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

A simple technique to examine the effects of drugs on the gastric secretion response to the secretagogues without anesthesia was shown in this paper. The administration of bethanechol (1 mg/kg, s.c.), histamine (15 mg/kg, s.c.) or pentagastrin (0.25 mg/kg, i.p.) significantly increased the gastric volume and the total acid output in the pylorus-ligated rat. These responses to the secretagogues were inhibited by N-butylscopolamine, urogastrone or cimetidine dose-dependently. N-butylscopolamine (0.5 mg/kg, i.p.) inhibited the response to bethanechol but not that to pentagastrin or histamine. Cimetidine (5 mg/kg, i.p.) inhibited not only the response to histamine but also the acid response to bethanechol or pentagastrin. Urogastrone (5 mg/kg, i.p.) inhibited the response to these three secretagogues. The ratio of the total acid output to the gastric volume was also examined in each of the cases. Somatostatin (0.1 mg/kg, i.p.) inhibited the response to pentagastrin, but not that to bethanechol or histamine. On the other hand, an analogue of somatostatin (SS-1; 0.1 mg/kg, i.p.) inhibited the response to bethanechol but not that to pentagastrin or histamine.
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PMID:[Effects of somatostatin and its analog on gastric secretion. An application of the secretagogues to gastric secretion]. 286 56

Lys-beta-urogastrone, an analogue of human beta-urogastrone with an additional N-terminal lysine, was shown to have similar effects in mice and sheep to mouse epidermal growth factor (mEGF). Lys-beta-urogastrone in doses of 0.18-3.24 micrograms g-1 body weight caused both precocious separation of eyelids and eruption of incisors in neonatal mice. In 17 sheep, intravenous infusion of the urogastrone analogue over c. 24 h led, towards the end of infusion, to erythema of the muzzle, caused reductions in voluntary food intake (with doses greater than or equal to 50 micrograms kg-1) and generally easier manual harvesting of the fleece (with infusions greater than or equal to 81 micrograms kg-1), with spontaneous shedding of the fleece (c. 14 days after infusions of greater than or equal to 116 micrograms kg-1). In five sheep infusions of 25, 38, 50, 83 and 118 micrograms kg-1 fleece-free body weight, plasma concentrations of lys-beta-urogastrone were near maximal 20 h after the infusions started and were, respectively, 1.1, 1.7, 5.5, 18 and 79 micrograms l-1 plasma. Plasma concentrations of gastrin, somatostatin and pancreatic polypeptide were determined in these five sheep. Plasma gastrin rose sixfold by the end of infusions of 25 micrograms kg-1 of the urogastrone analogue, and tenfold with the higher doses of infusion. Although plasma somatostatin concentrations were variable, a consistent trend was observed; lower levels were apparent during the lys-beta-urogastrone infusions. There was no discernible trend in pancreatic polypeptide concentrations.
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PMID:Effects of lys-beta-urogastrone in vivo. 290 24

In experimental studies, 0.6 N HCl-induced gastric mucosal injury was significantly severe in submandibularectomized rats (SMR rats) than that in either SMR rats receiving exogenous mouse EGF (SMR + EGF rats) or controls. This was also true in gastric injury induced by 0.4 N HCl under pretreatment with indomethacin to reduce gastric mucosal prostaglandins (PGs). Somatostatin (SLI), PGE2, and PAS-stained mucus in the corpus were significantly reduced in SMR rats in comparison to SMR + EGF and control rats. In clinical studies, salivary EGF secretion was much higher in peptic ulcer patients than healthy controls. beta-Urogastrone was effective in the treatment of gastric ulcers. On the basis of experimental studies, we conclude that the protective effect of EGF on the gastric mucosa is, in part, mediated indirectly by increases in SLI, PGE2, and mucus production. However, endogenous, as well as exogenous, EGF has an important direct, cytoprotective effect on the gastric mucosa. From the clinical studies, we also conclude that salivary EGF secretion in ulcer patients increases in a homeostatic response to the presence of an ulcer, facilitating ulcer healing. Furthermore, we believe that beta-urogastrone, human EGF, might prove to be an effective drug in the clinical treatment of gastric ulcers.
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PMID:Experimental and clinical studies on epidermal growth factor for gastric mucosal protection and healing of gastric ulcers. 326 11

Luminal application of acid was recently shown to stimulate surface epithelial HCO3(-) transport in stomach and duodenum. Effects of some potential transmitters of this response were therefore studied in amphibian gastric fundic and proximal duodenal mucosa in vitro. Duodenal HCO3- transport, which could be titrated directly, was stimulated by dibutyryl cAMP (DBcAMP, 10(-6) M), the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (10(-6) M), noradrenaline (10(-6) M), pancreatic glucagon (10(-8) M), and gastric inhibitory peptide (GIP, 10(-10) M). Stimulation by glucagon, but not by prostaglandin E2 (PGE2, 10(-6) M), required Cl- in the luminal solution and was prevented by furosemide (10(-3) M). This suggests that glucagon may affect HCO3(-)-Cl- exchange at the luminal membrane while transport stimulated by prostaglandins may be electrogenic. Stimulatory effects of glucagon and PGE2 were also additive. Gastric HCO3- transport, studied in tissues after inhibition of H+ secretion by histamine H2-antagonists, clearly differed from duodenum in that noradrenaline and GIP were inhibitory and DBcAMP was without effect. Stimulation of gastric HCO3- transport was observed with glucagon (10(-8) M), natural cholecystokinin (CCK, 10(-8) M), and CCK octapeptide (10(-7) M), CCK preparations had no effect in the duodenum. Although tested over a wide range of concentrations, no effect on either duodenal or gastric HCO3- transport was observed with histamine, pentagastrin, tetragastrin, urogastrone, ACTH, bombesin, motilin, secretin, serotonin, somatostatin, substance P, or vasoactive intestinal peptide.
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PMID:Gastric and duodenal HCO3- transport in vitro: effects of hormones and local transmitters. 697 77

Somatostatin (SMS) is administered to patients with short bowel syndrome and enterocutaneous fistulae. Previous studies have shown detrimental effects of SMS on intestinal adaptation after bowel resection. We examined whether administration of epidermal growth factor (EGF) could reverse the deleterious effects of SMS seen after enterectomy. Sixty-four Sprague-Dawley rats underwent an 80% small bowel resection or transection as control. Rats received either SMS at 50 ng x kg(-1) x h(-1), EGF/Urogastrone at 1.5 microg x kg(1-) x h(-1), or both via subcutaneous miniosmotic pumps. Samples were obtained at 1 day and 1 week after surgery for histologic examination, analysis of apical Na+/glucose cotransporter protein and mRNA expression, and analysis of basolateral Na+/K+ ATPase protein and mRNA expression. Protein expression was analyzed by Western blotting whereas mRNA expression was compared by ribonuclease protection assay. Histologically, villus to crypt length after intestinal resection showed increased adaptation in EGF/SMS vs SMS treated animals in both jejunum and ileum. Analysis of mRNA and protein of epithelial transporters show early increases when EGF is administered with SMS vs SMS only. We conclude that combination therapy using EGF and SMS may be beneficial to intestinal adaptation after small bowel resection. Both histologic and molecular data suggest an enhanced absorptive potential and adaptation of the remaining intestine when EGF is administered.
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PMID:Epidermal growth factor improves intestinal adaptation during somatostatin administration in vivo. 866 Nov 91

At the turn of XIX and XX century, the principal concept explaining the mechanism of secretory activity of the digestive glands was nervism proposed by I. P. Pavlov at Russian physiological school in St Petersburg, and this dogma was widely recognized for several years in other countries. The discovery of secretin in 1902 by W.B. Bayliss and E.H. Starling, and then of gastrin in 1906 by J.S. Edkins, emphasized the hormonal regulation of pancreatic and gastric secretion, respectively. In 1943, A.C. Ivy and E. Olberg discovered a hormone, which contracts the gallbladder - cholecystokinin (CCK), while A. Harper and H.S. Raper described another hormone, pancreozymin, which stimulated pancreatic enzymes. It required over twenty years, however, for these and many other hormones to be identified, purified and synthesized due to the extensive work of several teams including R. Gregory, G. Dockray and Kenner of the UK; J. Rehfeld of Denmark and E. Wunsch of Germany for their work on gastrin; E. Jorpes and V. Mutt of Sweden and N. Yahaihara of Japan for their work on secretin and other GI hormones including, CCK, vasoactive intestinal peptide (VIP), gastric inhibitory peptide (GIP), motilin, gastrin-releasing peptide (GRP) and others peptides. CCK and pancreaozymin were found by E. Jorpes and V. Mutt to represent structurally a common messenger for pancreatico-biliary secretion. This rapid development of GI endocrinology in the 1960s and 1970s could be attributed to the application of peptide biochemistry in characterizing various peptide hormones. The technique of radioimmunoassay by S.A. Berson and R.S. Yalow in 1959 measured minute amounts of hormones in the circulation and tissue, and the technique of immunocytochemistry detected the cellular origin of these hormones. Further progress in molecular biology led to sequencing GI hormones and their prohormones, and opened a new area of investigation for the physiological role of these hormones in the mechanism of digestive gland secretion, motility of gastrointestinal tract, visceral blood flow, tissue growth and integrity in health, as well as in various digestive diseases. Overall, apparent divergent concepts, the nervous control (Pavlov) and hormonal control (Bayliss and Starling), greatly facilitated the elucidation of the interacting neurohormones during the cephalic, gastric, and intestinal phases of gastric and pancreatic secretion in health and digestive diseases. Although Polish contributions in the early phase of GI endocrinology concerned mostly gastric inhibitory hormones such as enterogastrone and urogastrone, major Polish traces can be detected in the elucidation of origin and physiological role and pathological involvement of gastrin, CCK, secretin, motilin, gastric inhibitory peptide and the most recent additions of enterohormones such as epidermal growth factor, somatostatin, leptin or ghrelin. Major achievements have been obtained in gastric and colorectal cancerogenesis involving gastrin and its precursor, progastrin.
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PMID:The history of gastrointestinal hormones and the Polish contribution to elucidation of their biology and relation to nervous system. 1507 66