitory effects on gastric acid secretion. Many of these hormones, including enteroglucagon and glucagon-like peptide, may act through paracrine release of somatostatin, which in turn acts as the final mediator of acid inhibition. In addition, several peptides contained in nerves, including gastrin releasing peptide and vasoactive intestinal peptide, have been shown to regulate gastric acid secretion and motor function. With the creation of specific monoclonal antibodies for use in in vivo immunoneutralization studies, and the development of selective chemical antagonists for use in receptor blockade experiments, the specific contributions of the different gut hormones in the regulation of gastric function, can be assessed.
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PMID:Gut hormones in gastric function. 790 60

The neurohormonal structures of two human intestines removed due to rejection 22 months and eight months after intestinal transplantation were studied by an indirect immunohistochemical method and compared with normal ileum. The distribution and density of neurons immunoreactive for tyrosine hydroxylase, substance P, calcitonin gene-related peptide, neuropeptide Y, vasoactive intestinal peptide, galanin, gastrin-releasing peptide, L-enkephalin, and somatostatin were examined. Mucosal endocrine cells immunoreactive for somatostatin, peptide YY, and glucagon were also examined. Extrinsic adrenergic fibers and perivascular fibers were absent in all intestinal layers of the failed grafts. The distribution of intrinsic neurons was unchanged; however, the density was decreased by one rank. Distribution of endocrine cells of the first graft was similar to the normal. Extrinsic fibers were not detected by immunohistochemistry in human small intestinal grafts following long-term survival and eventual rejection, while the immunohistochemical expression of intrinsic neural and endocrine transmitters were well preserved.
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PMID:Immunohistochemical study of enteric nervous system after small bowel transplantation in humans. 795 15

Medullary thyroid carcinoma (MTC) can be important for gastroenterologists because 20-30% of patients with MTC suffer from chronic diarrhea and the tumor is capable of producing--besides other bioactive substances--a multitude of gastroenteropancreatic hormones. Gastrointestinal hormone profiles of 5 patients with MTC were determined both basally and after intravenous stimulation with secretin and calcium respectively. Diagnosis of MTC was confirmed histologically or cytologically and by demonstration of elevated serum concentration of calcitonin both basally and after calcium stimulation. 4/5 patients had chronic diarrhea. Normal values or only borderline increases were found for the following hormones: vasoactive intestinal polypeptide (VIP), neurotensin, substance P, growth hormone releasing hormone (GRH), glucagon, neurokinin A, peptide YY, and pancreatic polypeptide. Somatostatin was elevated after calcium stimulation in 1/5 patients only. The main findings were increased basal concentrations for GAWK in 5/5 patients and elevated concentrations for gastrin-releasing peptide (GRP, human bombesin) after calcium stimulation in 4/5. Probably as a consequence of the GRP increase, an increase in gastrin occurred in parallel, indicating bioactivity of the GRP released from the tumor. Besides calcitonin as the main tumor marker for MTC, determination of GAWK and GRP seems to provide helpful additional markers in laboratory diagnosis of MTC. GRP determination after i.v. calcium infusion allowed identification of patients with normal basal plasma GRP concentration.
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PMID:[Gastrointestinal hormone profile in medullary thyroid carcinoma]. 801 6

The occurrence of endocrine cells in 350 cases of colorectal adenocarcinoma was studied by immunohistochemistry for chromogranin A (CGA). The hormone profile of endocrine tumor cells, the correlation between endocrine differentiation and presence of other colorectal epithelial-cell lineages and the prognostic relevance of endocrine differentiation in colorectal cancer were investigated. CGA-positive tumor cells were found in 30% of cases, 21% showing moderate positivity and 9.0% extensive positivity. Of CGA-positive tumors, 70% additionally produced neurohormones, mainly indigenous to normal colorectal epithelium: 55% showed immunoreactivity for glucagon-like substances, 20% for serotonin and 10% for somatostatin, PYY and HCG. No immunoreactivity was found for various neurohormones not normally produced by colorectal endocrine cells. CGA-positive tumors tended to be more aggressive than CGA-negative tumors. Especially, tumors with extensive CGA positivity showed shorter survival, which was most apparent within Dukes' stage C. In multivariate analysis, extensive CGA positivity was an independent indicator of poor prognosis. CGA immunoreactivity significantly correlated with mucin production, but not with expression of secretory component (SC), a columnar-cell marker. Mucin production significantly correlated with SC expression. Tumors positive for CGA but not for mucin and/or SC showed the worst prognosis. SC expression was a relatively favorable feature, and mucin-producing tumors showed intermediate behavior.
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PMID:Endocrine cells in colorectal adenocarcinomas: incidence, hormone profile and prognostic relevance. 810 Aug 8


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