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)

We have studied the role of vitamin D in the regulation of gastrin and gastric somatostatin secretion from the isolated perfused rat stomach. In Ca-deficient vitamin D-deficient rats (Ca(-)D(-) group), the basal and bombesin-stimulated gastrin and gastric somatostatin release (basal IRGa, basal IRS, sigma delta IRGa, and sigma delta IRS) all were significantly lower than in Ca-replete vitamin D-replete rats (Ca(+)D(+) group), and also lower than in Ca-replete vitamin D-deficient rats (Ca(+)D(-) group) except for the basal IRGa. In the Ca(+)D(-) group, the basal IRGa and IRS, and sigma delta IRS were not significantly lower than in the Ca(+)D(+) group. Although there was no significant impairment in basal IRGa, sigma delta IRGa in the Ca(+)D(-) group was significantly lower than in the Ca(+)D(+) control group. Thus, the gastrin and gastric somatostatin secretion from the Ca-deficient vitamin D-deficient rats were impaired. In addition, the impaired gastrin and gastric somatostatin secretions seem to be caused not only by a decrease in serum Ca but also by the reduced effect of the vitamin D on the G and gastric D cells.
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PMID:Effect of vitamin D on gastrin and gastric somatostatin secretion from the isolated perfused rat stomach. 289 57

Nineteen rats were parathyroidectomized by electrocauterization, resulting in pronounced hypocalcaemia. Seven of these rats were then given vitamin D3 in a dose causing hypercalcaemia, while 7 received a dose which normalized serum calcium and 5 received no vitamin D. Ten further animals were sham-operated and were not given any extra vitamin D. The experimental period was 16 weeks. No significant differences in serum gastrin values were found between the different groups. Quantitative studies of the antral gastrin cells showed no difference in the number of gastrin cells per unit volume or unit segment between the different groups of vitamin-D-treated animals and sham-operated animals. However, the number of gastrin cells per unit segment was significantly higher in the hypocalcaemic animals than in the sham-operated animals, as a result of an increase in mucosal thickness. The amount of antral mucosal gastrin did not differ between the different groups. Thus the results of this study indicate that experimentally induced hypercalcaemia in parathyroidectomized rats does not influence the serum gastrin, the number of gastrin cells or antral gastrin.
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PMID:Vitamin-D-induced hypercalcaemia and its effect on serum gastrin, gastrin cells and antral gastrin in parathyroidectomized rats. 629 54

Endocrine abnormalities are common symptoms in patients with chronic renal failure. They are characterized by: 1. excessive somatotropin and prolactin secretion, 2. increased peripheral conversion of T4 to rT3, 3. secondary hyperparathyroidism accompanied by a relative insufficiency of calcitonin secretion, 4. hypogonadism, 5. hyperinsulinism and 6. decreased erythropoetin and 1,25-dihydroxy-vitamin D synthesis. In patients with chronic renal insufficiency normal function of the renin-angiotensin-aldosterone system, and pituitary-adrenal axis and normal PgA and PgE2 secretion are found. Increased blood levels of some peptide hormones (e.g. glukagon, gastrin) in patients with chronic renal failure seem to be caused, at least partially by secretion of biologically inactive prohormones and their decreased renal clearance.
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PMID:[Endocrine changes in chronic renal failure]. 700 96

22-Oxacalcitriol the analog with low calcemic effect and the original hormone 1,25(OH)2 vitamin D3 were localized by autoradiography in mouse stomach at different time intervals after intravenous injection. Both compounds showed a distinct nuclear concentration and retention in neck mucous cells of gastric and pyloric glands, and in dispersed endocrine cells in the antrum region. When the nuclear binding of radioactively labelled compound was compared between gastric neck cells and duodenal absorptive cells, binding was low but sustained in neck cells. Peak uptake after the injection was between 8 and 12 h in neck cells, but between 15 min and 30 min in duodenal villous epithelium. In the duodenum, weak nuclear labelling appeared at 8 h and was undetectable at 12 h under the conditions of the experiment. Nuclear labelling of neck cells remained detectable at 12 h and even after 24 h, similarly for both OCT and 1,25(OH)2 vitamin D3. These results suggest that the stomach is an important target tissue for vitamin D and its analog OCT. Regulation of neck cell functions is suggested, such as proliferation and differentiation of surface epithelium and gastric gland epithelium, and neck cell secretion of acidic mucus. Regulation is also indicated of G-cell gastrin secretion associated with gastrin paracrine effects on parietal cell HCl and intrinsic factor secretion, chief cell pepsinogen secretion, neck cell proliferation, as well as endocrine effects on systemic calcium homeostasis.
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PMID:Nuclear receptors for 1,25-dihydroxy-22-oxavitamin D3 (OCT) and 1,25-dihydroxyvitamin D3 in gastric gland neck mucous cells and gastrin enteroendocrine cells. 764 98

Highly selective vagotomy (HSV) or sham operation was performed in male rats. Fifteen weeks later bone mineralization, fractional intestinal absorption and balance, urinary excretion, and serum levels of calcium, magnesium and phosphorus, together with serum gastrin, parathyroid hormone, calcitonin, vitamin D metabolites, osteocalcin, isoenzymes of alkaline phosphatase, and the urinary excretion of cyclic AMP and hydroxyproline were assessed. HSV induced chronic hypergastrinemia and enhanced the weight of the fundus, antrum, and pancreas. Body weight, food intake, intestinal absorption, mineral balance, and bone mineralization were unaffected by HSV, whereas serum parathyroid hormone levels and urinary hydroxyproline excretion were increased. It is concluded that in the rat 1) HSV has a trophic effect on gastric and extragastric tissues; 2) gastric acid production is not a major determinant of intestinal calcium absorption; and 3) normal bone mass in the presence of signs of hyperparathyroidism indicates an intrinsic capacity of HSV to interfere with calcium metabolism, probably via hypergastrinemia, gastrin being an element of the gastro-parathyroid axis. Our present findings underscore the fact that osteopenia after HSV in man may be a rare finding, but it cannot be ruled out that bone disease found after partial or total gastrectomy may be due in part to concomitant vagotomy.
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PMID:Highly selective vagotomy in the rat: effects on bone and mineral metabolism. 820 82

Young male rats (100 g body weight) were fed diets containing varying amounts of calcium. Body weight and bone development were studied together with various endocrine parameters, including blood levels of Ca2+, calcitonin, parathyroid hormone, vitamin D, and gastrin, and the enterochromaffin-like (ECL) cell-related parameters gastric mucosal histidine decarboxylase activity and histamine concentration. A diet containing 0.5% calcium resulted in optimum body weight gain and bone development. A lower calcium intake impaired body weight gain and bone development. The impairment was manifested in reduced bone calcium content whereas the size of the bones was unaffected. The net absorption of calcium seemed to be proportional to the calcium intake. A low calcium diet (0.03%) raised the circulating levels of 1,25(OH)2D and parathyroid hormone and lowered 25(OH)D3 and Ca2+, whereas a high calcium diet (5.46%) raised calcitonin, Ca2+, 25(OH)D3, and 1,25(OH)2D. In addition, the low calcium diet lowered the circulating gastrin concentration and the histidine decarboxylase activity and histamine content of the ECL cells in the gastric mucosa. A high calcium diet raised the circulating gastrin concentration, but the rise was not associated with an increase in the histidine decarboxylase activity and histamine content.
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PMID:The effect of high or low dietary calcium on bone and calcium homeostasis in young male rats. 836 95

In humans, gastric surgery results in in osteopenia via mechanisms that are insufficiently understood; surgery-induced changes in the hormonal axes involving the stomach, thyroid, and the parathyroids may play a role. To study this in more detail, we evaluated calcium (Ca), magnesium (Mg), and phosphorus (P) metabolism as well as physical, chemical, and histomorphometric bone parameters in rats rendered hypergastrinemic by fundectomy (FX). In independent experiments, the response to an oral Ca challenge was investigated in intact rats versus FX, and in thyroidectomized versus thyroid-intact FX rats. Sixteen weeks following FX, body weight was approximately 80% that of sham-operated controls. In urine, P excretion was elevated fivefold, the pH was significantly decreased, and cAMP excretion was elevated as compared with controls; serum parathyroid hormone (PTH), calcitonin, 25OHD, Ca, Mg, and P were normal; gastrin and 1,25(OH)2D were elevated. On the basis of bone ash mineral content, FX rats developed significant osteopenia, and histomorphometry indicated only slightly elevated bone turnover and mineralization. Following oral Ca, thyroid-intact FX rats developed hypercalcemia, serum gastrin decreased, and calcitonin increased significantly; in thyroidectomized FX rats, calcitonin remained at baseline levels although there was a similar degree of hypercalcemia; PTH decreased during the hypercalcemic period in both groups. Serum gastrin did not correlate with calcitonin or PTH, and in multivariate regression analysis the only predictor of serum 1, 25(OH)2D was urinary phosphorus. It was concluded that in the FX rat (1) osteopenia is not caused by intestinal Ca malabsorption, vitamin D, Ca deficiency, or secondary hyperparathyroidism; (2) osteopenia may be related to PTH-independent urinary hyperexcretion of P, followed by a rise of serum 1,25(OH)2D; (3) the existence of endocrine axes among gastrin, calcitonin, and PTH cannot be substantiated. FX osteopenia appears to be related to gastric acid abolition, and the reactive hypergastrinemia probably stabilizes the mass and turnover of bone.
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PMID:Gastric fundectomy in the rat: effects on mineral and bone metabolism, with emphasis on the gastrin-calcitonin-parathyroid hormone-vitamin D axis. 979 30

The ECL cells are peptide hormone-producing cells, rich in histamine and chromogranin A (CGA)-derived peptides, that operate under the control of gastrin. Gastrin and the ECL cells form a functional unit, the gastrin-ECL-cell axis. The aims of the present study were to examine (1) if calcitonin (CT), parathyroid hormone (PTH) and vitamin D affect the gastrin-ECL-cell axis (by measuring the activity of the histamine-forming enzyme, histidine decarboxylase (HDC), and the expression of HDC mRNA and CGA mRNA in the ECL cells), and (2) if activation of the gastrin-ECL-cell axis affects the parathyroid glands (by measuring plasma PTH and mRNA expression). We also examined the possibility that the oxyntic mucosa harbours vitamin D receptors. Fasted rats received intravenous infusion of PTH and CT with or without gastrin. PTH raised the blood Ca2+ concentration, whereas CT infusion lowered it. Plasma PTH rose in response to CT, while serum gastrin remained unaffected. ECL-cell HDC was activated by gastrin but not by CT and PTH. Five daily subcutaneous injections of large amounts of ergocalciferol raised the blood Ca2+ concentration, while reducing the oxyntic mucosal HDC activity and the expression of HDC and CGA mRNA. The serum gastrin concentration was not affected. The findings are in line with the idea that the gastrin-ECL-cell axis can be suppressed by vitamin D or by vitamin D-dependent mechanisms. Western blot analysis revealed the presence of vitamin D receptor immunoreactivity and reverse transcription PCR detected vitamin D receptor gene expression in the rat oxyntic mucosa. Hypergastrinemia was induced by daily peroral treatment with the H+/K+-ATPase inhibitor, omeprazole, for 2 weeks or by continuous subcutaneous infusion of gastrin for 7 days. Elevated serum gastrin concentration was associated with increased HDC activity and increased HDC and CGA mRNA expression in the oxyntic mucosa. There was no elevation of plasma PTH or PTH mRNA expression in the parathyroid gland.
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PMID:Rat stomach ECL-cell histidine decarboxylase activity is suppressed by ergocalciferol but unaffected by parathyroid hormone and calcitonin. 1010 Sep 26

The bone mineral density (BMD) and the associated extracellular status of mineral and acid-base metabolism were evaluated in 11 males, 3-18 years after total gastrectomy (GX). In the lumbar spine, but not in the femoral neck, BMD was decreased in seven, normal in three, and falsely high in one individual. Relative to the limits of normalcy, fasting serum levels of gastrin were low, but normal for calcium, phosphorus, parathyroid hormone, calcitonin and vitamin D, while the level of total alkaline phosphatase was elevated; fasting urine pH and calcium were low, while phosphorus and net acid were high. Regression analyses revealed serum gastrin and phosphorus, and urinary net acid as possible predictors of BMD. It was concluded that over the long-term GX evokes low BMD, but not hyperparathyroidism and deranged vitamin D metabolites. Future studies may focus on gastrin, parathyroid hormone-independent hyperphosphaturia and disturbed acid-base metabolism as indicators of a new extra-cellular equilibrium of minerals.
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PMID:Low bone mineral density after total gastrectomy in males: a preliminary report emphasizing the possible significance of urinary net acid excretion, serum gastrin and phosphorus. 1051 Jul 32

An important role for beta-catenin pathways in colorectal carcinogenesis was first suggested by the protein's association with adenomatous polyposis coli (APC) protein, and by evidence of dysregulation of beta-catenin protein expression at all stages of the adenoma-carcinoma sequence. Recent studies have, however, shown that yet more components of colorectal carcinogenesis are linked to beta-catenin pathways. Pro-oncogenic factors that also release beta-catenin from the adherens complex and/or encourage translocation to the nucleus include ras, epidermal growth factor (EGF), c-erbB-2, PKC-betaII, MUC1, and PPAR-gamma, whereas anti-oncogenic factors that also inhibit nuclear beta-catenin signaling include transforming growth factor (TGF)-beta, retinoic acid, and vitamin D. Association of nuclear beta-catenin with the T cell factor (TCF)/lymphoid enhancer factor (LEF) family of transcription factors promotes the expression of several compounds that have important roles in the development and progression of colorectal carcinoma, namely: c-myc, cyclin D1, gastrin, cyclooxygenase (COX)-2, matrix metalloproteinase (MMP)-7, urokinase-type plasminogen activator receptor (aPAR), CD44 proteins, and P-glycoprotein. Finally, genetic aberrations of several components of the beta-catenin pathways, eg, Frizzled (Frz), AXIN, and TCF-4, may potentially contribute to colorectal carcinogenesis. In discussing the above interactions, this review demonstrates that beta-catenin represents a key molecule in the development of colorectal carcinoma.
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PMID:Beta-catenin--a linchpin in colorectal carcinogenesis? 1183 57


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