Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The receptors for the brain and gastrointestinal peptide, cholecystokinin, can be classified into CCKA and CCKB subtypes. Having recently cloned the rat CCKB receptor, we used it's cDNA to isolate the human CCKB receptor homologue from brain and stomach which encodes a 447 amino acid protein with 90% identity to both rat CCKB and canine gastrin receptors. Northern hybridization identifies transcripts from stomach, pancreas, brain and gallbladder. The CCKB receptor gene maps to chromosome 11. Expression of the receptor cDNA in COS-7 cells was characteristic of a CCKB receptor subtype pharmacology. These data confirm that we have cloned a novel gene for the human brain and stomach CCKB receptor.
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PMID:Molecular cloning of the human brain and gastric cholecystokinin receptor: structure, functional expression and chromosomal localization. 128 Apr 19

The purpose of this investigation was to determine the influence of long-distance running on the secretion of the gastrointestinal peptide hormones cholecystokinin (CCK) and gastrin. Several known stress hormones, ACTH, cortisol and norepinephrine, were also measured. The hormones were estimated before and after a competitive marathon run of 46.5 km and under control conditions a few weeks later. Except gastrin, all hormones were significantly higher under prerun conditions than under control conditions and were highest after the run. The most marked prerun elevation was in CCK. Therefore, CCK seems to be an important regulation factor in response to anticipatory stress.
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PMID:Cholecystokinin, gastrin and stress hormone responses in marathon runners. 132 Feb 60

To determine the response of the preterm infant's intestine to entire feedings at different postnatal ages, we recorded results of manometry of the gastroduodenum and determined fasting plasma concentrations of gastrin, gastric inhibitory peptide, neurotensin, and peptide YY three times in each of two groups: 27 preterm infants were randomly assigned to receive hypocaloric enteral nutrition on postnatal days 3 to 5 (early feeding) or on days 10 to 14 (late feeding). Initial observations (study 1) were performed by the fifth postnatal day; study 2 was performed on days 10 to 14, and study 3 on days 24 to 28. Early-fed infants received hypocaloric feedings immediately after study 1; late-fed infants did not receive enteral feedings until the completion of study 2. Although motor activity and fasting gastrointestinal peptide concentrations did not differ between groups at study 1, at study 2 early-fed infants had significantly more mature motor patterns than did babies not being fed. Early-fed infants also had significantly higher plasma concentrations of gastrin and gastric inhibitory peptide than did late-fed infants; neurotensin and peptide YY values were similar in both groups. By the time of study 3, when late-fed infants had also received enteral feedings, gut development was not different in the two groups. However, early-fed infants were able to tolerate full oral nutrition sooner, had fewer days of feeding intolerance, and had shorter hospital stays. Thus the provision of early hypocaloric nutrition was associated with earlier nutrition of preterm infants' intestinal function and resulted in improved feeding tolerance. These findings support the use of early feedings in preterm infants.
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PMID:Effect of early feeding on maturation of the preterm infant's small intestine. 159 57

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

Gallbladders removed at cholecystectomy are a potentially useful source of human receptor for the gastrointestinal peptide hormone cholecystokinin (CCK). Seven healthy gallbladders (removed incidentally at time of resection of hepatic metastases) and 50 diseased gallbladders were studied. Cholecystokinin radioligand binding to an enriched plasma membrane preparation from these tissues was shown to be rapid, reversible, temperature-dependent, saturable, specific, and high-affinity. Computer analysis of equilibrium binding data using the Ligand program best fit a single class of binding sites with Kd = 1.0 +/- 0.1 nM (mean +/- SEM). This was similar in health and disease, with no apparent differences related to age, gender, or body habitus. The structural specificity for binding to this site correlated well with relative potencies for CCK-gastrin peptides to stimulate gallbladder contraction. To biochemically characterize this receptor, we used a battery of reagents, including "long" (125I-Bolton Hunter-CCK-33) and "short" 125I-D-Try-Gly-[(Nle28,31)CCK-26-33] probes that were cross-linkable through their amino terminus and a monofunctional probe with a photolabile group at its carboxyl terminus 125I-D-Tyr-Gly[(Nle28,31,pNO2-Phe33)CCK-26-33]. All probes specifically labeled a human gallbladder muscularis protein of Mr = 85,000-95,000, which was also independent of diagnosis. Labeling of this band was inhibited in a concentration-dependent manner by CCK-8 and by L-364,718. Thus, the CCK receptor present on the very common surgically removed human gallbladder is functionally and biochemically intact and is useful for further characterization.
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PMID:Functional and biochemical characterization of the human gallbladder muscularis cholecystokinin receptor. 292 56

Enprostil, a long-acting, orally active dehydroprostaglandin E2 with cytoprotective and gastric antisecretory properties, is a potent inhibitor of meal-stimulated gastrin release. Recent data have suggested suppression of additional other gastrointestinal peptide hormones following single doses of enprostil. The current investigation was conducted to further clarify the effects of enprostil administration on gastrointestinal hormones and glucose metabolism under physiologic conditions and to determine whether these effects were present following multiple doses of the agent. Enprostil 70 mcg/d and its placebo were each administered for 7 1/2 days to eight normal male subjects in a study of crossover design, each treatment period lasting 7 1/2 days and separated by a 7 day washout period. Subjects received a test meal on days 1 and 8 and an oral glucose challenge on day 3 of each treatment period following enprostil or its placebo. Following the test meal, there was a delay and suppression of the maximum measured serum glucose levels. Mean overall peak glucose concentrations were lower during the enprostil phase compared to placebo (112 vs. 121 mg/dd, P = 0.025) with a trend toward delay in the time to achievement of peak glucose concentrations. Mean overall peak levels for insulin, C-peptide, and glucose-dependent insulinotropic peptide (GIP) were significantly suppressed by 36%, 16% and 60%, respectively by enprostil when compared to placebo. The overall integrated postprandial responses for insulin, C-peptide, and GIP were significantly reduced by 42%, 39% and 90%, respectively while that for glucose above baseline was reduced by 44% (P = 0.098). Similar effects were present following the oral glucose challenge.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Suppression of postprandial glucose, insulin, C-peptide, and glucose-dependent insulinotropic peptide (GIP) in man by oral administration of a prostaglandin analogue (enprostil). 314 39

The adaptation to extrauterine nutrition involves complex physiological changes at birth which may be regulated by genetic endowment; enteral nutrients, secretions, and bacteria; and endogenous hormones and exogenous hormones in breast milk. The hypothesis is explored that enteral feeding after birth may trigger key adaptations in the gut and in metabolism partly through the mediation of gastrointestinal hormone secretion. Gut peptides are found in the early human fetal gut and by the second trimester some are found in high concentrations in the fetal circulation and amniotic fluid. Major plasma hormonal surges occur during the neonatal period in term and preterm infants: notably in enteroglucagon, gastrin, motilin, neurotensin, gastrointestinal peptide, and pancreatic polypeptide. These events do not occur in neonates deprived of enteral feeding. A progressive development of dynamic gut hormonal responses to feeding is observed. The pattern of gut endocrine changes after birth is influenced by the type and route of feeding. Potential pathophysiological effects of depriving high risk neonates of enteral feeding are considered. It is speculated that infants committed to prolonged total parenteral nutrition from birth may benefit from the biological effects of intraluminal nutrients used in subnutritional quantities.
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PMID:Gastrointestinal peptides and the adaptation to extrauterine nutrition. 389 39

Administration of a small dose of pentagastrin, a synthetic pentapeptide containing the biologically active portion of the native hormone gastrin, results in a marked, rapid, transitory increase in thyrocalcitonin secretion in the pig. Gastrin or a related gastrointestinal peptide may be important in the physiological secretion of thyrocalcitonin, such as that which occurs when calcium salts are introduced into the gastrointestinal tract.
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PMID:Thyrocalcitonin: stimulation of secretion by pentagastrin. 557 57

The review article summarizes the results obtained in the author's laboratory during the last few years concerning the action of number of neurohormones such as ACTH, vasopressin, oxytocin, TRH and TRH analogues, human chorionic gonadotropin (HCG) LH-RH, gastrin and gastrin C-terminal fragments and cholecystokinin octapeptide on certain behavioural reactions and brain transmitters. The results obtained suggests that in some of the behavioural reactions elicited by these peptide hormones are brought about by modulatory action of these peptide on brain transmitters. These neurohormones, including gastrointestinal peptide hormones have a time dependent, locus and transmitter specific action on the brain function.
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PMID:The effect of neurohormones on the brain and the endocrine system. 611 Mar 9

The proposal that some post-prandially released alimentary hormones modify ingestive behaviour and gastric emptying by altering impulse activity in alimentary enteroceptors has been tested using a number of gastrointestinal peptide hormone analogues. These and other drugs were applied to single-unit afferent preparations of duodenal tension receptors in chloralose-anaesthetized sheep. In separate experiments the effect of pentagastrin and cholecystokinin on duodenal motor activity was recorded without unitary afferent activity measurements. Local intra-arterial bolus injections of pentagastrin, cholecystokinin, insulin, prostaglandin, acetylcholine, phenylbiguanide, veratrine, 5-hydroxytryptamine and bradykinin aroused or enhanced activity in tension receptors. With the exception of a short-latency effect of insulin B.P., these responses occurred together with local increases in tension and electromyographic activity of the duodenum. Combinations of atropine and hexamethonium reduced duodenal motor activity and abolished most drug-evoked afferent responses. Intracarotid bolus injections of pentagastrin at first increased, then reduced duodenal tension, electromyographic activity and impulse activity of tension receptors. Cholecystokinin (CCK-8) injected by this route caused similar alterations of these parameters, and the response was characterized by periods of reduced activity followed by a prolonged excitation of duodenal motility. From the responses to bolus injections of humoral agents it is concluded that some alimentary hormones released after a meal may have a peripheral excitatory action on the tension receptor environment which causes increased afferent activity. The mechanism probably involves both an alteration in duodenal motility and a sensitization of the receptor ending. In addition, the peptide hormones gastrin and cholecystokinin may act centrally to alter duodenal motor control and thus may influence gastric emptying and post-prandial satiety mechanisms.
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PMID:The responses of duodenal tension receptors in sheep to pentagastrin, cholecystokinin and some other drugs. 614 12


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