Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ability of infantile hypercalcemic tumors (three rhabdoid renal tumors, one cellular mesoblastic nephroma, and one hepatoblastoma) to produce parathyroid hormone (PTH) was tested using RNA-DNA hybridization. Results were compared with those obtained in one lung epidermoid carcinoma and one parathyroid adenoma from adult patients. Elevated plasma immunoreactive PTH (iPTH) concentrations were observed in three of five children. The only tumor in which PTH-RNA hybridization could be detected was the parathyroid adenoma. The integrity of the RNA preparations was further confirmed by positive hybridization obtained with a glucagon DNA probe in both normal pancreas and the rhabdoid tumors. Quantitative bone histomorphometry of tumor-bearing nude mice showed a reduction in bone formation and increased bone resorption, the opposite of what occurs in hyperparathyroidism. The PTH-like protein, which was detected by radioimmunoassays (RIA) in the sera of three patients, could not be correlated with tumor PTH mRNA transcription within the limits of our assays. In order to explain this discrepancy, we suggest that the tumors produce a factor (not PTH) which, in turn, elicits the excess iPTH which we detected by RIA.
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PMID:PTH mRNA transcription analysis in infantile tumors associated with hypercalcemia. 338 30

Four weeks after 70% resection of the pancreas in the rat, serum levels of calcium, inorganic phosphate, magnesium, parathyroid hormone and calcitonin, as well as femur dry weight, volume, mean specific density, and mineral content were investigated. The urinary excretion of cAMP and hydroxyproline was measured. Additionally, residual pancreatic amylase content, fasting blood levels of insulin, glucagon, somatostatin and glucose were determined, and the mineral balance (calcium, phosphate) studied. Residual pancreatic amylase content was decreased to 22% of control values, fasting serum glucose and plasma glucagon were increased. Fecal excretion of calcium and phosphate was unchanged, but their balance was increased. Serum calcitonin and the mean specific density of femurs were decreased. All the other variables were unchanged. We conclude that in the rat, 70% pancreatic resection 1) probably does not have any harmful effects on calcium metabolism and bone mineralization in the short term postoperatively, 2) provokes mild hyperglucagonemia, the molecular nature and the origin of which need further elucidation.
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PMID:Influence of 70 percent pancreatic resection on serum and bone calcium in the rat--a preliminary report. 342 61

Clearance experiments were performed to characterize the sensitivity to vasopressin of the thick ascending limbs and collecting duct system of the rat kidney. The response of the thick ascending limbs was evaluated by measuring the Mg2+ excretion rate in the urine, since the [arginine-8] vasopressin-mediated effects on Mg2+ excretion are the direct result of a stimulation of Mg2+ reabsorption in this nephron segment, and the response of the collecting ducts was evaluated by changes in urine flow. To avoid the effects of parathyroid hormone, glucagon, and calcitonin, which stimulate Mg2+ reabsorption in the thick ascending limb and distal tubule, and of calcitonin, which increases the permeability of the cortical collecting ducts to water, experiments were performed on Brattleboro D. I. rats (with hereditary diabetes insipidus, due to a lack of [Arg8]vasopressin) acutely deprived of endogenous parathyroid hormone, calcitonin, and glucagon. Vasopressin infused at rates up to 5 pg/min did not reduce the Mg2+ fractional excretion rate, whereas at 5 pg/min water excretion was decreased by 50%. The half-maximal reduction of Mg2+ excretion occurred at vasopressin infusion rates 4-6 times higher than those necessary to diminish the water excretion rate to the same extent. We conclude that in vivo, two segments involved in the production of concentrated urine have different sensitivities to vasopressin and that this difference in sensitivity is very similar for the biological response in vivo and the adenylate cyclase activation in vitro. We suggest that both the magnitude and the nature of the effects of [Arg8]vasopressin on the kidney may vary according to the required antidiuretic response.
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PMID:Sensitivities of rat kidney thick ascending limbs and collecting ducts to vasopressin in vivo. 345 86

The effects of the cytosol activator protein obtained from rat reticulocytes (RCAP) were investigated in a heterologous membrane system--partially purified cell membranes from dog renal cortex. RCAP enhanced the response of dog renal cortical adenylate cyclase to bovine parathyroid hormone (1-34) [bPTH (1-34)] from two- to three-fold. RCAP also enhanced the response to 5 microM arginine vasopressin, 10 microM glucagon, and 10 microM isoproterenol. Analysis of double-reciprocal plots of substrate concentration and enzyme activity indicated that bPTH (1-34) alone and together with RCAP increased the Vmax of the adenylate cyclase enzyme and did not alter the apparent Km of the enzyme for MgATP. Membranes from dog renal cortex contain 42K and 39K proteins that are ADP-ribosylated by cholera toxin and pertussis toxin, respectively, and appear to be the stimulatory (Ns) and inhibitory (Ni) guanine nucleotide binding proteins described in many other hormone-responsive membrane preparations. Similar to its effects in rat reticulocytes, RCAP inhibited ADP-ribosylation of Ns and enhanced ADP-ribosylation of Ni. The muscarinic agonist, carbachol, inhibited PTH-responsive adenylate cyclase activity in dog renal cortical membranes and this inhibition was reversed by RCAP. These results indicate that RCAP enhances stimulation of adenylate cyclase by a variety of hormones in a heterologous membrane preparation and supports the hypothesis that RCAP's site of action is common to all adenylate cyclase systems. RCAP may facilitate coupling between Ns and the catalytic unit of adenylate cyclase by a pertussis toxin-like effect to inactivate Ni. The dual effects of RCAP upon ADP-ribosylation of Ni and Ns alpha subunits suggest that a binding site for RCAP may exist at a site of homology between Ns alpha and Ni alpha.
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PMID:Enhancement of parathyroid hormone-responsive renal cortical adenylate cyclase activity by a cytosol protein activator from rat reticulocytes. 350 32

In eight normal pregnant women and in eighteen women with a family history of diabetes, plasma calcitonin (CT), parathyroid hormone (PTH), insulin and glucagon variations and total plasma calcium levels were investigated. Calcitonin, parathyroid hormone and glucagon were all increased during the 2nd and 3rd trimester of pregnancy in normal women (N.W.) and in women with a family history of diabetes (W.F.H.D.). Plasma calcitonin levels were statistically significantly different between the two groups only in the 3rd trimester (118 +/- 4.9 vs 139 +/- 3.6 pg/ml p less than 0.01 in N.W. and W.F.H.D. respectively). Total plasma calcium levels were decreased significantly in the 3rd trimester in both groups: 3rd vs 1st trimester p less than 0.005 and p less than 0.001 in N.W. and W.F.H.D. respectively. Statistically significant difference between the two groups in total insulinemic area (p less than 0.001), in the rapid phase area (p less than 0.01) and insulinogenic index (p less than 0.05) were observed in the 3rd trimester.
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PMID:Plasma calcitonin variations in normal women and in women with family history of diabetes during pregnancy. 354 28

The effects of 1-desamino-8-D-arginine vasopressin (dDAVP) on superficial and juxtamedullary nephrons were investigated by micropuncture in diabetes insipidus (DI) Brattleboro rats chronically treated with the peptide. The rats, acutely deprived of endogenous calcitonin, parathyroid hormone (PTH), and glucagon [hormone-deprived (HD) rats], were examined either 4 days after cessation of dDAVP treatment (HDT, control diuretic rats) or when the treatment was continued until the micropuncture experiment, during which dDAVP was also given intravenously (HDT + dDAVP, experimental nondiuretic rats). In the presence of dDAVP, the reabsorption of Cl, Na, Mg, and Ca by the superficial loop of Henle was significantly increased, as previously observed in HD-untreated rats during acute infusion of dDAVP. The effects on the superficial distal tubule were also similar. The effects on K, however, were different both in the loop and in the distal tubule. At the bend of the juxtamedullary nephrons, the treatment alone (HDT rats) increased fractional delivery (FD%) of Na and Cl, whereas FD% of Mg, Ca, K, and P was unaltered. In HDT + dDAVP rats, FD% of H2O, Cl, Na, and Ca was significantly lower than in HDT rats, and FD% of K, Mg, and P did not differ significantly. In conclusion, in the presence of dDAVP, the FD% of H2O, Na, and Cl at the bend of the long-loop nephrons decreases, in accordance with our previous hypothesis that water removal along the rat descending limb increases outward NaCl diffusion along this segment.
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PMID:NaCl and Ca delivery at the bend of rat deep nephrons decreases during antidiuresis. 359 53

We investigated by micropuncture the effects of glucagon and parathyroid hormone (PTH) on thin limbs of juxtamedullary nephrons of rats with reduced plasma concentration of endogenous glucagon, PTH, antidiuretic hormone (ADH) and calcitonin, all four hormones enhancing the adenylate-cyclase activity in the thick ascending limbs and the distal nephron. Such a hormonal depletion suppresses the corticomedullary concentration gradient, making favourable conditions for studying the influence of these hormones on the renal concentrating mechanism. Administration of glucagon (4.4 ng/min-1) or PTH (5 mU/min-1) to these hormone-deprived rats elicited the expected decrease in urinary Mg and Ca fractional excretion without modifying either fractional or absolute excretion of water. At the tip of the loop, glucagon enhanced the loop fluid osmolality by 20%, but left the delivery of water unchanged. The Na and Cl concentrations increased significantly with the osmolality, resulting in a positive correlation between the fractional delivery of either ion and the loop fluid osmolality. PTH increased the fraction of filtered phosphate delivered to the thin limbs, as expected, but, in contrast to glucagon, did not alter either the Na, Cl, or total solute fractional deliveries. The Mg, Ca and K deliveries were unaffected by glucagon and PTH. In conclusion, glucagon, which activates the cyclase system of both the medullary and cortical portion of the thick ascending limb, enhances the delivery of salt to the tip of the loop by net sodium chloride addition to the descending limb. PTH which activates the adenyl-cyclase system only in the cortical thick ascending limb cannot enhance such NaCl delivery. NaCl, when added, might therefore originate from the medullary thick ascending limb.
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PMID:Effects of glucagon and PTH on the loop of Henle of rat juxtamedullary nephrons. 371 66

The effects of synthetic human calcitonin (HCT) on water and electrolyte deliveries to the thin limbs of Henle's loop of juxtamedullary nephrons were investigated by micropuncture in the rat. To avoid undesirable interference with exogenous calcitonin, experiments were performed in hormone-deprived rats with reduced circulating calcitonin, antidiuretic hormone, parathyroid hormone and glucagon, all four of which stimulate the adenylate-cyclase activity in the thick ascending limb and the distal tubule. Administration of HCT (1.0 mU/min X 100 g body wt) to such rats significantly reduced the urinary fractional excretion rate of water, Mg, Ca and K. At the tip of the longlooped nephrons, the fractional delivery of water diminished in the presence of HCT, although the glomerular filtration rate of these nephrons was unaltered. Simultaneously, the loop fluid osmolality rose significantly. HCT, however, did not alter the fraction of total filtered solutes remaining in the thin limbs, nor the NaCl fractional delivery. As previously observed in this laboratory with dDAVP, the reduced fractional delivery of water at the hairpin turn was accompanied by a decrease in Mg and Ca deliveries in rats given HCT, indicating that the handling of these two ions along the descending limb may be linked in part to the water movements in this nephron segment. The fractional deliveries of K at the hairpin turn and in urine were significantly correlated, and both decreased in the presence of HCT. Since, as shown previously, HCT reduces the net addition of K along the superficial distal tubule, it is concluded that calcitonin inhibits the medullary recycling of K between the nephron terminal segments and the loop of Henle of juxtamedullary nephrons.
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PMID:Effects of human calcitonin on water and electrolyte movements in rat juxtamedullary nephrons: inhibition of medullary K recycling. 371 48

The effects of subclinical vitamin D deficiency and vitamin D supplementation on oral glucose tolerance and secretion of pancreatic hormones were studied in 10 diphenylhydantoin-treated epileptic patients and 15 geriatric patients. Their mean serum concentrations of 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3 decreased markedly, but returned to normal within 2 weeks of oral supplementation with 25-hydroxyvitamin D3. The serum concentration of ionized calcium was within the normal range before treatment, and remained unchanged. Serum parathyroid hormone was increased during vitamin D deficiency, but decreased significantly (p less than 0.05) afterwards. In vitamin D-deficient epileptic and geriatric patients, the 2- and 3-h insulin levels after glucose ingestion were increased when compared with control values, and glucagon secretion was not suppressed by glucose. Oral glucose tolerance of both groups of patients did not change after 25-hydroxyvitamin D3 supplementation. Insulin secretion remained unchanged in geriatric patients, but was reduced to normal values in epileptic patients. Glucagon suppressibility by glucose was partly restored after vitamin D supplementation in epileptic patients but not in geriatric patients. In contrast to that observed in severely vitamin D-deficient rats or rabbits, correction of subclinical vitamin D deficiency failed to enhance insulin secretion or to improve glucose tolerance in man.
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PMID:Pancreatic secretion in man with subclinical vitamin D deficiency. 375 30

Previous studies demonstrated that in rat kidney, arginine-vasopressin (AVP), glucagon (GLU), calcitonin and parathyroid hormone exert similar effects on the thick ascending limb of Henle's loop (TALH). To ascertain the physiological significance of such multiple hormonal control of TALH function, it is necessary to establish whether one hormone can exert its effect on TALH, even when other hormones are present. We therefore compared renal responses to submaximal (1 ng/min) and maximal (10 ng/min) doses of glucagon in rats deprived of endogenous AVP, GLU, calcitonin and parathyroid hormone with the responses of similar rats given a maximal dose of AVP (40 pg/min). Administration of glucagon or AVP alone reduced Mg fractional excretion, but the reduction was more marked when both hormones were given together. Consequently, their effects were additive, at submaximal and maximal doses. In the presence of AVP + glucagon, urinary osmolality was also higher than in the presence of AVP alone (Umax: 1242 +/- 49 vs. 936 +/- 50 mosmol/kg; p less than 0.001). This latter effect may indicate that AVP and glucagon also exert additive effects on Na reabsorption in the TALH.
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PMID:Additive effects of glucagon and vasopressin on renal Mg reabsorption and urine concentrating ability in the rat. 382 66


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