UNIPROT:P61278 - FACTA Search

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Query: UNIPROT:P61278 (somatostatin)
22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fetal parietal cerebral cortex was transplanted to the anterior eye chamber of adult Sprague-Dawley rats. After two to three months the grafts, with or without colchicine treatment, were subjected to immunohistochemical analysis using antibodies against cholecystokinin (CCK), somatostatin (SOM), neuropeptide tyrosine (NPY), vasoactive intestinal polypeptide (VIP), peptide histidine isoleucine (PHI) and the GABA-synthesizing enzyme glutamic acid decarboxylase (GAD). Cerebral cortex in situ of untreated and colchicine-treated rats was always analyzed in parallel. A dense plexus of CCK-immunoreactive fibers was distributed in all parts of the transplants, and after colchicine treatment a large number of CCK-positive cells was observed. These cells were markedly increased in number as compared to normal cortical tissue in colchicine-pretreated rats. The amount of NPY-immunoreactive cells was also markedly increased, whereas somatostatin-positive cells were found in numbers similar to those seen in cortex in situ. In the grafts only a few VIP- and PHI-positive fibers were seen with a few VIP-positive cell bodies, but no clearly discernible PHI-positive cells. A very dense plexus of GAD-positive fibers with an even distribution throughout the grafts was observed. Cortex in situ exhibited a lower density of GAD-immunoreactive fibers. Even after colchicine treatment the number of GAD-positive cells in the grafts was low. Using double-staining techniques, it was found that most of the few GAD-positive cells in the grafts were also NPY-positive, SOM-positive or, to a minor extent, CCK-positive. The present results demonstrate that several peptides and transmitter markers are expressed in cortical grafts in oculo, but marked differences in their expression can be observed in cortical tissue that has developed in isolation. Thus, the intraocular cortex graft, alone and in combination with other brain areas, should provide a useful model in which to study factors that regulate brain development.
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PMID:Glutamic acid decarboxylase- and peptide-immunoreactive neurons in cortex cerebri following development in isolation: evidence of homotypic and disturbed patterns in intraocular grafts. 290 91

We have evaluated the potential of the clonal insulin-secretory cell line HIT-T15 as a model system for investigating stimulus-secretion coupling in pancreatic B cells. In contrast to other cell lines, HIT cell insulin secretion was consistently stimulated 2- to 3-fold by D-glucose. The maximally effective concentration of glucose was 10 mmol/l; between 2 and 10 mmol/l glucose the increase in insulin release was paralleled by an increased rate of glucose oxidation. The main characteristics of glucose-stimulated insulin release by HIT cells were essentially similar to those of normal islets. Thus, the response was specific for metabolizable sugars (D-mannose and D-glyceraldehyde stimulated insulin release but L-glucose and D-galactose were ineffective); markedly dependent on extracellular Ca2+ concentration; potentiated by forskolin, glucagon, acetylcholine and 12-O-tetradecanoyl phorbol 13-acetate; inhibited by adrenaline or somatostatin; showed a biphasic pattern of release in perifusion experiments, with both phases being potentiated by forskolin. The secretory response of the HIT cells to amino acids was also similar to that of normal islets. Thus, L-leucine and its deamination product 2-ketoisocaproate were effective stimuli, whereas L-isoleucine and L-glutamine were ineffective. Insulin release from HIT cells could also be evoked by the sulphonylureas glibenclamide and tolbutamide and by an increase in concentration of extracellular K+ to 40 mmol/l. The content of cyclic AMP in HIT cells was increased modestly by glucose but not by an increase in extracellular K+. Forskolin elicited a 4-fold increase in cyclic AMP content. We conclude that HIT cells retain the essential features of the insulin secretory response of normal B cells and represent an important tool for further biochemical characterization of the secretory system.
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PMID:Insulin secretory responses of a clonal cell line of simian virus 40-transformed B cells. 302 78

Using an antiserum (no. 373) raised against a tyrosinated analog of preproTRH53-74 [( Tyr1]preproTRH53-74 or pYT 22), we have demonstrated the presence of a discrete population of immunoreactive neurons in the midbrain periaqueductal gray (PAG). Relative to the distribution of serotonin, somatostatin, peptide histidine isoleucine (PHI), methionine enkephalin, substance P and neurotensin-containing neuronal perikarya in the PAG, neurons containing immunoreactive pYT 22 occupied a unique location in the ventrolateral PAG. In contrast, terminal fields containing these neuroactive substances with the exception of PHI, were seen in abundance in the region of the ventrolateral PAG neurons. These studies indicate that a non-TRH sequence contained within the N-terminal portion of the TRH prohormone are expressed in a distinct group of neurons in the ventrolateral PAG. The location of these neurons in the PAG in a region richly innervated by nerve terminals containing analgesia-mediating substances, suggests a possible role for proTRH-derived peptides in the modulation of nociception.
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PMID:Neurons containing a N-terminal sequence of the TRH-prohormone (preproTRH53-74) are present in a unique location of the midbrain periaqueductal gray of the rat. 314 23

Bombesin-like immunoreactivity (BLI), a putative peptidergic neurotransmitter of the gastrointestinal intrinsic nervous system is released from the isolated perfused rat stomach in response to the classical neurotransmitter acetylcholine and in response to other putative peptidergic neurotransmitters such as vasoactive intestinal peptide (VIP), peptide histidine isoleucine (PHI) or growth hormone releasing factor (GRF). The secretion of BLI is modulated not only by gastric factors such as the intragastric pH but also by changes of perfusate glucose concentrations indicating that alterations of carbohydrate metabolism might have an effect on gastric neuroendocrine regulation. Since previous studies have shown that insulin, the major regulatory hormone of glucose metabolism, reduces gastric somatostatin and glucagon secretion it was of interest to determine the effect of insulin on gastric BLI and gastrin secretion. The experiments were performed in the isolated perfused rat stomach model. The addition of porcine insulin to the perfusate at concentrations of 50 and 100 microU/ml had no effect on basal BLI and gastrin secretion. The infusion of acetylcholine (2 X 10(-6)M and 4 X 10(-6)M) elicited a stimulation of BLI and gastrin secretion which was not altered by the addition of insulin (100 microU/ml). On the other hand, significant effects of insulin were observed during administration of the two putative peptidergic neurotransmitters VIP and leu-enkephalin. The infusion of VIP at 10(-11)M and 10(-8)M had no effect on BLI and gastrin secretion in the absence of insulin, however, with the addition of insulin (100 microU/ml) the higher dose of VIP (10(-8)M) elicited a significant stimulation of BLI secretion while both doses of VIP (10(-11)M and 10(-8)M) significantly increased gastrin release. Similar to VIP the infusion of leu-enkephalin at doses of 10(-9)M and 10(-6)M had no effect on BLI and gastrin secretion in the absence of insulin. When insulin was added to the perfusate both doses of leu-enkephalin elicited a significant stimulation of BLI secretion while gastrin remained unchanged. The addition of the specific opiate receptor antagonist naloxone (10(-5)M) did not block the effect of leu-enkephalin in the presence of insulin. In addition the effect of naloxone was also examined during cholinergic stimulation. The addition of naloxone (10(-5)M) during the infusion of acetylcholine abolished the stimulatory effect on BLI secretion in the absence of insulin, whereas in the presence of insulin naloxone did not alter cholinergically-induced BLI secretion.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effect of insulin on secretion of bombesin-like immunoreactivity and gastrin from the isolated rat stomach in response to acetylcholine, VIP and leucine-enkephalin. 351 44

In cultured rat hepatocytes, the effects of gut hormones on bile acid uptake and release were studied. It was found that cultured hepatocytes continued to secrete bile acids into the culture medium and incorporated them effectively as a function of incubation time. Gut hormones such as secretin, glucagon, vasoactive intestinal polypeptide (VIP), peptide histidine isoleucine (PHI), gastric inhibitory polypeptide (GIP), tetragastrin, cholecystokinin-octapeptide (CCK-8), pancreatic polypeptide (PP), neurotensin substance P, beta-endorphin (beta-End), methionine-enkephalin (Met-enk), motilin, bombesin and somatostatin (SS) had no effect on bile acid uptake by cultured hepatocytes. In bile acid release studies, only secretin caused a dose-dependent stimulation of bile acid release, while other gut hormones had no effect on bile acid release into medium. These results indicate that secretin acts directly on cultured rat hepatocytes and/or bile canaliculi, besides its effect on the bile duct, and influences bile acid metabolism.
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PMID:Effects of gut hormones on bile acid uptake and release in cultured rat hepatocytes. 359 53

Gastric acid secretion is known to be controlled by a complex system of interacting factors. Amongst these, regulatory peptides make a significant contribution. In the present study, immunocytochemistry and radioimmunoassay were used to investigate gastric regulatory peptides in animals with pharmacologically reduced gastric acid secretion. Increased numbers of densely immunostained antral gastrin-immunoreactive (G) cells were seen in rats which had been rendered virtually achlorhydric by administration of high-dose (400 mumol/kg daily) omeprazole over a 10-week period. These morphological changes were accompanied by increases in the plasma, antral and fundic concentrations of gastrin, as measured by radioimmunoassay. In contrast, antral somatostatin-containing cells were reduced, and there was a corresponding fall in the tissue content of the peptide. Ten weeks after treatment had ceased, the peptide profiles had returned to normal. No other regulatory peptide, whether endocrine or neural, appeared to alter during treatment with high-dose omeprazole. Treatment with high-dose (700 mumol/kg daily) ranitidine also caused an elevation in the G cell population and the antral and plasma content of gastrin, but to a lesser extent than that observed during omeprazole treatment. Somatostatin cells and tissue levels did not alter in these animals, and no other morphological changes could be detected. Radioimmunoassay, however, measured reduced quantities of vasoactive intestinal peptide, peptide histidine isoleucine and calcitonin gene-related peptide. Achlorhydria, induced by omeprazole at a dosage of 250-500 times that required for effective acid inhibition in man and animals, therefore resulted in reciprocal changes in gastrin and somatostatin cells. These changes are support for the postulated roles of these peptides in the control of gastric acid secretion.
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PMID:Gastric regulatory peptides in rats with reduced acid secretion. 379 73

The gastric autonomic innervation of the dogfish was examined for regulatory peptides and serotonin by immunochemical techniques. Bouin's-fixed, paraffin-embedded or benzoquinone-fixed frozen sections were used for light microscopical immunocytochemistry and glutaraldehyde-fixed resin-embedded sections for electron microscopical immunocytochemistry. Bombesin-, somatostatin-, gastrin/cholecystokinin-, substance P-, peptide histidine isoleucine-, vasoactive intestinal peptide- and serotonin-immunoreactive nerves were found in all layers of the stomach wall. Bombesin and vasoactive intestinal peptide-containing nerves were identified at ultrastructural level. Radioimmunoassay of acetic acid extracts of tissue confirmed the presence of immunoreactivity for bombesin, somatostatin, substance P, peptide histidine isoleucine and vasoactive intestinal peptide. Reverse phase high performance liquid chromatography indicated that the peptides identified were broadly similar to their mammalian counterparts.
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PMID:Neuropeptides and 5-HT immunoreactivity in the gastric nerves of the dogfish (Scyliorhinus stellaris). 391 13

The effects of iontophoretically applied human pancreatic growth hormone-releasing factor (hpGRF), peptide histidine isoleucine (PHI-27), and somatostatin (SS) on the extracellular activity of single cells in the hypothalamus, thalamus, and cortex of the rat brain were studied in urethane-anesthetized, male rats. Neurons with membrane sensitivity to hpGRF, PHI-27, and SS were present in each brain region. Although neurons excited by these peptides were encountered in thalamus and hypothalamus, depression of neuronal firing was the predominant response observed. Overall, the neurons responding to hpGRF also possessed membrane sensitivity to PHI-27, whereas, the hpGRF sensitive neurons appeared to be more divided as to their ability to respond to SS. The results clearly demonstrate that hpGRF and PHI-27 are capable of affecting the membrane excitability of neurons in several brain regions. The distribution of neurons sensitive to hpGRF suggests that hypothalamic GRF, in addition to its well documented role in the regulation of pituitary growth hormone secretion, may subserve other physiological events in the rat central nervous system as a neurotransmitter and/or neuromodulator.
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PMID:Sensitivity of rat forebrain neurons to growth hormone-releasing hormone. 393 50

1. Somatostatin (SRIF, somatotropin release inhibiting factor), at a concentration of 2 x 10(-8) M (32 ng/ml) decreased the rat of alanine release (approximately 45%) and increased glutamine release (approximately 30%) in in vitro preprations of m. extensor digitorum longus (EDL) muscle from 35--40 day old Wistar rats. These effects of SRIF were observed under both aerobic and anaerobic conditions. 2. SRIF increased the formation of 14CO2 from alanine but not from glutamine, glutamate, leucine, isoleucine or valine. 3. The incorporation of alanine, glutamine, glutamate, leucine, isoleucine and valine into muscle protein was unaffected by the presence of SRIF.
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PMID:The effect of somatostatin (SRIF) on the release of amino acids from skeletal muscle. 610 70

Studies were conducted to explore the effects of vasoactive intestinal peptide (VIP), histamine, somatostatin-14 and -28 (S-14 and S-28), and prostaglandin E2 (PGE2) on cAMP production in gastric glands isolated from the guinea pig. VIP (EC50 = 5 X 10(-10) M) and PGE2 (EC50 = 10(-8) M) induced cAMP accumulation in glands isolated by means of EDTA from the fundus or antrum. The structurally related peptides PHI (peptide with N-terminal histidine and C-terminal isoleucine amide) and secretin also increased cAMP production in the system, but with 200 to 2000 times lower potencies than VIP. Combinations of VIP with PHI or secretin do not produce additive stimulation, indicating that PHI or secretin interact with the receptor-cAMP system highly sensitive to VIP. Histamine was about 10 times more potent in fundus (EC50 = 10(-5) M) than in antrum (EC50 = 9 X 10(-5) M) and did not produce any stimulation in enterocytes isolated from the upper part of the duodenum. Complete inhibitions caused by the H2 receptor antagonist cimetidine (Ki = 0.15-0.16 X 10(-6) M) (Ki is the inhibition constant) or by the H1 receptor antagonist diphenhydramine (DPH) (Ki = 13-17 X 10(-6) M) indicate that H interacts with typical H2 receptors mediating adenylate cyclase activation in fundic (Ka = 10(-5) M) (Ka is the association constant) or antral membranes (Ka = 3 X 10(-5) M). In fundus, S-14 inhibited partially (about 60%) cAMP production evoked by H or by its H1 or H2 agonists. The kinetics and the inhibitory potencies (2 X 10(-8) M) or efficacies of S-14 and -28 were identical. No effect of S-14 was found on basal or on cAMP production induced by VIP or PGE2 in either fundic or antral glands or by H in antral glands. The results support the hypothesis of a regulatory role for VIP and/or secretin in mucous and/or peptic secretions via a cAMP-dependent mechanism in gastric mucosa in mammals. Second, we propose that S-14 as well as S-28 may inhibit gastric acid secretion by a direct and selective control of H-induced cAMP production in parietal cells, through a common recognition site (receptor?) distinct from the H2 receptor. Third, not only parietal cells, but also nonparietal cells of the antrum possess an H2 receptor-cAMP system. This finding could be related to the in vivo regulation by cimetidine of endocrine (somatostatin) and exocrine (pepsin) secretions by the stomach.
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PMID:Regulation by vasoactive intestinal peptide, histamine, somatostatin-14 and -28 of cyclic adenosine monophosphate levels in gastric glands isolated from the guinea pig fundus or antrum. 613 13

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