Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Receptors for regulatory peptides (hormones or neurotransmitters) play a pivotal role in the ability of cells to taste the rich neuroendocrine environment of the gut. Recognition of low concentration of peptides with a high specificity and translation of the peptide-receptor interaction into a biological response through different signalling pathways (adenylyl cyclase-cAMP or phospholipase C-phosphatidylinositol) are crucial properties of receptors. While many new receptors have been identified and thereafter characterized functionally during the 1980s, molecular biology now emerges as the privileged way for the structural characterization and discovery of receptors. Different strategies of receptor cloning have been developed which may or may not require prior receptor purification. Among cloning strategies that do not require receptor purification, homology screening of cDNA libraries, expression of receptor cDNA or mRNA in Xenopus laevis oocytes or in COS cells, and the polymerase chain reaction method achieved great success, e.g. cloning of receptors for cholecystokinin, gastrin, glucagon-like peptide 1, gastrin-releasing peptide/bombesin, neuromedin K, neuropeptide Y, neurotensin, opioids, secretin, somatostatin, substance K, substance P and vasoactive intestinal peptide. All these receptors belong to the superfamily of G-protein-coupled receptors which consist of a single polypeptide chain (350-450 amino acids) with seven transmembrane segments, an N-terminal extracellular domain and a C-terminal cytoplasmic domain. In this chapter, we have detailed the properties of three receptors which play an important role in digestive tract physiology and illustrate various signal transduction pathways: pancreatic beta-cell galanin receptors which mediate inhibition of insulin release and intestinal epithelial receptors for vasoactive intestinal peptide and peptide YY, which mediate the stimulation and inhibition of water and electrolyte secretion, respectively.
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PMID:Receptors for gut regulatory peptides. 751 Sep 49

Morphological and functional modifications have been described in the gastrointestinal tract of germ-free rodents in comparison to their conventional counterparts. These differences have been related to the absence of normal flora, but peptides and biogenic amines may also be involved. Enteroglucagon-, peptide YY-, somatostatin-, serotonin-, neurotensin-, chole-cystokinin-, and secretin-producing cells were studied by immunocytochemistry in the ileum, cecum and colon of 10 germ-free, 10 conventional and 5 conventionalized CFW adult male mice. In the cecum and colon of germfree mice, enteroglucagon- and peptide YY-positive cells appeared enlarged, were globular in shape and strongly immunostained. Enlarged and strongly immunostained serotonin- and neurotensin-positive cells were also seen in some germ-free mice. Somatostatin-positive cells and all the endocrine cells of the ileum were similar in the 3 groups, and no cholecystokinin- or secretin-positive cells were observed. Our results are consistent with higher enteroglucagon and peptide YY production in germ-free mice that may be related to the lower cellular renewal rates and slower gastrointestinal transit reported in these animals. Locally produced biogenic amines and peptides may be important factors in the mediation of the effect of the intestinal flora on gastrointestinal structure and function and germ-free mice seem to be a good model for the study of the mechanisms involved.
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PMID:Immunocytochemical study of intestinal endocrine cells in germ-free mice. 753 May 14

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

Reperfusion of ischaemic intestine is characterised by an initial hyperaemia with ensuing mucosal repair. This study investigated possible roles for gut vasoactive neuropeptides and trophic peptides in these phenomena. Groups of rats were monitored during superior mesenteric artery occlusion for five or 20 minutes, with or without subsequent reperfusion for five minutes. Peptide concentrations (fmol/ml) in arterial blood, were measured using specific radioimmunoassays. Intestinal ischaemia alone did not cause haemodynamic disturbance or peptide release. Reperfusion, after five minutes of ischaemia, resulted in arterial hypotension and a rise in plasma vasoactive intestinal polypeptide (mean (SEM)) (37 (3), control 11 (4), p < 0.001). After 20 minutes of ischaemia, reperfusion resulted in greater hypotension (p < 0.05) and release of both vasoactive intestinal polypeptide (31 (3), p < 0.05 v control) and the more potent vasodilator beta-calcitonin gene related peptide (49 (3), control 23 (1), p < 0.001). By contrast, the vasodilators alpha-calcitonin gene related peptide and substance P and the vasoconstrictors neuropeptide Y, peptide YY, and somatostatin were not released. Bombesin, a stimulatory neuropeptide, was released after 20 minutes of ischaemia/reperfusion (13 (2), control 7 (3), p < 0.05). Plasma enteroglucagon rose from control (51 (4)) to 110 (16) (p < 0.001) and to 158 (27) (p < 0.005) after five and 20 minutes of ischaemia/reperfusion. The potent enteric vasodilators vasoactive intestinal polypeptide and beta-calcitonin gene related peptide, unopposed by vasoconstrictors, may promote post-ischaemic intestinal hyperaemia. The rise in plasma enteroglucagon may point to diffuse mucosal injury and is consistent with the putative trophic role of this peptide.
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PMID:Release of vasodilator, but not vasoconstrictor, neuropeptides and of enteroglucagon by intestinal ischaemia/reperfusion in the rat. 782 5

The release of pancreatic polypeptide (PP) and peptide YY (PYY) is regulated by the vagal nerve, and the inhibitory effect of these peptides on pancreatic exocrine secretion shows indirectly via a neural mechanism. To determine the role of the vagal nerve on the inhibitory action of these peptides on the pancreas, we compared the effect on the pancreatic response to bile and pancreatic juice diversion in conscious rats with and without vagotomy. We also studied this response in rats treated with capsaicin, because bile-pancreatic juice diversion is the most potent endogenous stimulation of pancreatic secretion in conscious rats. In addition, since somatostatin potently inhibits of pancreatic enzyme secretion, the effects of PP and PYY were compared with somatostatin. An intravenous infusion of 2.5 nmol/kg per h of PP and PYY significantly inhibited the pancreatic responses of bile and pancreatic juice diversion in animals with an intact vagal nerve and in those treated with capsaicin, whereas the same dose of peptides failed to inhibit pancreatic secretion in vagotomized rats. Somatostatin inhibited pancreatic secretion under all conditions tested. We concluded that the inhibitory action of PP and PYY on pancreatic secretion is fully mediated by the vagal efferent nerve although other multiple mechanisms are involved for the inhibitory action of somatostatin.
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PMID:Vagal efferent nerve-dependent inhibitory action of pancreatic polypeptide and peptide YY in conscious rats: comparison with somatostatin. 788 53

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


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