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)

Upon investigation of pig intestinal peptides for effects on the release of endocrine hormones from the isolated perfused rat pancreas, we reported earlier that glucose-stimulated insulin release was inhibited by PEC-60, a peptide with marked sequence similarity to PSTI (pancreatic secretory trypsin inhibitor). Continuing this study we found a polypeptide, which inhibited glucose-induced insulin release but enhanced glucose-induced somatostatin secretion. Determination of the amino acid sequence of this polypeptide revealed that it is identical to that of PSTI. Thus, PSTI modulates islet hormone release.
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PMID:Pancreatic secretory trypsin inhibitor (PSTI) isolated from pig intestine. Influence on insulin and somatostatin release. 167 2

Octreotide acetate is a long-acting analogue of the naturally occurring inhibitory gastrointestinal peptide, somatostatin. We tested the efficacy of octreotide in controlling the symptoms of dumping syndrome in response to a provocative meal in a randomized, double-blinded, crossover trial in nine severely affected patients. Pretreatment with octreotide acetate (100 micrograms injected subcutaneously) reduced postprandial dumping symptoms from a mean +/- SEM score of 15.7 +/- 1.6 (placebo treatment day) to 4.6 +/- 1.7. With placebo treatment, all nine patients became symptomatic in response to the meal, whereas with octreotide treatment, symptoms occurred in only two of nine patients. Similarly, all placebo-treated patients showed a postprandial increase in pulse rate to a mean +/- SEM of 105 +/- 6 beats per minute, whereas only one of nine octreotide-treated patients showed an increase in pulse rate (mean +/- SEM, 80 +/- 3 beats per minute). These differences were also statistically significant. While no significant changes were observed in postprandial hematocrit values or osmolality between placebo and octreotide treatments, octreotide prevented hypoglycemia in four affected patients and significantly inhibited insulin release. We conclude that octreotide is a useful tool in the treatment of patients with severe, refractory dumping syndrome.
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PMID:Control of dumping symptoms by somatostatin analogue in patients after gastric surgery. 192 23

Sandostatin (SMS 201-995 (SMS)), a potent, long acting analog of native somatostatin was used in five patients with functional endocrine tumors (gastrinoma, two patients; insulinoma, one patient; glucagonoma, one, and adult onset nesidioblastosis, one). Primary and secondary peptide levels were obtained during provocation with a test meal, a calcium infusion, a secretin bolus and either a glucagon or tolbutamide bolus. During provocation test, the levels of the primary peptides insulin and C-peptide (nesidioblastosis and insulinoma), gastrin (gastrinoma), glucagon (glucagonoma) and the secondary peptides calcitonin, gastrointestinal peptide, gastrin releasing peptide, motilin, neurotensin, pancreatic polypeptide, somatostatin, substance-P and vasoactive intestinal peptide were obtained at predetermined intervals and quantitated by radioimmunoassay. SMS therapy was begun and peptide levels were again obtained during provocation. SMS suppressed basal primary peptide levels in all patients by more than 50 per cent. In 23 of 26 provocative tests, SMS effectively decreased circulating peptide levels by more than 50 per cent. Thirteen instances of elevated basal secondary peptides were discovered, and SMS universally suppressed these levels by a mean of 54 per cent. Of the 44 provocative tests performed, elevated secondary peptide levels were present in 41. SMS was effective in 31 of these 41 tests. The mean suppression of these provoked secondary peptide levels was 70 per cent. SMS effectively suppresses both basal and provoked peptides and, thus, provides relief of the clinical symptoms induced by pathologic elevations of primary and secondary peptides.
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PMID:Suppression of primary and secondary peptides with somatostatin analog in the therapy of functional endocrine tumors. 246 Sep 58

Since endogenous cholecystokinin (CCK) is released after oral administration of camostate, it has been suggested that camostate-induced pancreatic growth is mediated via circulating CCK. To test this concept, we investigated the effects of three potentially inhibitory substances on rat pancreatic hypertrophy caused by feeding of camostate over 2 weeks: (1) L-364,718, the novel specific highly potent nonpeptide CCK receptor antagonist, (2) octreotide (SMS 201-995), a potent long-lasting somatostatin analogue and (3) pancreastatin (33-49), the biologically active C-terminal fragment of the novel gastrointestinal peptide pancreastatin. Camostate feeding (200 mg/kg) once daily for 14 days induced a significant increase in pancreatic weight, total protein, trypsinogen and polyamine levels, whereas total amylase content was substantially diminished. Simultaneous oral or subcutaneous treatment with L-364,718 (0.3 mg/kg twice daily) completely suppressed all trophic effects of camostate. Octreotide (25 micrograms/kg twice daily s.c.) and pancreastatin (33-49) (10 micrograms/kg twice daily s.c.) did not change any trophic parameter. In case of octreotide it could be shown that two daily injections only partially suppressed elevated CCK levels. Pancreatic DNA and putrescine levels were slightly reduced in rats receiving the CCK antagonist alone. These results demonstrate that camostate-induced pancreatic hypertrophy in rats is caused by the release of endogenous CCK which may contribute to the maintenance of normal pancreatic DNA and putrescine concentrations.
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PMID:Influence of CCK antagonist L-364,718, pancreastatin (33-49) and a somatostatin analogue on camostate-induced rat pancreatic hypertrophy. 261 49

Somatostatin, the hypothalamic release-inhibiting factor, has been found to stimulate gluconeogenesis in rat kidney cortical slices. Stimulation by somatostatin was linear and dose-dependent. Other bioactive peptides such as cholecystokinin, gastrointestinal peptide, secretin, neurotensin, vasoactive intestinal peptide, pancreatic polypeptide, beta endorphin and substance P did not affect the renal gluconeogenic activity. Somatostatin-induced gluconeogenesis was blocked by phentolamine (alpha adrenergic antagonist) and prazosin (alpha1 adrenergic antagonist) but not by propranolol (beta adrenergic antagonist) and yohimbine (alpha2 adrenergic antagonist) suggesting that the effect is via alpha1 adrenergic stimuli. Studies on the involvement of Ca2+ revealed that tissue depletion and omission of Ca2+ from the reaction mixture would abolish the stimulatory effect of somatostatin. Furthermore, somatostatin enhanced the uptake of 45calcium in renal cortical slices which could be blocked by lanthanum, an inhibitor of Ca2+ influx. It is proposed that the stimulatory effect of somatostatin on renal gluconeogenesis is mediated by alpha1 adrenergic receptors, or those which functionally resemble alpha1 receptors and that the increased influx of Ca2+ may be the causative factor for carrying out the stimulus.
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PMID:Somatostatin: a metabolic regulator. 286 45

The effect of gastric secretory inhibitors, vasoactive agents and gastrointestinal peptide hormones were investigated on gastric mucosal blood flow (MBF) and HCl secretion in 197 subjects. Changes in MBF were estimated by a new clearance substance, 99mTc-4-methyl-aminophenazone originally described by the authors. The procedure seemed to be suitable for characterizing changes in MBF without any toxic side effect or considerable radioactive loading of the patient or its surroundings. The studies were performed after a secretory steady state had been achieved by continuous pentagastrin infusion. Some experiments were done in the fasting stomach instilled with 0.160 N HCl. Secretory inhibition following atropine, pirenzepine, ranitidine and somatostatin was a primary effect of these substances, the observed MBF decrease being a secondary one. In contrast, vasopressin caused a fall in mucosal blood supply through vasoconstriction, the concomitant secretory inhibition being a secondary phenomenon. Certain doses of dopamine and terbutaline increased MBF without influencing HCl secretion. Glucagon in the dose used did not influence either mucosal blood flow or acid secretion. Synthetic secretin in the fasting stomach increased MBF without affecting HCl production; during pentagastrin stimulation it inhibited acid production while MBF remained unchanged. Cholecystokinin-octapeptide proved to be a direct vasodilating agent with a slight acid output increasing effect. Divergent effects of some drugs on mucosal blood flow and HCl production may be important in the pathology of hypoxic ulcerative damage and in the reparative processes of gastric ulceration. The 99mTc-4-methyl-aminophenazone clearance technique proved to be a reliable method for screening of drugs possessing vasoactive or secretion influencing properties.
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PMID:Mucosal blood flow changes in the human stomach measured by the 99mTc-4-methylaminophenazone clearance technique. 368 45

The effects of a porcine gastric fundic mucosal extract (molecular weight less than 10 000) has been compared with the effects of eight candidate gastrointestinal peptides on glucose absorption from the jejunum in a rat model. Bolus injection of the extract produced immediate and marked depression of glucose absorption. None of the candidate peptides tested produced this response, although somatostatin and substance P depressed absorption as a late phenomenon after 30 minutes. We conclude that the effects of the fundic extract are not reproduced by any of these candidate peptides. This strengthens the evidence for a novel gastrointestinal peptide, resident in fundic mucosa, which affects absorption from upper small bowel.
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PMID:Effects of porcine gastric fundic factor, somatostatin, substance P, glucagon, neurotensin, bombesin, VIP, motilin, and pentagastrin on jejunal glucose absorption in the rat. 618 32

The gastrointestinal peptide response to food was assessed in 6 healthy subjects following oral administration of 40 mg omeprazole. There was a small but statistically significant increase in basal plasma gastrin six hours after the dose of omeprazole, but the post-prandial plasma gastrin was not significantly increased. There was no significant effect on basal or post-prandial levels of somatostatin, insulin, pancreatic glucagon, enteroglucagon, gastric inhibitory polypeptide, pancreatic polypeptide, motilin, neurotensin, cholecystokinin, secretin, vasoactive intestinal peptide and gastrin-releasing peptide or blood glucose concentration.
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PMID:Effect of single dose of omeprazole on the gastrointestinal peptide response to food. 636 14

Motilin, a gastrointestinal peptide recently detected in the rat brain, was capable of stimulating growth hormone (GH) release from dispersed anterior pituitary cells in a dose-related fashion. In initial experiments, the minimum effective concentration was 10(-7) M and the effect was specific for just GH. Subsequent experiments demonstrated that concentrations of synthetic motilin as low as 10(-9) M could significantly stimulate GH release. Only large IV doses (100 micrograms) of motilin significantly elevated circulating GH levels in vivo. However, administration of antiserum to porcine motilin (100 microliters, IV) significantly depressed plasma GH levels, suggesting a physiologic role for median eminence and hypothalamic motilin in the control of GH secretion. Furthermore, infusion of motilin into the third ventricle of conscious rats resulted in a significant depression of GH levels, suggesting an ultrashort loop feedback action of motilin on the release of motilin itself or somatostatin. In light of motilin's only minor structural similarity to human pancreatic tumor GH-releasing factor (GRF) and the ability of passive immunoneutralization of motilin to lower GH, this 22-amino acid peptide must now be considered a physiologic GRF.
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PMID:Motilin: a novel growth hormone releasing agent. 642 71

Streptozotocin diabetes prevents induction of pancreatic tumors in several animal models, suggesting a pivotal role for islet cell products in the pathogenesis of pancreatic cancer. To test the hypothesis that altered gastrointestinal peptide levels in streptozotocin diabetes influence tumor growth, human pancreatic cancer cells (MIA PaCa-2) were implanted subcutaneously into streptozotocin diabetic nude mice. After 3 weeks, tumors in the control group weighed 43 mg and tumors in the diabetic group weighed 12 mg (P < 0.001). Plasma insulin and IGF-1 levels were significantly decreased in the streptozotocin-treated animals compared to those of control (insulin: 23 microU/ml vs 31 microU/ml, P < 0.001; IGF-1: 254 ng/ml vs 324 ng/ml, P < 0.001). In contrast, somatostatin and glucagon were significantly elevated in the streptozotocin diabetic group relative to control levels (somatostatin: 179 pg/ml vs 54 pg/ml, P < 0.001; glucagon: 290 pg/ml vs 134 pg/ml, P < 0.001). Competitive binding studies revealed specific cell surface receptors for insulin (Kd = 15.5 nM), IGF-1 (Kd = 30.0 nM), and somatostatin (Kd = 2.5 nM) on the MIA PaCa-2 cells. Receptors for glucagon were absent. In an in vitro cell proliferation assay, cell division was promoted by insulin (P < 0.01, max + 11%) and IGF-1 (P < 0.01, max + 10%). Somatostatin inhibited cell division (P < 0.01, max - 18%). No effect was seen with glucagon. The growth of pancreatic cancer, particularly in diabetes, may be influenced by gut peptides in a receptor-dependent fashion.
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PMID:GI hormonal changes in diabetes influence pancreatic cancer growth. 779 56


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