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Query: UNIPROT:P01350 (
gastrin
)
9,683
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
In tests on dogs with innervated and vagus denervated miniature stomaches and gastric fistula the action of
secretin
on the gastric secretion provoked by food stimulants-pentagastrin, histamine and parenteral introduction of casein hydrolysate was studied. Experiments showed the
secretin
to produce an inhibiting action only on the 2nd phase of the gastric secretion after feeding on 100 g of meat, depresses secretion, called forth with pentagastrin, but it does not affect the secretion induced by sham feeding, histamine and intravenous administration of casein hydrolysate. Hence,
secretin
displays specific properties, by arresting only the action of
gastrin
on the gastric glands.
...
PMID:[Action of secretin on the gastric secretion induced by food stimuli, pentagastrin, histamine and the parenteral administration of casein hydrolysate]. 10 52
Studies were performed in four dogs with chronic gastric and pancreatic fistulas following intraduodenal perfusion with 10 mmole hr-1 of sodium oleate for 30 minutes. Radioimmunoassay (RIA) of plasma CCK LI was undertaken by an RIA method using labeled, desulfated CCK 8 I125 and an antiserum raised to CCK 8. The detection limit for the assay was 0.25 to 0.5 fmole and the lowest detectable plasma level was 5 to 10 fmoles ml-1. Since there was equal cross-reactivity to
gastrin
, a
gastrin
-specific assay also was employed to evaluate any changes in
gastrin
levels. After oleate infusion the plasma CCK increment above basal was 50 +/- 11 fmoles ml-1, with return to basal levels after 60 minutes. Administration of atropine significantly (P less than 0.01) inhibited the release of CCK in the first 20 minutes. Thereafter CCK release was not reduced. Plasma
gastrin
values did not change before and after oleate perfusion. Pancreatic protein output increased from 72 +/- 12 to 420 +/- 55 mg/10 min-1 after oleate administration. However, after atropinization the rise in pancreatic protein output was significantly lower (152 +/- 36 mg/10 min-1) (P less than 0.01). We have shown that, using our RIA method, there is a measurable rise in plasma CCK LI after intraduodenal oleate. After atropinization the CCK response was decreased significantly during the first 30 minutes, but was virtually unchanged during the second 30 minutes, when the fall in pancreatic protein output was most marked. We conclude that the cholinergic mechanism which plays a role in the endogenous stimulation of pancreatic protein secretion by intraduodenal oleate cannot be explained simply be decreased CCK release. This mechanism may be hormonal, distinct from
secretin
, or neural possibly, via activation of an enteropancreatic reflex.
...
PMID:Evidence that the cholinergic enteropancreatic reflex may be independent of cholecystokinin release. 11 64
Reliable and specific radioimmunoassays have been developed for the gut hormones
secretin
,
gastrin
, cholecystokinin, pancreatic glucagon, VIP, GIP, motilin, and enteroglucagon. Using these assays, the relative pattern of distribution of the gut hormones has been determined using the same bowel extracts for all measurements. VIP occurred in high concentration in all regions of the bowel, whereas
secretin
, GIP, motilin, and CCK were predominantly localised in the proximal small intestine. Pancreatic glucagon was almost exclusively confined to the pancreas. Like VIP, enteroglucagon also exhibited a wide pattern of distribution but was maximal in the ileum. The acid ethanol extraction method that was used was found to be unsuitable for
gastrin
. On gel chromatography of the extracts, motilin and VIP eluted as single molecular species in identical position to the pure porcine peptides. CCK, pancreatic glucagon, enteroglucagon and GIP were all multiform.
...
PMID:Distribution of the gut hormones in the primate intestinal tract. 11 57
The effects of a number of peptides which are found in the gastrointestinal tract have been ascertained on the direct current recorded dorsal and ventral root responses of the isolated hemisected toad spinal cord. Motilin, substance P, bombesin, neurotensin, and thyrotropin releasing hormone had potent depolarizing actions on dorsal root terminals and motoneurons. These substances evoked discernable effects at concentrations as low as 10--7 M, or even lower with motilin. The effects of motilin, neurotensin, and thyrotropin-releasing hormone were greatly reduced or abolished by perfusion of the preparation with tetrodotoxin. Adrenocorticotrophic hormone,
secretin
, and pancreozymin (cholecystokinin) also depolarized dorsal root terminals and motoneurons. The effects of
secretin
and cholecystokinin were not abolished by tetrodotoxin. Leu- and Met-enkephalin had weak hyperpolarizing actions on the dorsal and ventral root potentials of repetitively stimulated preparations.
Gastrin
, gastric inhibitory peptide, glucagon, and somatostatin had no apparent effects on the responses of the preparation. Angiotensin and vasopressin both had rather weak depolarizing effects on the dorsal and ventral roots.
...
PMID:Actions of various gastrointestinal peptides on the isolated amphibian spinal cord. 11 60
After a review on the historical development of morphological investigations of entero-endocrine cells, dating back to 1870, a detailed synoptical review of the current stage of findings in this field is given. At the present time nine different endocrine cell types can be distinguished in the epithelium of the gastrointestinal tract. Criteria for this differentiation are properties concerning specific staining methods, aldehyde-induced fluorescence, immunohistochemistry, and ultrastructure. From present results it is obvious that distinct cell types are responsible for the synthesis of defined polypeptide hormones (e.g.
gastrin
,
secretin
, enterogastrone). The metabolism of amines, in relation to the endocrine cells of the gastrointestinal tract is of particular interest here. Points investigated include the uniqueness of endocrine cells, with regard to the metabolism of biogenic amines ("APUD-cells") and the possibility of serotonin synthesis by a definite cell type, i.e. by the EC-cell ("enterochromaffin" cell). In our experimental animal, male Wistarrats, seven different entero-endocrine cell types can be discerned by ultrastructural means: EC-, ECL-, G-, AL-, EG-, D- and D1-cells. The I-cell (found in other species) can hardly be distinguished from the AL-cell by ultrastructural means and the S-cells, as found in other species, are not to be found at all. Only some of the cited cell types can be seen by fluorescence microscopy. After formaldehyde-treatment of the tissue, the "enterochromaffin" cell shows a yellow, serotonin-specific fluorescence. This cell corresponds in shape, number and distribution to the ultrastructurally defined EC-cell. EC-cells are found predominantly in the pyloric region and the duodenum and less frequently in the middle- and hindgut and the cardiac region; seldomly EC-cells are encountered in the oxyntic gland area of the stomach. In the rat gastro-intestinal tract, number and fluorescent intensity of EC-cells does not always correspond with the serotonin content of a certain region--sometimes the level of serotonin is largely determined by the mast cells, which in the rat also contain serotonin. For example, the high serotonin content of the oxyntic gland area, which contains very few EC-cells, has to be contributed nearly exclusively to mast cell serotonin. Mast cells can be domonstrated by fluorescence microscopy, due to their histamine content, after treatment of the tissue with o-phthalaldehyde (OPD). It seems likely that the histamine content, especially that of the so-called "atypical mast cells" of the mucosa, is inversely related to their respective serotonin content. --In addition to mast cells, OPD-treatment leads to a fluorescence in some of the entero-endocrine cells of the gastrointestinal epithelium. In the gastric epithelium these fluorescing cells should be regarded as histamine-containing ECL-cells and glucagon-containing AL-cells while in the colonic epithelium they are considered to be glucagon-containing AL-cells...
...
PMID:[The endocrine cells of the gastrointestinal epithelium and the metabolism of biogenic amines in the gastrointestinal tract (author's transl)]. 13 9
Functioning tumors of the pancreatic islets are now recognized as the source of clinical syndromes affecting the gastrointestinal tract which have a wide variety of catastrophic symptoms. Experiences with thirty-six cases suggest at least four separate diagnostic categories in the ulcerogenic tumor syndrome. These include: a typical history, gastric analysis, and roentgenographic findings with boderline fasting serum
gastrin
levels; ulcerogenic tumor with evidence of hyperparathyroidism; iatrogenic ulcerogenic syndrome associated with failure of a previous operation for duodenal ulcer; and the classic ulcerogenic syndrome associated with a fulminating ulcer diathesis or diarrhea and high serum
gastrin
levels. The problems presented at operation include: decisions to be make in the presence of a negative exploration; the finding of a solitary tumor in the wall of the duodenum; solitary pancreatic tumors particularly in the body and tail; ulcerogenic tumors in the very young; liver metastases in the elderly; and the wisdom of removing gross metastases in combination with total gastrectomy. The long-term survival in the ulcerogenic tumor syndrome approximated 50 per cent, with 40 per cent of those having proved malignancy living five years. Evidence of hyperparathyroidism is relatively common in association with both the ulcerogenic and the diarrheogenic tumor syndromes. The association may by a result of a congenital abnormality, metabolic alkalosis, or a direct effect of the islet cell tumor. Parathyroidectomy may be indicated when both the serum calcium and parathormone levels are elevated in the presence of borderline fasting
gastrin
levels. The latter may return to normal after parathyroidectomy. The evidence of hyperparathyroidism closely parallels the episodes of diarrhea in the diarrheogenic syndrome, and hyperparathyroidism may regress spontaneously after total removal of the pancreatic tumor. Just as routine calcium determinations made the diagnosis of hyperparathyroidism more commonplace, it is suggested that the gastrointestinal syndromes associated with islet cell tumor would receive wider recognition if radioimmunoassays for
gastrin
as well as
secretin
, and the other
secretin
-like polypeptides, were carried out routinely.
...
PMID:Islet cell tumors of the pancreas and the alimentary tract. 16 36
1. Intracellular recordings of membrane potential and input resistance have been made in vivo and in vitro from the exocrine acinar cells of rat pancreas using indwelling glass micro-electrodes. 2. The resting cell membrane potential and input resistance in the in vivo experiments were not markedly different from the values obtained in the in vitro experiments. The effect of both acetylcholine (ACh) and pancreozymin (CCK-Pz) on the pancreas in vivo as well as in vitro was to reduce both the acinar cell membrane potential and the input resistance narkedly. The amplitude of the evoked depolarization and the change in input resistance evoked by supramaximal stimuli were of the same magnitude in both types of preparations. 3.
Gastrin
had an effect on the acinar cell potential and resistance which was indistinguishable from that of CCK-Pz or ACh. The effect of
gastrin
or CCK-Pz was, in contrast to that of ACh, not influenced by the presence of atropine. The reversal potential for the
gastrin
evoked potential change was about -20 mV. 4.
Secretin
in doses producing maximal volume secretion in vivo had no effect on acinar cell membrane potential and input resistance. 5. Dibutyryl cyclic AMP (5mM) and cyclic GMP (1mM) had no effect on cell membrane potential or resistance. 6. It is concluded that the in vitro superfused pancreas segment preparation is a useful model system in electrophysiological studies since it functions essentially as the in vivo preparation. In contrast to both
gastrin
and CCK-Pz,
secretin
has no effect on the bioelectrical properties of the acinar cells, indicating that there are no physiologically important
secretin
receptors in rat acinar cells.
...
PMID:Pancreatic acinar cells: effect of acetylcholine, pancreozymin, gastrin and secretin on membrane potential and resistance in vivo and in vitro. 16 55
1. Secretagogues of pancreatic enzyme secretion: pancreozymin, carbamylcholine,
gastrin
I, the octapeptide of pancreozymin, caerulein and the Ca2+ ionophore A 23187 stimulate 45Ca uptake into isolated rat pancreatic cells, whereas adrenaline, isoproterenol,
secretin
, dibutyrylic cyclic adenosine 3',5'-monophosphate and dibutyrylic cyclic guanosine 3',5'-monophosphate have no effect on 45Ca uptake. 2. A graphical analysis of the Ca2+ uptake curves reveals at least two phases: a fast phase, probably due to binding of Ca2+ to the membrane and a slow phase representing Ca2+ transport into cells. Both phases are stimulated by pancreozymin and carbamylcholine. 3. The 45Ca-exchangeable pool size is increased by both carbamylcholine and pancreozymin, whereas a significant increase of total content of cell calcium was too small to be detected. 4. Atropine blocks the stimulatory effect of carbamylcholine completely but not that of pancreozymin. The Ca2+ antagonist D600 blocks the stimulatory effects of both carbamylcholine and pancreozymin only partially. 5. The data suggest that secretagogues of pancreatic enzyme secretion act by increasing the rate of Ca2+ transfer into the cell most probably through an increase of the cell membrane permeability for Ca2+.
...
PMID:Calcium ion uptake in isolated pancreas cells induced by secretagogues. 17 97
In the presence of 5 mM theophylline,
secretin
and vasoactive intestinal peptide (VIP) each increased cyclic adenosine 3':5'-monophosphate (cyclic AMP) in acinar cells isolated from guinea pig pancreas. Without theophylline, neither peptide altered cellular cyclic AMP. Glucagon, which is similar to
secretin
and VIP both in chemical structure and spectrum of biologic activities, neither stimulated cellular cyclic AMP nor inhibited the stimulation produced by
secretin
or by VIP. Other agents which were tested and found not to increase cellular cyclic AMP were cholecystokinin, carboxyl-terminal octapeptide of cholecystokinin,
gastrin
I,
gastrin
II, bovine pancreatic polypeptide, carbamylcholine, and prostaglandin E1. Neither carboxyl-terminal octapeptide nor
gastrin
I altered the stimulation of cellular cyclic AMP produced by
secretin
or VIP. With natural
secretin
a significant increase in cellular cyclic AMP could be detected at concentrations as low as 3 x 10(-10) M and maximal stimulation occurred at 10(-8) M. VIP was approximately 1% as potent as natural
secretin
and maximal concentrations of
secretin
plus VIP increased cellular cyclic AMP to the same value as was obtained with a maximal concentration of
secretin
alone.
...
PMID:Cyclic AMP in pancreatic acinar cells: effects of gastrointestinal hormones. 17 15
A case of watery diarrhea, hypokalemia and hypercalcemia associated with an islet cell tumor was described. A 62-year old man exhibited frequent watery diarrhea and hypokalemia for two years. He had no peptic ulcer and serum
gastrin
level was normal. His serum calcium was abnormally high and serum phosphate was lowered. He had
secretin
-like activity in his plasma. Autopsy revealed a small islet cell tumor in the pancreas and several metastatic masses in the liver. Microscopic examination revealed the tumor cell was not beta, alpha nor D cells. By electron microscopy the secretion granules of the tumor cell resembled those of S, M and T cells. It was not possible to decide which of the tree cell types was responsible for the pancreatic cholera.
...
PMID:A case of watery diarrhea, hypokalemia and hypercalcemia associated with nonulcerogenic islet cell tumor of the pancreas. 17 23
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