Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies have suggested that certain gastrointestinal peptides exert a trophic effect on the small intestine. We chose to evaluate the effect of glucagon and cholecystokinin-octapeptide (CCK-OP) on absorption of substrates in both developing and mature small intestine. Developing small intestine was evaluated in a rat fetal intestine transplant model, and mature rat small intestine was studied in in situ but isolated 10 cm segments of jejunum and ileum. Glucagon, 10 micrograms/kg/day, and CCK-OP, 45 micrograms/kg/day, were delivered continuously for 14 days through a subcutaneous osmotic pump. Intestinal absorption was determined with labeled substrates (14C-galactose and 14C-glycine) by a recirculation perfusion technique. Absorption results were expressed as percentage increase over control. The fetal intestine response to glucagon infusion was a 13% rise in galactose absorption and a 27% rise in glycine absorption. After CCK-OP infusion, fetal galactose absorption was 11% and glycine absorption rose 17%. Mature jejunal galactose absorption rose 53% and glycine absorption rose 55% after glucagon infusion. The ileal response to glucagon was a 271% rise in galactose absorption (p less than 0.05) and a 21% increase in glycine absorption. Infusion of CCK-OP decreased jejunal galactose absorption 3% but increased glycine absorption 41%. The ileal response was a 224% increase in galactose absorption (p less than 0.05) and a 19% increase in glycine absorption. Our data suggest that chronic administration of glucagon and CCK-OP can increase substrate absorption in developing and mature rat small intestine. Perhaps manipulation of the gastrointestinal hormone environment may result in increased absorption in man.
 ...
PMID:Can gastrointestinal hormones enhance intestinal absorption? 403 65

The distribution and quantification of enteroendocrine cells exhibiting immunoreactivities to nine peptides and one amine were examined in the gastrointestinal mucosa of the adult opossum using specific immunocytochemical methods. In the stomach, 90% of the enteroendocrine cells are confined to the pyloric glands and this region contained 73% of the gastrin-containing cells, 60% of the somatostatin-containing cells and 9% of cells reactive for 5-HT. Enteroendocrine cells showing immunoreactivities to glucagon, pancreatic polypeptide, somatostatin and 5-HT were observed scattered within the oxyntic glands. Only somatostatin and 5-HT positive cells were found in the cardiac glands. Immunoreactivities to CCK, glucagon, gastrin, BPP, somatostatin, secretin, motilin, neurotensin, GIP and 5-HT were observed in the epithelium of the small intestine. Although considerable variation exists in the distribution of individual enteroendocrine cell types along the intestinal tract, nearly equal numbers of enteroendocrine cells were observed in each segment. The percentage of enteroendocrine cells increases distally in the colon. Of the three enteroendocrine cell types present, somatostatin- and 5-HT-immunoreactive cells are evenly distributed, whereas neurotensin-immunoreactive cells increase in numbers distally, resulting in an increase in total number.
 ...
PMID:Quantitative distribution of enteroendocrine cells in the gastrointestinal tract of the adult opossum, Didelphis virginiana. 407 99

A sensitive and specific radioimmunoassay for cholecystokinin-pancreozymin (CCK-PZ) has been developed, using rabbit antisera to crude porcine hormone. Highly purified porcine CCK-PZ, labelled with (131)I, and repurified by column chromatography on Sephadex G15, was used as tracer. Separation of free from antibody-bound labelled CCK-PZ was carried out using charcoal, ion-exchange resin, or a double antibody procedure. Non-specific interference with the assay system by serum factors was abolished (as judged by in-vitro and in-vivo recovery studies) by boiling and diluting the serum samples before assay. Ninety-nine per cent pure porcine CCK-PZ (standard), commercial CCK-PZ preparations, caerulein, the C-terminal 8- and 12-amino acid fragments of the CCK-PZ molecule, and endogenous human CCK-PZ all cross reacted in the assay system and showed parallel inhibition curves. No significant cross reaction was found with gastrin, secretin, glucagon, or insulin. The sensitivity of the assay is approximately 5 pg per ml of test solution, which proved adequate for measuring physiological levels of CCK-PZ in peripheral blood in man.The mean immunoreactive CCK-PZ concentration in 50 fasting normal subjects was 60.4 pg per ml. The distribution of individual values was skewed, however, so that the median was much lower (30 pg per ml). Older subjects had higher fasting levels of CCK-PZ than were found in young adults.
 ...
PMID:Radioimmunoassay of cholecystokinin-pancreozymin. 443 83

1. The role of extracellular and intracellular Ca(2+) in pancreatic enzyme secretion has been assessed by correlating the exchange of (45)Ca with amylase secretion in the isolated uncinate pancreas of baby rats.2. The rate coefficient of (45)Ca efflux from pre-loaded glands declined continually (indicating that (45)Ca is retained in several different pools) and probably reflects changes in the concentration of cytoplasmic free (45)Ca, which is determined by the rate at which (45)Ca is released from intracellular organelles into the cytoplasm.3. The rate coefficient of (45)Ca release was not influenced by extracellular Ca(2+) or Mg(2+) concentrations.4. Cholecystokinin-pancreozymin (CCK-PZ) and acetylcholine accelerated the release of both (45)Ca and amylase in a dose-dependent fashion, even when extracellular Ca(2+) was reduced to 0.1 mM, but did not affect the initial rate of (45)Ca uptake by the tissue.5. In Ca(2+)-free media (containing 0.5 mM-EGTA) basal amylase secretion slowly declined and stimulated secretion was virtually abolished, but the accelerated release of (45)Ca was maintained.6. These observations indicate that natural stimuli of pancreatic enzyme secretion alter (45)Ca distribution in the cell by a process which is independent of extracellular Ca(2+) and which is associated with amylase secretion provided that the plasma membrane has not been depleted of Ca(2+).7. Secretin, glucagon and insulin did not influence (45)Ca release. Secretin slightly increased amylase secretion, but this may have been a washout effect.8. Replacement of extracellular Na(+) by Li(+) increased the release of (45)Ca and amylase, but only in the presence of extracellular Ca(2+). Li(+)-substitution also increased (45)Ca uptake. Thus, under special conditions, secretion may be stimulated when increased amounts of Ca(2+) are made available from extracellular sources.9. Hyperosmolarity (known to increase (45)Ca release in muscle) also accelerated (45)Ca release and amylase secretion.10. 2,4-Dinitrophenol markedly accelerated (45)Ca efflux but did not stimulate amylase secretion, indicating that a rise in cytoplasmic Ca(2+) will not initiate secretion if energy metabolism is impaired.11. CCK-PZ slightly increased the rate coefficient of (42)K release, indicating a changed membrane permeability.12. The stimulatory effects of CCK-PZ and acetylcholine were suppressed during Na(+)-substitution by Li(+), suggesting that the Na(+) concentration gradient across the membrane is important in secretion.13. It is concluded that the primary action of CCK-PZ and acetylcholine may be to increase the influx of Na(+) into the cell by changing membrane permeability. This in turn is responsible for the release of Ca(2+) from intracellular stores (probably endoplasmic reticulum), leading to a rise in Ca(2+) concentration close to the structures involved in enzyme secretion. Secretion then follows provided that ATP is available and the plasma membrane is not depleted of Ca(2+).
 ...
PMID:The relationship between calcium exchange and enzyme secretion in the isolated rat pancreas. 477 43

Previously, we reported that pancreatic acini have specific receptors for the insulin-like growth factors (IGF) I and II. We now report that the binding of 125I-labeled IGF II to mouse pancreatic acini is maximally increased by 100 nM insulin (51%) and is maximally reduced by 10 nM cholecystokinin octapeptide (CCK8) (34%), but is not affected by other regulatory peptides such as somatostatin or glucagon. Since many polypeptide hormones are internalized, we determined whether this regulation of IGF II binding occurred via a change in internalization. Acid washing or trypsinization has been shown to remove surface-bound hormone while the acid- or trypsin-resistant radioactivity represents internalized radioligand. Insulin increased and CCK8 decreased the internalization of IGF II as determined by these techniques. Studies of IGF II binding to acini at low temperature (15 degrees C) and binding to particulate fractions from acini were also consistent with the effect of insulin to increase and CCK8 to decrease the internalization of IGF II. When insulin and CCK8 were added together, the inhibitory effect of CCK8 predominated, indicating that CCK8 acted distal to the effect of insulin. Several lines of evidence suggest that this effect of CCK8 was via the CCK receptor and was mediated via a change in intracellular Ca2+: the effect of CCK8 on inhibiting IGF II binding was blocked by the cholecystokinin antagonist N2,O2'-dibutyryl cGMP; the cholinergic agent carbachol (1-100 microM), which acts through the muscarinic receptor to increase intracellular Ca2+, also inhibited IGF II binding; the Ca2+ ionophore A23187 (1-5 microM) mimicked the effects of CCK8 and carbachol. These data indicate, therefore, that CCK8 and possibly insulin may regulate the internalization of IGF II via intracellular Ca2+. Moreover, the data raise the possibility that alterations of hormone internalization may be a general phenomenon of hormone-hormone interaction.
 ...
PMID:Effect of intracellular Ca2+ on insulin-like growth factor II. internalization into pancreatic acini. Roles of insulin and cholecystokinin. 609 32

1. The effects of secretin, glucagon, cholecystokinin-pancreozymin (CCK-PZ), gastric inhibitory peptide (GIP), vasoactive intestinal peptide (VIP), somatostatin, neurotensin and enkephalin on basal, pentagastrin- and histamine-stimulated gastric acid secretion were investigated in the conscious fistula rat. 2. Glucagon and GIP were ineffective inhibitors of basal and pentagastrin-stimulated secretion. CCK-PZ stimulated acid secretion at a low dose level but at higher doses it inhibited both pentagastrin- and histamine-induced secretions. VIP was ineffective at low doses and at high doses its action was complicated by reflux of stimulated pancreatic and intestinal secretions into the stomach. Met-enkephalin inhibited histamine- but not pentagastrin-stimulated secretion. Neurotensin inhibited the response to pentagastrin but had no effect on histamine-stimulated secretion. Secretin and somatostatin were potent inhibitors of basal and pentagastrin-stimulated acid secretion with little or no effect on the response to histamine. 3. At doses completely inhibitory to pentagastrin-stimulated secretion secretin and somatostatin did not block the mobilization of gastric mucosal histamine by pentagastrin, although somatostatin caused partial competitive inhibition at lower doses of pentagastrin. Thus secretin and somatostatin inhibited pentagastrin-induced secretion neither by blocking gastric mucosal histamine mobilization nor by abolishing the direct action of histamine on the parietal cell -- findings which are inconsistent with the proposed role of histamine as the mediator of the action of gastrin on the parietal cell.
 ...
PMID:Effects of various gastrointestinal peptides on parietal cells and endocrine cells in the oxyntic mucosa of rat stomach. 610 65

Fifteen male Holstein X Frisian calves, weighing 65 +/- 3 kg and fed a milk replacer twice daily were fitted with a return cannula loop, chronically implanted at 10 days of age in the pancreatic duct, were used. In six successive experiments we have observed the influence of an intravenous infusion of secretin, cholecystokinin pancreozymin (CCK-PZ), vasoactive intestinal peptide (VIP), glucagon, gastrin and somatostatin on pancreatic juice flow rate, and on the excretion of proteins, calcium, inorganic phosphorus, zinc and amylase activity of pancreatic juice. In two other experiments, we have studied the interaction of secretin (or CCK-PZ) with somatostatin (SRIF). Each experiment was performed 5 h after calves feeding and no milk was given to the animals during the time of sampling. Our results indicate that the endocrine regulation of the exocrine pancreas in young calves is similar to that described in other mammals. Secretin and CCK-PZ increased significantly excretion of water, calcium, magnesium, inorganic phosphorus, zinc, proteins and amylase activity. Somatostatin and glucagon inhibited effects observed with two precedent hormones. Gastrin increased pancreatic juice flow rate but excretion of protein and amylase activity do not varied significantly. VIP showed no significant effect on pancreatic excretion of water, minerals, proteins and amylase activity. However, our animals seem to be characterized by a more intense excretion of proteins and amylase in the pancreatic juice following secretin than after CCK-PZ infusion.
 ...
PMID:The endocrine regulation of exocrine pancreas in preruminant milk-fed calves. 610 15

Using a new model of a reversible pancreatic fistula which allows the long-term-investigation under nearly physiological conditions on the unrestrained dog, we tested the effect of somatostatin (50 micrograms), calcitonin (4 micrograms), glucagon (1 microgram), and prostaglandin E1 (150 micrograms) on the exocrine pancreatic function in 45 experiments over a period of 13 h: SST inhibits the basal as well as the secretin or CCK-stimulated secretion: calcitonin shows inhibition of the stimulated secretion only; glucagon blocks the secretin-stimulated pancreatic function; and PGE1 reduces the bicarbonate concentration and trypsin output in secretin stimulation, but in one of the two series it stimulates the basal secretion.
 ...
PMID:The effect of SST, glucagon, calcitonin and PGE1 on exocrine pancreatic secretion in the unrestrained dog in long-term experiments. 611 65

Immunocytochemical methods for light and electron microscopy were used to demonstrate the regulatory peptides present in the endocrine pancreas of the alligator, Alligator mississippienses. The peptides studied included insulin, glucagon (pancreatic and enteric), somatostatin, pancreatic polypeptide (avian, bovine and human), vasoactive intestinal polypeptide, substance P, metenkephalin, beta-endorphin, C-terminal gastrin/CCK and gastric inhibitory polypeptide. Endocrine cells were detected using antisera to insulin, pancreatic glucagon, somatostatin and avian pancreatic polypeptide, whereas peptidergic nerves were stained with antisera to vasoactive intestinal polypeptide. All other antisera were unreactive in the alligator pancreas. The peptide-containing structures were identified ultrastructurally by both the semithin/thin and immuno-gold methods. The results showed that five of the regulatory peptides commonly detected in the mammalian pancreas were immunologically recognisable in the alligator. In addition, the ultrastructural appearance of the peptide-containing cells was clearly distinct from that reported in mammals.
 ...
PMID:The endocrine pancreas of Alligator mississippiensis. An immunocytochemical investigation. 612 17

Dibutyryl cyclic guanosine monophosphate (dbcGMP), a specific competitive inhibitor of the gastrin, cholecystokinin-pancreozymin (CCK-PZ) family of peptides in pancreas, gallbladder and ileum, had no effect on basal acid secretion in the isolated mouse stomach nor on secretion stimulated by bethanechol or histamine. Secretion evoked by low doses of pentagastrin were likewise unaffected by dbcGMP but responses to high doses of pentagastrin were augmented. CCK-PZ and glucagon each inhibited acid secretion evoked by pentagastrin. DbcGMP blocked CCK-PZ-mediated inhibition but was without effect on inhibition by glucagon. These observations suggest that in the gastric glands there exist two receptors with different affinities for gastrin and CCK-PZ which mediate excitation and inhibition respectively.
 ...
PMID:The effect of dibutyryl cyclic guanosine monophosphate, a competitive antagonist to cholecystokinin-pancreozymin, on gastric acid secretion in the isolated mouse stomach. 612 63


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>