Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three experiments were carried out in each of 6 healthy students on separate days, in a randomized order. Intravenous saline infusions were given for one hour basally in each experiment. During the second hour either pentagastrin, pentagastrin and somatostatin, or somatostatin alone were given. Gastric juice was collected continuously during all experiments. Somatostatin decreased the volume of gastric secretion and the concentrations of acid and pepsin, and output of acid, pepsin, and intrinsic factor (IF). The plasma gastrin concentration was not changed by somatostatin. A rebound effect was seen on pepsin and IF outputs after cessation of somatostatin, and on blood sugar concentration. The present study suggests that somatostatin acts on gastric secretion either directly or by mechanisms other than by inhibition of gastrin. The rebound of pepsin and IF indicates a release-inhibiting action on these substances similar to the effect of somatostatin on the release of some hormones.
 ...
PMID:The effect of somatostatin on pentagastrin-stimulated gastric secretion and on plasma gastrin in man. 33 22

Somatostatin (SRIF), a tetradecapeptide, has been reported to suppress gastrin release and hence inhibit acid secretion in vivo. This study was performed to determine whether SRIF has any direct effect on parietal cell (PC). Isolated gastric cells were prepared by collagenase digestion and calcium chelation of rabbit fundic mucosa. PC enrichment (75% +/- 5%) was accomplished by velocity sedimentation with an elutriator rotor. Acid, as assessed by the accumulation of 14C-aminopyrine (AP) and macromolecular (intrinsic factor [IF]) secretion were used as markers of PC function. Cells were stimulated with histamine (H) (10(-6) mol/L). SRIF (10(-10) to 10(-6) mol/L) significantly inhibited H-stimulated 14C-AP accumulation (p less than 0.05). Inhibition of H-stimulated IF release was less sensitive, occurring at 10(-8) and 10(-7) mol/L (p less than 0.05), and loss of inhibition was observed at 10(-6) mol/L (p less than 0.05). These results demonstrate a direct inhibitory action of SRIF on PC secretion. The difference in inhibitory effect on IF and proton secretion is consistent with the postulation that SRIF may function at more than one site within the PC.
 ...
PMID:Evidence for nongastrin-mediated somatostatin inhibition of parietal cell function. 287 98

The aim of our study was to examine the direct effect of somatostatin on histamine- and pentagastrin-stimulated intrinsic factor (IF) release in collagenase-dispersed guinea pig gastric glands. The effect of somatostatin (10(-11) M to 10(-6) M) on half-maximal doses of histamine (10(-6) M), pentagastrin (10(-6) M), and both histamine and pentagastrin together was tested. All tested concentrations of histamine significantly stimulated IF release. Pentagastrin (10(-10) M to 10(-6) M) inconsistently stimulated IF release. The quantity of IF release stimulated by histamine and pentagastrin together was approximately the additive sum of that produced by either agent alone. Somatostatin (10(-6) M) inhibited histamine-stimulated (10(-6) M) IF release by 69.9 +/- 7.2% and the combination of histamine (10(-6) M) and pentagastrin (10(-6) M) by 64.2 +/- 9.1%. This is the first in vitro demonstration that somatostatin inhibits IF release.
 ...
PMID:Somatostatin inhibition of intrinsic factor secretion from isolated guinea pig gastric glands. 288 25

Records of the 30 cases of gastric carcinoid at the Mayo Clinic showed that the gastric mucosa was normal, hyperplastic, or atrophic (nonantral) in 12, 2, or 16 patients, respectively. In the atrophic group, the tumors were in the gastric body and fundus; small, polypoid, and multicentric; and associated with fundal argyrophil cell hyperplasia. In immunocytochemical studies, minor tumor cell populations stained positively for 5-hydroxytryptamine, gastrin, and somatostatin in 1 case and for 5-hydroxytryptamine in 3 others. Metastasis occurred in 3 patients. Twelve patients had pernicious anemia. Parietal cell or intrinsic factor antibodies or both were present in all 12 patients tested. Each of the 7 patients with an intact antrum had massive hypergastrinemia. No common HLA-A, -B, or -DR antigen pattern was detected among the 10 patients tested. The results suggest that nonantral gastric atrophy predisposes to gastric carcinoid as well as to gastric carcinoma.
 ...
PMID:The syndrome of gastric argyrophil carcinoid tumors and nonantral gastric atrophy. 619 1

The cellular content and secretion of intrinsic factor was measured by [57Co]cyanocobalamin binding using isolated rat gastric mucosal cells. The intrinsic factor/R-protein ratio was above 9:1 as evaluated by specific anti-intrinsic factor antibodies. In unfractionized cells with 23 +/- 1.3% parietal cells the intrinsic factor content of 148 +/- 47 fmol/10(6) cells remained almost unchanged over 3 h, whereas basal secretion rose up to 57 +/- 10. In fractionized cells (Percoll) with 3-85% parietal cells most intrinsic factor was found in the parietal cell-depleted fraction (content: 441 +/- 30, secretion/3 h: 139 +/- 16, mean formation/h: 50 +/- 12 fmol/10(6) cells). The intrinsic factor content of the different cell fractions correlated with that of pepsin. [14C]Aminopyrine uptake, an indirect measure of parietal cell H+ production, was inversely related. Carbachol (1 X 10(-6)-10(-3) mol/l) stimulated intrinsic factor secretion, 1 X 10(-3) mol/l being maximally effective (90 +/- 8% above basal). This response was inhibited by atropine and pirenzepine, but not by prostaglandin E2 (PGE2) and somatostatin. Dibutyryl cyclic adenosine monophosphate (dibutyryl cAMP, 43 +/- 7%) and hexoprenaline (24 +/- 5%) enhanced intrinsic factor secretion less effectively and pentagastrin like histamine lacked any stimulatory effect. We conclude that in the rat intrinsic factor is produced and released from chief cells mainly under cholinergic control.
 ...
PMID:Cellular origin and release of intrinsic factor from isolated rat gastric mucosal cells. 641 15

An account is given of the clinical and serological associations between diabetes and autoimmune diseases, especially those between diabetes and antihyperoglobulin, antithyroid, anti-intrinsic factor, anticorticoadrenal cell, and anti-nucleic acid autoantibodies. Body fluid antipancreas autoimmunity is examined from various standpoints relating to antipancrease cell antibodies (ICA), autoantibodies against glucagon-secreting cells (ECA) and somatostatin-secreting cells (SCA), and anti-islet cell surface antibodies (McLaren and Lernmark antibodies). Particular attention is directed to ICAs, since these have supplied the background for the recent division of type I diabetes into Ia viral and Ib autoimmune. Stress is laid on both the soundness and the problems forming part of ICAs, since their actual pathogenetic role (cytoplasmic markers?) still has to be determined, even though their persistent and significant association with autoimmune polyendocrinopathies is certain.
 ...
PMID:[Diabetes and autoimmune diseases. I]. 704 53

Baby formula acidification can be used to reduce diarrhea. Calcium formate is a dietary acidifier frequently used in animal weaning diets; it is also a source of available calcium. Gastric acidification reduces gastrin release and hydrochloric acid (HCl) secretion. To study the medium-term effects on fundic gastric mucosa, we fed weaning pigs control diets or diets supplemented with free or fat-protected calcium formate. We evaluated the following: 1) the number of HCl-secreting parietal cells, by immunohistochemistry using an antibody against H(+)/K(+)-ATPase; 2) the number of enteroendocrine cells immunohistochemically stained with chromogranin A (CGA), somatostatin, and histamine (HIS); and 3) the expression of the H(+)/K(+)-ATPase gene, by real-time RT-PCR in the oxyntic mucosa. Cells co-staining for CGA and HIS were defined as enterochromaffin-like (ECL) cells. Pigs fed calcium formate had fewer parietal cells and a lower expression of the H(+)/K(+)-ATPase gene than the controls (P < 0.05). This reduction did not occur in pigs fed fat-protected calcium formate. Somatostatin immune-reactive cells were also more numerous in pigs fed free calcium formate than in controls (P < 0.05). The number of ECL cells was not affected. Using covariance analysis, the number of parietal cells explained part of the differences in the expression of H(+)/K(+)-ATPase gene (positive correlation, r = 0.385, P < 0.01), and excluded the statistical significance of the diet. In the future, the effects on the oxyntic mucosa should be checked when the diet supplemented with calcium formate is discontinued. Furthermore, a reduction in the number of parietal cells could impair the absorption of vitamin B-12 due to a reduced secretion of the intrinsic factor by these cells.
 ...
PMID:A continuous dietary supply of free calcium formate negatively affects the parietal cell population and gastric RNA expression for H+/K+-ATPase in weaning pigs. 1661 9

We have previously reported that a synergistic interaction between hypergastrinemia and Helicobacter felis (H. felis) infection accelerates gastric carcinogenesis in mice, but the precise mechanism for this interaction has not been clarified. Consequently, we undertook an oligonucleotide cDNA microarray study to investigate changes in gene expression in this model system. Male hypergastrinemic transgenic (INS-GAS) mice with 6-months H. felis infection were compared with three different age, strain and gender-matched control groups: (i) INS-GAS mice without H. felis infection; (ii) non-transgenic FVB/N mice with H. felis infection; and (iii) non-transgenic FVB/N mice without H. felis infection. Complementary RNA derived from whole stomach were hybridized to the Affymetrix GeneChip murine U74Av2 array. Among 12 000 cDNA spotted on each chip, 35 cDNA were upregulated and 41 cDNA were downregulated more than twofold in H. felis-infected INS-GAS mice compared with all three control groups. Expression changes were validated in 12 selected genes by northern hybridization and/or quantitative real-time reverse transcription polymerase chain reaction (RT-PCR). Confirmed upregulated genes included Reg I, amphiregulin, MMP-10, MMP-13, claudin-7 and chitinase 3-like 1, while confirmed downregulated genes included H/K-ATPase alpha and beta subunits, intrinsic factor, somatostatin, galectin-2 and apolipoprotein A-I. Immunohistochemical analysis of MMP-10, amphiregulin, H/K-ATPase beta subunit and galectin-2 confirmed these expression changes at the protein level, and MMP-10 was mainly detected in stromal cells of submucosal region, while the other three genes were expressed in gastric epithelial cells. Taken together, gene expression profiling of this mouse model may provide novel insights into Helicobacter-induced gastric carcinogenesis.
 ...
PMID:Gene expression profiling in a mouse model of Helicobacter-induced gastric cancer. 1727 17