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 15,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In antrectomized (B-I) and control rats, bone mineralization, the fractional intestinal absorption of calcium, magnesium and phosphorus, the balances of these minerals, their serum concentration and renal excretion, together with serum gastrin, calciotropic hormones (parathyroid hormone, calcitonin, 1,25-dihydroxyvitamin D), and osteocalcin were assessed four months after surgery. B-I evoked hypogastrinemia, but no changes in the serum concentrations of minerals and calciotropic hormones, or urinary cyclic AMP. The major significant changes brought about by B-I were: (1) a decrease in bone dry weight, specific density, bone ash calcium and magnesium content; (2) a decrease in the fractional absorption and urinary excretion of calcium and magnesium; (3) an increase in urinary hydroxyproline and serum osteocalcin in the presence of normal serum bone isoenzyme of alkaline phosphatase. It is concluded that in the rat (1) B-I over the long term decreases both bone mineral content and calcium and magnesium absorption, in the absence of any counterregulation; (2) B-I rats may have attained a new equilibrium which is characterized by decreased absorption and urinary excretion of calcium and magnesium, but maintenance of normocalcemia at the expense of bone; (3) the concomitant changes of serum bone markers are contradictory, which makes their interpretation and use in the present context difficult.
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PMID:Disturbances of mineral and bone metabolism following gastric antrectomy in the rat. 133 20

An acute challenge with gastrin-17 enhanced the uptake of 45Ca into sternum and several long bones in rats by about 10-30%; gastrectomy prevented this effect. Long-term treatment with (Leu15)-gastrin-17 (continuous infusion via osmotic minipumps for 4 weeks) enhanced the uptake of 45Ca into bone (examplified by radius and sternum) by 18-26% (tested on the last day of the infusion). Surgical removal of the acid-producing part of the stomach (fundectomy) or treatment with the anti-ulcer drugs, ranitidine (a histamine H2-receptor antagonist administered by continuous infusion) or omeprazole (an H+/K(+)-ATPase inhibitor administered daily by gastric tube for 4 weeks), induced sustained hypergastrinemia (through loss of acid feedback inhibition of gastrin release). The ranitidine- and omeprazole-evoked hypergastrinemia was associated with 32-62% enhancement of bone 45Ca uptake but the hypergastrinemia of fundectomized rats was not. Gastrectomy abolished the effect of omeprazole. We suggest that exogenous and endogenous gastrin influences calcium uptake into bone indirectly by releasing a calciotropic hormone (gastrocalcin) from the acid-producing part of the stomach. The bone ash weight was reduced by gastrectomy or fundectomy (4 weeks), but neither ranitidine nor omeprazole-evoked hypergastrinemia (4 weeks) raised the bone ash weight. The stimulated calcium uptake into bone of hypergastrinemic rats treated with ranitidine or omeprazole was associated with a 22-32% increase in the density of osteoclasts in the tibia. This finding is in line with the hypothesis that long-lasting hypergastrocalcinemia produces accelerated turn-over of bone rather than increased bone calcium content.
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PMID:Evidence that gastrin enhances 45Ca uptake into bone through release of a gastric hormone. 232 3

Diets containing egg white, casein, menhaden fish meal, soy protein or wheat gluten were fed to rats to assess the impact of dietary protein (and other nutrients) on gastric functions. The menhaden fish meal group exhibited increases in stomach histidine decarboxylase (HDC) activity, histamine concentration, as well as acid secretion when compared with the control, casein group. When rats were fed amino acid-supplemented casein or fish meal diets to simulate each other's amino acid profile, a small increase in gastric HDC activity, histamine content and acid secretion was observed in comparison with the unsupplemented casein or fish meal groups. The high mineral content of menhaden fish meal (15%) was thought to be a potential inducing factor for gastric histamine metabolism and acid secretion. Adding fish meal ash to the casein diet or to a cod fillet diet elevated stomach HDC activity and histamine concentration significantly. Furthermore, when calcium (Ca) was added to the casein diet to simulate its high content in menhaden fish meal (7.8%), similar elevated levels of gastric histamine were obtained for the Ca-supplemented casein group as for the fish meal group. The role of Ca could be due to release of gastrin, which results in release of stomach histamine, or by facilitating mast cell histidine incorporation with subsequent histamine synthesis.
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PMID:Gastric histamine metabolism and acid secretion in rats as influenced by diet and nutrient content. 682 9

Treatment with omeprazole, a long-acting proton pump inhibitor of acid secretion, induces hypergastrinemia. In chickens, omeprazole induces growth not only of the acid-producing mucosa (probably reflecting the trophic action of gastrin), but also of the parathyroid glands (hypertrophy + hyperplasia), while suppressing bone density and body weight gain without affecting blood calcium. The first part of the present study was concerned with the effect of omeprazole, ergocalciferol (vitamin D2), and restricted food intake on the gene expression of parathyroid hormone (PTH) in the parathyroid glands of the chicken. Chickens were treated with omeprazole (400 micromol/kg/day, I.M.), food restriction, omeprazole + food restriction, ergocalciferol (250 000 IU/kg/day, S.C.), or ergocalciferol + omeprazole for 5 weeks. The weight gain of the chickens was monitored, and the weights of the parathyroid glands and femurs were determined at sacrifice. PTH mRNA in the parathyroid glands was analyzed by Northern blot. The second part of the study examined the effect of 3 weeks of continuous gastrin infusion (chicken gastrin 20-36, 5 nmol/kg/hour, S.C.) on the expression of PTH mRNA in the parathyroid glands. Omeprazole reduced the body weight and femur density (ash weight per volume) while greatly increasing the weight of the parathyroid glands and the PTH gene expression. Food restriction alone and ergocalciferol alone (at a dose that raised blood Ca2+) were without effect, but food restriction greatly enhanced the omeprazole-evoked increase in parathyroid gland weight and PTH gene expression. Gastrin increased the weight of the parathyroid glands and reproduced the effect of omeprazole on PTH gene expression. Hence, it seems likely that the effect of omeprazole reflects the ensuing hypergastrinemia.
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PMID:Chicken parathyroid hormone gene expression in response to gastrin, omeprazole, ergocalciferol, and restricted food intake. 926 12

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

In man and experimental animals, partial and total gastrectomy and gastric vagotomies disturb extracellular mineral homeostasis, osteopenia being among the late outcomes. The sequence of events is complex and insufficiently understood. We report on the long-term effects of gastric fundectomy (FX; FX-1, n=11; sham-operated controls, n=14) sparing gastric vagal fibers at the lesser curvature in the rat, a procedure eliminating gastric acid production but preserving gastric reservoir function. After FX-1 there was a marked increase of gastrinemia [FX-1: 590 (SE 95); controls: 82 (5) pg-equiv/ml; P<0.001], serum 1,25-dihydroxyvitamin D [FX-1: 188 (17); controls: 86 (6) pg/ml; P<0.001], phosphaturia [FX-1: 32 (2); controls 23 (2) micromol/h; P<0.001] due to increased fractional phosphate clearance, elevated urinary net acid [FX-1: 21 (2); controls: 16 (1) micromol/h; P=0.03], and low urinary pH. The urinary excretion of hydroxyproline was increased [FX-1: 137 (15); controls: 99 (8) micromol/h; P=0.01], and crosslinks were also high. These changes were associated with a significant decrease of bone ash calcium, magnesium, and phosphorus. Bone histomorphometry revealed signs of high bone turnover. No signs of hyperparathyroidism were detectable. Acute stimulation of serum gastrin by gastric acid abolishing omeprazole failed to provoke extra-osseous changes, as seen in the long-term after fundectomy. It was concluded that the described type of fundectomy disturbs gastrinemia, acid-base and phosphorus metabolism, thereby initiating osteopenia. This animal model may be suitable for research into post-gastrectomy bone disease.
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PMID:Vagus-sparing gastric fundectomy in the rat: development of osteopenia, relationship to urinary phosphate and net acid excretion, serum gastrin and vitamin D. 1119 17