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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of vitamin D3 on rat kideney metabolism under conditions of experimental hypercalcemia. Acta Physiol. Pol., 1978, 29 (2) 153--159. The effect of vitamin D3 on renal gluconeogenesis processes was studied in the rat. The performed estimations of gluconeogenesis rate from malate and lactate demonstrated significant increases of glucose formation rate when kidney cortex slices of the vitamin D3 treated animals were analyzed. Further studies on the mechanism of the observed phenomenon were performed using kidney cell fractionation procedure and fluorometric estimation of the concentration of selected gluconeogenetic metabolites. Significant increases of phosphoenolpyruvate concentration in the cytosol fraction and citrate concentration in the mitochondrial fraction were observed. Comparison of the described action of vitamin D3 on gluconeogenesis and the effect of parathyriod hormone, as known from the literature suggests similar mechanism of both factor actions. A possibility of vitamin D3 action through the increase in intracellular calcium has been discussed.
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PMID:The effects of vitamin D on the rat kidney metabolism under conditions of experimental hypercalcemia. 20 82

The effect of somatostatin on the insulin response to an acute intravenous glucose load was studied in five normal subjects before and after induction hypercalcaemia. In the normocalcaemic state, the insulin response to glucose was depressed by somatostatin. In the hypercalcaemic state, insulin responses to glucose in the presence of somatostatin, were partially restored and appeared to be related to the level of increment of serum ionized calcium. It is concluded that, in the human being, hypercalcaemia and somatostatin have opposite actions on glucose-stimulated insulin secretion.
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PMID:The effect of serum ionized calcium elevation on somatostatin inhibition of glucose-induced insulin release in humans. 74 92

Parathyroid hormone (PTH) was given intravenously to anesthesized adult dogs. Blood flows were measured with electromagnetic probes in different vascular areas concomitant with analysis of glycerol, free fatty acid, calcium, glucose, sodium, potassium, albumin, carbon-dioxid and creatinine. PTH consistently caused an immediate increment in blood flow in the celiac vasculature and a following, less pronounced increase in the renal artery. These changes were effectuated by a vasodilatation. The degree and duration of the flow increments were dose dependent; The celiac artery was more sensitive to the effect of PTH than the renal artery. In celiac artery maximal increase above basal flow was 58 +/- 27% (Mean +/- S.D.), in renal artery 25 +/- 12%. A significant lipolytic action of PTH was consistently notable within minutes after the administration of PTH. The other parameters analysed in blood remained unchanged sixty to ninety minutes after the PTH injections. Then a hypercalcemic effect of PTH appeared. A lipolytic action of PTH could be demonstrated with PTH doses which did not induce hypercalcemia.
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PMID:Circulatory and lipolytic effects of parathyroid hormone. An experimental study in dogs. 92 52

The relative contributions of Ca++, phosphorus, and parathyroid hormone (PTH) on insulin secretion were evaluated in three groups of dogs. Dogs were studied with glucose infusions (group I) or standard intravenous glucose tolerance tests (IVGTT) (group II) before and after the development of diet-induced hypophosphatemia. Mean serum phosphorus levels for both groups fell from 4.1 to 1.1 mg/100 ml. Animals in group I demonstrated a fall in glucose disappearance rates (Kg) from 5.3+/-0.6% min to 3.5+/-0.5% after induction of hypophosphatemia (P less than 0.001). Mean insulin response was significantly greater in the hypophosphatemic animals than in controls in this group. In group II animals, mean insulin areas obtained during the IVGTT increased from 1,426+/-223 to 2,561+/-141 muU/ml/60 min after induction of hypophosphatemia, and were unaffected by Ca++ or PTH administration. Ca++ administration, but not hypophosphatemia or PTH infusion, increased significantly the mean insulin response to tolbutamide. Secondary hyperparathyroidism was induced by dietary manipulation in four dogs (group III). Mean PTH values increased from 71.4+/-2.1 to 3,012+/-372 pg/ml (P less than 0.001). Mean insulin response to an IVGTT was similar to group III animals, but increased from 1,352+/-128 to 1,894+/-360 muU/ml/60 min after the excessive dietary phosphorus was reduced for 3 mo, and plasma phosphorus fell from 3.2+/-0.1 to 2.8+/-0.3 mg/100 ml. PTH values decreased to 647+/-53 pg/ml. The insulin response to tolbutamide was comparable to that in group II animals, but increased significantly after calcium administration. Immunoreactive insulin disappearance rates were unaffected by hypophosphatemia or diet-induced secondary hyperparathyroidism. These data demonstrate that hypophosphatemia is associated with an augmented glucose-stimulated insulin release, without any effect on tolbutamide-stimulated insulin release. Hypercalcemia produces an augmented tolbutamide-stimulated insulin release with no apparent effect on glucose-stimulated insulin release. Finally, PTH does not appear to be an insulin antagonist and has no apparent effect on either glucose- or tolbutamide-stimulated insulin release in animals with dietary-induced secondary hyperparathyroidism.
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PMID:The relative roles of calcium, phosphorus, and parathyroid hormone in glucose- and tolbutamide-mediated insulin release. 95 71

Deficiencies in acid excretion during hypercalcemia have been reported, and this defect has been ascribed to a deficiency in ammonia excretion. Because no changes in urine pH and urine flow occurred to explain decreased ammonia excretion, this suggested to us that decreased excretion was secondary to decreased renal ammonia production. To test this hypothesis, we investigated the ability of kidney slices from rats to produce ammonia and glucose and to consume oxygen when incubated in varying concentrations of calcium. High medium concentrations of calcium (3 and 4 mM) decreased kidney slice ammonia-genesis from glutamine and glutamine and kidney slice oxygen consumption while not affecting gluconeogenesis. Based upon our findings, we propose that hypercalcemia decreases urine ammonia excretion by depressing renal ammonia production.
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PMID:The effects of high calcium concentrations on renal ammoniagenesis by rat kidney slices. 101 6

In the experimentally-induced hyper- or hypoglycemic state, perilymph glucose concentration paralleled the blood concentration, although a delay of about one hour was observed between the time of maximum concentration of glucose in perilymph and its concentration in blood. In hypercalcemia, perilymph calcium concentration steadily increased over a three-hour period, although blood calcium concentration fluctuated during this time. After an initial increase in the CSF calcium concentration, there were insignificant changes during the second and third hours. In animals with thyrocalcitonin-induced hypocalcemia, although blood calcium concentration steadily decreased, its concentration in perilymph and CSF remained practically constant. The present findings suggest that the chemical composition of perilymph can be altered by changing the blood concentration of glucose or calcium. The marked difference of behavior noted between glucose and calcium in these experiments would indicate the existence of different mechanisms for maintaining the homeostatic state for these two substances.
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PMID:The effect on perilymph of the alteration of serum glucose or calcium concentration. 105 75

The growth hormone response to acute hypercalcemia was studied in 9 normal subjects. Growth hormone, calcium, glucose, phosphate and magnesium levels were determined at 30-min intervals during 4-h infusions. Infusions, performed in random order in the subjects, consisted of either normal saline at 3 ml/min for / h or 15 mg calcium/kg (calcium gluconate at 3 ml/min for 3 h followed by normal saline for the fourth hour. Significant hypercalcemia (P less than 0.05) was achieved within 60 min and maintained throughout the infusion. No change in calcium concentrations occurred during normal saline infusions, and phosphate, glucose and magnesium were unchanges in all studies. Growth hormone levels were significantly higher (P less than 0.05) at 60 min and all subsequent determinations during calcium infusion when compared to normal saline infusions. In 6 of the subjects, standard l-dopa provocative testing with an oral dose of 500 mg was preformed during normal saline and calcium infusions identical to those described above. Peak growth hormone responses did not differ significantly following l-dopa during saline or calcium infusion. These results suggest that an acute increase in circulating calcium promotes greater basal growth hormone secretion without a synergistic increase in hypothalamic mediated growth hormone release by l-dopa.
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PMID:The effect of acute hypercalcemia on growth hormone release in man. 112 88

The alterations in carbohydrate metabolism which attend the uremic syndrome have been recognized for some time. Recently, an interaction between hyperparathyroidism and these alterations in intermediary metabolism has been postulated. To further define any such interaction, 6 stable dialysis patients with significant secondary hyperparathyroidism were studied prior to and after subtotal parathyroidectomy. Glucose utilization and insulin secretion were estimated by use of a standard intravenous glucose tolerance test and the resistance of peripheral tissues to exogenous insulin was evaluated by insulin tolerance testing. All of peripheral tissues to exogenous insulin was evaluated by insulin tolerance testing. All patients were studied under baseline conditions, as well as induced hyper- and hypocalcemia, prior to and at least 2 months after surgery. Parathyroidectomy, per se, had no significant effect upon glucose utilization, insulin secretion, or the resistance of peripheral tissues to the action of exogenous insulin. Both induced hyper- and hypocalcemia, on the other hand, significantly diminished glucose utilization as judged by a reduced glucose disappearance rate during intravenous glucose tolerance testing. Hypocalcemia was associated with a markedly reduced insulin secretory response and normal tissue insulin sensitivity, while hypercalcemia was associated with a normal insulin response but reduced tissue sensitivity. The data suggest that calcium ion concentration may affect both glucose utilization and insulin secretion. As such, it must be adequately controlled in furture metabolic studies.
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PMID:The influence of serum calcium and parathyroid hormone upon glucose metabolism in uremia. 115 Nov 60

We studied calcium (Ca), magnesium (Mg) mass transfer (MT) in 10 and lactate balance in 5 CAPD patients using standard dialysis solution [(ST) (Ca 1.75 mmol/l; Mg 0.75 mmol/l; lactate 35 mmol/l)] and with reduced Ca/Mg, high lactate solution [(LC) (1.25 mmol/l; 0.25 mmol/l; 40 mmol/l respectively)]. Exchanges were performed with 1.36% and 3.86% glucose solutions. MT was calculated as mmol/exchange. Ca MT was +0.96 and +0.39 with ST 1.36% and 3.86% glucose respectively. Serum ionised Ca (iCa++) levels were less than fluid Ca during these exchanges. With LC 1.36% glucose it was -0.66 when ICa++ was more than dialysate Ca, but +0.66 when iCa++ was less than dialysate Ca. Ca MT was negative with LC 3.86% glucose irrespective of iCa++ levels. All patients were hypermagnesaemic (mean 1.24 mmol/l. Mg MT was +0.21 and -0.04 with ST 1.36% and 3.86% glucose respectively and -0.62 and -1.13 with LC 1.36% and 3.86% glucose respectively. The difference between mean lactate gain and bicarbonate loss was less (-0.4) during exchange with LC 1.36% glucose. Mean plasma TCo2 and plasma pH did not differ between ST and LC solutions. We conclude that reduced Ca/Mg, high lactate solutions should reduce hypercalcaemia/magnesaemia and maintain a better acid base balance in CAPD patients who may require Ca/Mg containing phosphate binders.
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PMID:Calcium, magnesium mass transfer and lactate balance study in CAPD patients with reduced calcium/magnesium and high lactate dialysis fluid. 136 24

Theoretical and clinical studies suggest that reduction of PD fluid calcium to 1.25 mmol/liter allows administration of larger doses of calcium carbonate, improves phosphate control and obviates the need for aluminum gels in most CAPD patients, without increasing hypercalcemia or hyperparathyroidism. Hypermagnesemia can also be avoided by reducing PD fluid magnesium concentration to 0.25 mmol/liter. Although glucose is a safe, effective an cheap osmotic agent, it provides a short duration of ultrafiltration, and contributes to significant metabolic abnormalities. Amino acids and glucose polymer are potential alternatives to glucose, and early clinical studies are encouraging. The unphysiological concentration of lactate in PD fluids has been shown to have pathological consequences, and undoubtedly bicarbonate would be a preferable buffer. Manufacturing techniques are being developed to produce such a fluid. A fluid containing bicarbonate and the peptide glycylglycine (30:10 mmol/liter) gives a stable buffer with a pH of 7.35, but has only undergone animal studies so far. Glucose solutions have deleterious effects on the peritoneal membrane, particularly during episodes of severe peritonitis, and the high osmolality is toxic to peritoneal host defense cells. Prompt treatment of peritonitis, early removal of the catheter where necessary, and minimization of glucose exposure, may do much to lengthen the dialysis life of the peritoneum.
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PMID:Improved solutions for peritoneal dialysis: physiological calcium solutions, osmotic agents and buffers. 140 67


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