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)

Rats were fasted 48 h and then injected once with either saline, pentagastrin, EGF, secretin or combinations of secretin and pentagastrin or EGF. Another group of rats was fasted and refed. Animals were killed 4 h later and ODC assayed in mucosa of the cecum, proximal colon, and distal colon. EGF significantly increased ODC activity in all 3 tissues. Secretin had no effect by itself on ODC or ODC stimulated by EGF. Pentagastrin significantly increased ODC of the cecum, and secretin completely inhibited the effect of pentagastrin. Refeeding fasted rats significantly induced activity in all three tissues. Immunocytochemistry using a highly specific polyclonal ODC antibody showed that ODC was confined to the crypt cells of the proximal colon. Antibody dilution techniques demonstrated that gastrin, EGF and refeeding increased the level of enzyme in these cells. Refeeding in addition caused the appearance of enzyme in surface epithelial cells. These results showed that colonic mucosal ODC is present in proliferative cells and is regulated by the same peptides known to regulate growth in this tissue. Colonic mucosal ODC also responds the same way as it does in the oxyntic gland and small bowel mucosa.
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PMID:Ornithine decarboxylase in large bowel mucosa: regulation by gastrin, secretin and EGF. 145 Apr 33

The effects of treatment with the somatostatin analogue Sandostatin, separately and in combination with surgical castration, on the development of azaserine-induced lesions in rat pancreas and N-nitrosobis(2-oxopropyl)amine (BOP)-induced lesions in hamster pancreas were investigated. The animals were divided in 4 groups and treated as follows: (a) controls, injected s.c. with saline solution (0.9% NaCl); (b) orchiectomy directly after the last treatment with carcinogen; (c) Sandostatin (SMS 201-995) subcutaneously; (d) orchiectomy followed by treatment with Sandostatin. No significant suppressive effects on plasma EGF or IGF-I concentrations were noted after Sandostatin treatment, but plasma gastrin levels decreased slightly in the rats, not in the hamsters. In rats, Sandostatin treatment enhanced rather than inhibited growth of acidophilic atypical acinar cell nodules. In hamster pancreas, by contrast, Sandostatin inhibited the development of putative pre-neoplastic ductular lesions. There was no interaction between treatment with Sandostatin and surgical castration. It was concluded that Sandostatin, when administered prophylactically, has an inhibitory effect on the growth of putative pre-neoplastic ductular, but not acinar, lesions.
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PMID:Effects of sandostatin and castration on pancreatic carcinogenesis in rats and hamsters. 173 May 18

Proliferation and growth of gastroduodenal mucosal cells represent important elements of mucosal defense and any alterations in the balance between cell proliferation and cell loss may lead to trophic changes in mucosa. Acute mucosal lesions induced by local irritants such as bile salts, ethanol, aspirin, or stress are accompanied by widespread damage of surface epithelium followed by almost immediate repair due to mucosal cell restitution, which is unrelated to cell proliferation but does depend on the intrinsic property of mucosal cells to cover superficial defects. Cytoprotection involves the protection of the regeneration zone and the maintenance of blood flow to the mucosa. Various factors that exhibit mucosal growth-promoting action include EGF, gastrin, growth hormone, and GH-releasing factor. These factors protect the mucosa against acute injury but the mechanism of this effect is not clear. These trophic agents, especially EGF, accelerate the healing of chronic gastroduodenal ulceration and may contribute to the healing effects of sucralfate or De-Nol. These effects of trophic substances are related to their stimulation of cell proliferation and DNA, RNA, and protein synthesis and can be reversed by the suppression of mucosal growth. Prostaglandins, especially their stable methylated analogs, display trophic effects on the gastric mucosa but neither gastroprotective nor ulcer healing actions of PG can be attributed to their trophic effect. With increasing attention being paid to mucosal growth and repair as components of mucosal defense, the emphasis of drug therapy of acute or chronic gastroduodenal lesions is likely to move toward strengthening mucosal defense rather than the inhibition of aggressive factors.
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PMID:Role of growth factors in gastroduodenal protection and healing of peptic ulcers. 197 Mar 37

A sensitive radioimmunoassay was developed for human epidermal growth factor (hEGF) in saliva and gastric juice. This method was sufficiently sensitive for an accurate measurement of hEGF in these biological fluids. The minimal detectable concentration of EGF was 30 ng/L. The imprecision profile of EGF standard curve had a CV less than 10% in the range of 0.1-3.0 micrograms/L. Serial dilution curves of saliva and gastric juice paralleled that of standard EGF. The antibody to hEGF showed no cross-reactivity with a large excess of growth factors, such as human transforming growth factor alpha, human insulin-like growth factor I, and platelet-derived growth factor (c-sis). No detectable cross-reactivity was observed with some biological gut peptides: somatostatin, gastrin, secretin or pancreatic polypeptide. The intra-assay CV for saliva and gastric juice was less than 10%, and the recoveries were 93.9 +/- 8.7% and 93.7 +/- 11.3%, respectively for saliva and gastric juice. Gel exclusion chromatography revealed hEGF-like substances, heterogeneous in size in saliva and gastric juice, the origins and physiological functions of which are unknown.
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PMID:Radioimmunoassay of epidermal growth factor in human saliva and gastric juice. 204 84

Intestinal tissue mass was significantly reduced throughout the gastrointestinal tract (p less than 0.001) of intravenously fed (TPN) rats. Urogastrone-epidermal growth factor, (URO-EGF), reversed these changes. Although plasma enteroglucagon and gastrin levels showed a small increase with URO-EGF, this was far less than the gut tissue weight change, suggesting that it was unlikely that they were involved in modulating the proliferative response of the intestine to URO-EGF. Peptide tyrosine tyrosine (PYY) levels were however significantly increased by URO-EGF, indicating that PYY may possibly have a role in the modulation of intestinal cell proliferation.
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PMID:Plasma enteroglucagon, peptide YY and gastrin in rats deprived of luminal nutrition, and after urogastrone-EGF administration. A proliferative role for PYY in the intestinal epithelium? 249 89

Exposure of IEC-6 cells for 24 hr to either gastrin (50-500 ng/ml) or EGF (100-500 ng/ml) significantly stimulated (100-165%) the rate of [3H]thymidine incorporation into DNA (referred to as DNA synthesis) when compared with the corresponding basal levels. Somatostatin (10-500 ng/ml) produced no apparent change in DNA synthesis in IEC cells. On the other hand, somatostatin completely inhibited the EGF-induced rise in DNA synthesis. The gastrin-mediated stimulation in DNA synthesis was not affected by somatostatin. The rate of DNA synthesis in IEC cells in the presence of both gastrin and EGF was found to be greater (additive) than that caused by either of the peptides alone. A similar but less dramatic change in the actual number of cells (assessment of cell replication) was observed when the IEC cells were exposed for 24 hr to gastrin, EGF, and somatostatin, either alone or in combination. Whereas gastrin (250 ng/ml) and EGF (250 ng/ml) by themselves increased the number of cells significantly by 29 and 37%, respectively, together they caused a 72% stimulation, when compared with the basal levels. Somatostatin by itself caused no apparent change in IEC cell population, but it significantly inhibited the EGF- but not the gastrin-induced stimulation in IEC cell replication. It is concluded that both gastrin and EGF exert a direct proliferative effect on IEC cells, and the EGF action is regulated by somatostatin.
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PMID:The effects of gastrin, epidermal growth factor, and somatostatin on DNA synthesis in a small intestinal crypt cell line (IEC-6). 288 10

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

The current understanding in biology and function of 4 growth factors is reviewed. PDGF suggests functions for proto-oncogens in normal cells, which may interact in tightly linked hierachies to induce malignant growth. PDGF-requirement of normal fibroblast cell-lines is lost when the cells are infected with tumor viruses. TGF is able to stimulate growth of normally anchorage dependent cells in an anchorage independent manner in soft agar. This ability is thought to be the best in-vitro correlate of neoplastic transformation. The peptide hormones bombesin/gastrin releasing factor and EGF can act as autocrine growth factors in various lung cancer cell-lines and stimulate clonal tumor cell growth in-vitro. The potential clinical application of these types of growth factors may enable the in-vitro growth from any lung cancer patient and allow individual drug testing. TCGF produced by T-cells to activate T-cells, is central to immune stimulation and immune response. Models for potential indirect anticancer effects either by in-vivo administration or by in-vivo incubation plus passive transfer of T-cells are presented to be initiated in future clinical trials.
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PMID:[Growth factors. A new dimension in understanding oncogenesis]. 299 23

Effects of regulatory molecules on growth of mouse pancreatic acinar cells in culture were examined. The cholecystokinin (CCK) analogue caerulein and cholecystokinin octapeptide (CCK-8) each led to threefold increases in incorporation of [3H]thymidine into DNA. Gastrin, which interacts weakly with the CCK receptor, stimulated DNA synthesis, but only at much higher concentrations. In contrast, other secretagogues that utilize Ca2+ as an intracellular messenger, including carbachol, bombesin, substance P, and the ionophore A23187, did not induce trophic responses. Factors that affect intracellular cAMP concentration, such as secretin, somatostatin, VIP, DBcAMP, and forskolin, did not increase DNA synthesis in cultured pancreatic cells. Insulin and epidermal growth factor induced two- and threefold increases in [3H] thymidine incorporation into DNA, respectively. The effects of insulin were mediated via insulin-like growth factor I receptors. Steroid hormones had little effect on pancreatic acinar cell DNA synthesis. The stimulatory effects of CCK, insulin, and EGF were additive. The combination of caerulein, EGF, and insulin in a hormonally defined medium led to a tenfold increase in the incorporation of [3H]thymidine into DNA. These data indicate that CCK, EGF, and insulin directly increase DNA synthesis in pancreatic acinar cells.
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PMID:Stimulation of pancreatic acinar cell growth by CCK, epidermal growth factor, and insulin in vitro. 302 Sep 92

Large increases in gastric acid and pepsin secretion, antral gastrin concentration, and decreases in serum gastrin occur during the third week of life in the neonatal rat. At the same time gastrin receptors appear and gastrin release becomes sensitive to somatostatin, indicating that absence and then appearance of specific hormone receptors may be responsible for some of the ontogenic pattern. At this time the mucosa also begins to grow rapidly, with a greater proportion of cells leaving the proliferative pool and differentiating. For the first 2.5-3 weeks these ontogenic changes can be triggered by corticosterone. Their full expression depends on dietary changes associated with weaning. Neither hormones, dietary changes, nor the weaning process itself is essential for development, because in the absence of these, all of the changes still occur--although they may be delayed or be smaller in magnitude. Figure 1 provides a generalized summary of the normal functional development of the stomach and how it is altered by changes in corticosterone levels and the absence of weaning. These findings indicate that ontogeny is genetically programmed and that the full expression of this program depends on hormones, luminal contents, and other environmental factors. In comparison with the small intestine, for example, gastric ontogeny has not received adequate attention. There are essentially no studies directed toward understanding changes in motility during this period. There is really only one study examining the growth pattern of the mucosa during development, and this study is aimed at changes in DNA synthesis and cell loss. Experiments involving the cell cycle are needed to understand whether existing cells mature and differentiate or whether newly created cells suddenly leave the proliferative pool to differentiate. There have been no experiments in which the effects of thyroid hormone on gastric development have been adequately examined. In addition, little or nothing is known about EGF in the ontogenic process. Studies implanting fetal tissue into adult hosts are needed to determine which gastric functions can develop in the absence of luminal stimulation and hormone changes. The cell biology of the gastric mucosa is difficult to examine--especially that involving the cells concerned with growth and differentiation. The stem cells are dispersed throughout the tissue and are a small portion of the cell population. These have never been isolated for study. In vitro culture of mucosal cells, however, is a technique that can possibly be used to examine development at the cellular and molecular level.
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PMID:Functional development of the stomach. 392 87


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