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)

A number of regulatory peptides were investigated for their ability to elevate plasma cAMP. Pituitary adenylate cyclase activating peptide (PACAP)-27, PACAP-38, helodermin, helospectin I and II, vasoactive intestinal peptide (VIP), glucagon, parathyroid hormone (PTH), calcitonin and calcitonin gene-related peptide were among the peptides that were highly effective in raising plasma cAMP when given intravenously in equimolar doses to conscious mice. PACAP-27 and -38 were more effective than any of the other peptides. PACAP 16-38, secretin, gastrin-17, galanin, somatostatin, cholecystokinin-8s, pancreatic polypeptide, substance P, peptide YY and neuropeptide Y were inactive and also did not interfere with the PACAP-27-evoked rise in plasma cAMP levels. Repeated injections of PACAP-27 every 30 min caused a progressive reduction in the plasma cAMP response (measured 5 min after each injection). Forskolin, an activator of adenylate cyclase, dose-dependently raised the plasma concentration of cAMP and displayed a synergistic effect when given in a low dose concurrently with PTH or PACAP-38. The phosphodiesterase inhibitor rolipram dose-dependently raised the plasma concentration of cAMP. Combined treatment with PACAP-27 and a threshold dose of rolipram resulted in an exaggerated plasma cAMP response. Kidney hilus ligation suppressed the responses to PACAP-38, PTH, helodermin, helospectin, VIP, glucagon and calcitonin. Hepatectomy suppressed the response to glucagon but was without effect on the response to the other peptides. Pancreatectomy and spleenectomy reduced the response to VIP, but was without effect on the response to the other peptides. PACAP-27 stimulated cAMP efflux from the isolated rat tail vein. Hence, it cannot be excluded that blood vessels contribute to the peptide evoked plasma cAMP response in vivo.
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PMID:Neuropeptides of the vasoactive intestinal peptide/helodermin/pituitary adenylate cyclase activating peptide family elevate plasma cAMP in mice: comparison with a range of other regulatory peptides. 133 41

To ascertain whether certain gastro-entero-pancreatic hormones whose concentration in blood rises after ingestion of food could play a role in the elevation of plasma triglycerides (or hepatic triglyceride secretion) observed after oral vs parenteral feeding, studies were undertaken of their acute effects upon triglyceride synthesis and release by freshly isolated rat hepatocytes in vitro. The incorporation of radiopalmitate into hepatocyte triglycerides was significantly increased, by one-fourth to one-half, by each of pancreatic polypeptide, peptide YY, and an intermediate concentration (0.50 microgram/mL) of somatostatin. However, at a lower concentration (0.25 microgram/mL) somatostatin significantly decreased (by 14%) the incorporation of radiopalmitate into hepatocyte triglycerides. Release of labelled triglycerides from hepatocytes into the medium was significantly enhanced by both gastric inhibitory polypeptide (by 31%) and pancreatic polypeptide (22%), but was significantly reduced (by 28%) by somatostatin at a concentration of 1 microgram/mL. Neurotensin produced no detectable effect. Although there were similarities between the active hormones, each had a unique overall pattern of response on triglyceride synthesis and release and individually, or in concert with other hormones, could modulate hepatic triglyceride production and secretion, thereby explaining the differential effects of oral vs parenteral feeding on plasma triglycerides.
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PMID:Effects of gastro-entero-pancreatic hormones upon triglyceride synthesis and secretion by rat hepatocytes. 134 74

The endocrine cells of rainbow trout pyloric ceca and intestine have been investigated immunocytochemically using the avidin-biotin method. Twenty-six antisera were tested and 13 endocrine cell types immunoreacted with antisera to serotonin, somatostatin-25, bombesin, C-flanking bombesin, substance P, salmon PP, NPY, PYY, PP, glucagon, GLP1, Met-enkephalin, and CCK/G. Glucagon and GLP1 immunoreactivities appear in the same cells. Nerves positive to serotonin, substance P, PHI, and VIP were also found. The presence of cells positive to somatostatin-25, C-flanking bombesin, and salmon PP are described for the first time in fish intestine.
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PMID:Endocrine cells and nerves in the pyloric ceca and the intestine of Oncorhynchus mykiss (Teleostei): an immunocytochemical study. 138 78

Proliferative effects of hormones on the gastrointestinal mucosa are discussed according to literature data. There are presented the trophic effects of gastrin, cholecystokinin, secretin, enteroglucagon, somatostatin, growth hormone, thyroxine, peptide YY, epidermal growth factor and submaxillary growth factor.
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PMID:[The effect of hormones on the gastrointestinal mucosa]. 141 98

We studied the distribution of mucosal neuroendocrine (NE) cells in the colon from 13 patients with Hirschsprung's disease (HD) and from 8 controls. Immunohistochemical studies were carried out using monoclonal and polyclonal antibodies against chromogranin A and synaptophysin (general markers of NE cells), 5-hydroxytryptamine (5-HT) (a marker of amine), peptide YY (PYY), and somatostatin (markers of neuropeptides). Chromogranin A immunoreactive cells were significantly increased in the aganglionic bowel compared with ganglionic bowel and controls (P less than .05). There was an increase in the number of synaptophysin immunoreactive cells in the aganglionic bowel compared with ganglionic bowel and controls but the results were not statistically significant. 5-HT immunoreactive cells were also significantly increased in the aganglionic bowel compared with ganglionic bowel and controls (P less than .05). The immunostaining for PYY demonstrated abundance of this NE cell type in the aganglionic bowel and this was highly significant compared with ganglionic bowel and controls (P less than .001). There was a significant increase in somatostatin immunoreactive cells in the aganglionic bowel compared with ganglionic bowel (P less than .01). The increase in neuroendocrine cells was found over the entire length of the aganglionic segment in rectosigmoid HD as well as in long-segment HD. These results demonstrating the increased levels of NE cells in the mucosa of aganglionic colon suggest that the NE cells may have a role in regulating the sustained contraction of the aganglionic intestine in HD.
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PMID:Mucosal neuroendocrine cell abnormalities in the colon of patients with Hirschsprung's disease. 164 Mar 25

The isolated gastric gland preparation, with aminopyrine accumulation as an index of the parietal cell response, has been used to study the effects of somatostatin (S-14), gastrin-releasing peptide (GRP), cholecystokinin (CCK-8), vasoactive intestinal peptide (VIP), and peptide YY (PYY) on the in vitro acid secretion in human and rabbit oxyntic mucosa. Somatostatin was able to inhibit the parietal cell response to histamine in both human and rabbit isolated gastric glands (maximal inhibition, 22% and 34%, respectively) but failed to inhibit the parietal cell response to db-cAMP. However, other peptides capable of inhibiting gastric acid secretion in vivo, such as CCK, VIP, and PYY, were unable to induce any inhibition of the parietal cell response to db-cAMP or histamine in the isolated gastric gland preparation irrespective of the species studied. GRP was not able to induce a parietal cell response, a finding that is in accord with the assumption that the stimulatory effect of GRP on gastric acid secretion in vivo is by releasing gastrin from antral G-cells.
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PMID:Effects of some gastrointestinal peptides on isolated human and rabbit gastric glands. 167 70

The physiological regulation of intestinal proglucagon-derived peptide secretion has not been well studied. We have therefore used a fetal rat intestinal cell culture model to investigate the control of secretion of the gut glucagon-like immunoreactive (GLI) peptides by other intestinal regulatory peptides in vitro. Secretion of the intestinal GLI peptides was found to be stimulated in a dose-dependent fashion by the intestinal endocrine peptide, gastric inhibitory peptide (at greater than or equal to 10(-10) M, P less than 0.05), and by the neurocrine peptides, gastrin-releasing peptide (at greater than or equal to 10(-12) M, P less than 0.05), and calcitonin gene-related peptide (at greater than or equal to 10(-8) M, P less than 0.05). Gastrin-releasing peptide and its amphibian equivalent, bombesin were equipotent in stimulating GLI peptide secretion. In contrast, the endocrine and neurocrine intestinal somatostatin-related peptides, somatostatin-28 and -14, inhibited release of the GLI peptides, at concentrations of 10(-10) (P less than 0.01) and 10(-8) (P less than 0.01) M, respectively, with significant differences in potency between the two peptides detected at 10(-10) M (P less than 0.05). The inhibitory effects of both somatostatin-28 and -14 could be blocked by preincubation of the cells with pertussis toxin (P less than 0.05). Dose-dependent stimulation of gut GLI peptide secretion was also detected in response to treatment of cultured cells with sodium oleate (at 10(-4) M; P less than 0.05), or with the cholinergic agonist bethanecol (at greater than or equal to 100 microM; P less than 0.05). Other endocrine [cholecystokinin, glucagon, glucagon-like peptide-1(1-37), glucagon-like peptide-1(7-37), glucagon-like peptide-2, neurotensin, and peptide YY] and neurocrine (vasoactive intestinal peptide) peptides, and the synthetic glucocorticoid, dexamethasone, were without effect on secretion of the gut GLI peptides, at doses of 10(-12) to 10(-6) M. The results of the present study therefore demonstrate that secretion of the intestinal proglucagon-derived peptides is under the regulatory control of a wide variety of intestinal endocrine and neurocrine peptides, as well as nutrients (fats) and neurotransmitters (acetylcholine).
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PMID:Regulation of intestinal proglucagon-derived peptide secretion by intestinal regulatory peptides. 167 88

Delta-sleep-inducing peptide (DSIP), vasoactive intestinal peptide (VIP), peptide YY (PYY) and somatostatin (SOM) were assayed with specific radioimmunological methods in cerebrospinal fluid (CSF) of healthy volunteers, 12 patients with Alzheimer's disease (AD), 11 patients with multi-infarct dementia (MID) and 10 patients with normal-pressure hydrocephalus (NPH). Patients with NPH were reinvestigated 3 months after a ventriculoperitoneal shunt operation. DSIP, PYY and SOM levels in CSF were decreased in patients with NPH compared to controls. The CSF concentration of SOM was also significantly reduced in patients with AD. No correlations were found between the degree of dementia in any of the illnesses and the CSF concentrations of the peptides. The concentration of DSIP, VIP and SOM increased significantly in parallel to the clinical improvement after the shunt operation in NPH patients.
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PMID:Neuropeptides in cerebrospinal fluid in normal-pressure hydrocephalus and dementia. 167 71

The fasting plasma levels of 9 gastrointestinal regulatory peptides were measured by radioimmunoassay in 13 stable patients with chronic renal failure receiving hemodialysis treatment regularly and compared with those of 10 healthy controls. The plasma concentrations of gastrin-releasing peptide, motilin, neurotensin, pancreatic polypeptide, peptide YY, somatostatin, substance P, and vasoactive intestinal peptide were increased. The plasma level of gastrin was not statistically different from that of the controls (p = 0.077). We conclude that patients with chronic renal failure receiving hemodialysis treatment regularly have increased concentrations of eight of nine measured gastrointestinal regulatory peptides. The elevated levels of gastrointestinal peptides in patients with chronic renal failure may contribute to uremic gastrointestinal symptoms and dysfunctions. It is necessary to make a renal function evaluation before interpreting measured plasma levels of gastrointestinal regulatory peptides.
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PMID:Plasma levels of gastrointestinal regulatory peptides in patients receiving maintenance hemodialysis. 171 7

Neuropeptide Y (NPY) is a unique 36 amino acid peptide with strong sequence homology to pancreatic polypeptide and peptide YY. In the rat pancreas, NPY-positive fibers have been demonstrated in close association with exocrine structures, suggesting a regulatory role for the peptide. In conscious rats with pancreatic ductal cannulas, amylase output stimulated by cholecystokinin octapeptide (CCK-8: 0.2 microgram kg - 1 h -1) was dose-dependently inhibited by intravenous NPY infusion (20, 40, and 80 micrograms kg-1 h-1). Inhibitory effects were rapid in onset but reversed with cessation of NPY infusion. With continuous NPY infusion (40 microgram kg-1 h-1), prolonged inhibition of amylase output by the vagal stimulant 2-deoxyglucose (100 mg kg-1) was observed (greater than 50% inhibition in each of none consecutive 10-min periods). In contrast, NPY infusion in doses of 20, 40, or 80 micrograms kg-1 h-1 produced no alteration in immunoreactive somatostatin levels. In vitro, NPY incubation (10(-13)-10(-8) M) produced no change in basal amylase release from dispersed, purified acinar cells. In addition, co-incubation of NPY (10(-8)-10(-6) M) with CCK-8 (10(-13)-10(-8) M) produced no inhibition of CCK-stimulated amylase release from dispersed acini. In contrast, NPY (10(-6) M) produced significant inhibition of amylase release from pancreatic lobules that had been stimulated by 75 mM potassium (135 +/- 11% versus 177 +/- 18% of basal level) or by 25 microM veratridine (196 +/- 19% versus 398 +/- 152%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of rat pancreatic exocrine secretion by neuropeptide Y: studies in vivo and in vitro. 171 87


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