Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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 effects of insulin on the renal handling of sodium, potassium, calcium, and phosphate were studied in man while maintaining the blood glucose concentration at the fasting level by negative feedback servocontrol of a variable glucose infusion. In studies on six water-loaded normal subjects in a steady state of water diuresis, insulin was administered i.v. to raise the plasma insulin concentration to between 98 and 193 muU/ml and infused at a constant rate of 2 mU/kg body weight per min over a total period of 120 min. The blood glucose concentration was not significantly altered, and there was no change in the filtered load of glucose; glomerular filtration rate (CIN) and renal plasma flow (CPAH) were unchanged. Urinary sodium excretion (UNaV) decreased from 401 plus or minus 46 (SEM) to 213 plus or minus 18 mueq/min during insulin administration, the change becoming significant (P smaller than 0.02) within the 30-60 min collection period. Free water clearance (CH2O) increased from 10.6 plus or minus 0.6 to 13 plus or minus 0.5 ml/min (P smaller than 0.025); osmolar clearance decreased and urine flow was unchanged. There was no change in plasma aldosterone concentration, which was low throughout the studies, and a slight reduction was observed in plasma glucagon concentration. Urinary potassium (UKV) and phosphate (UPV) excretion were also both decreased during insulin administration; UKV decreased from 66 plus or minus 9 to 21 plus or minus 1 mueq/min (P smaller than 0.005), and tupv decreased from 504 plus or minus 93 to 230 plus or minus 43 mug/min (P smaller than 0.01). The change in UKV was associated with a significant reduction in plasma potassium concentration. There was also a statistically significant but small reduction in plasma phosphate concentration which was not considered sufficient alone to account for the large reduction in UPV. Urinary calcium excretion (UCaV) increased from 126 plus or minus 24 to 200 plus or minus 17 mug/min (P smaller than 0.01). These studies demonstrate a reduction in UNaV associated with insulin administration that occurs in the absence of changes in the filtered load of glucose, glomerular filtration rate, renal blood flow, and plasma aldosterone concentration. The effect of insulin on CH2O suggests that insulin's effect on sodium excretion is due to enhancement of sodium reabsorption in the diluting segment of the distal nephron.
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PMID:The effect of insulin on renal handling of sodium, potassium, calcium, and phosphate in man. 112 Jul 86

The difference in absorption of insulin and its glucose lowering-effect after the administration of crystalline insulin by the intravenous, intramuscular, and subcutaneous routes was compared in 14 lean normal subjects. Insulin in a dose of 0.1 U/kg body weight was given by the three different routes. Blood was drawn from the opposite arm at regular intervals for the determination of insulin, glucose, glucagon, cortisol, and potassium. Intravenous insulin produced the highest pharmacological level of insulin in 2 minutes (2099 +/- 414 muU/ml) with marked hypoglycemia at 30 minutes (a 68% drop). Intravenous insulin injection produced an increase in plasma glucagon and cortisol reaching a 2-fold increase above the fasting level 30 minutes after the glucose nadir. An equivalent amount of intramuscular insulin produced a maximal increase in plasma insulin at 50 minutes (45 +/- 4 muU/ml) and caused a 35% drop in plasma glucose at 60 minutes, which effects were greater than those caused by subcutaneous injection (highest IRI = 36 +/- 3.5 muU/ml and 23% glucose drop at 180 minutes). No significant increase in glucagon or cortisol was noted with equivalent amounts of subcutaneous or intramuscular insulin injection. Our studies suggest that, in normal lean subjects, insulin injection by the intramuscular route provides a faster absorption of insulin with a concomitant greater drop in plasma glucose than does injection by the subcutaneous route.
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PMID:Comparison of the effectiveness of various routes of insulin injection: insulin levels and glucose response in normal subjects. 127 May 78

Transgenic mice with elevated levels of beta-cell calmodulin develop severe diabetes even though pancreatic beta-cells contain reserve levels of insulin. Electron microscopic examination of transgenic pancreas confirmed the presence of abundant insulin secretory granules and failed to reveal obvious morphological abnormalities. These observations suggested that excess calmodulin may specifically impair the secretory process. To directly assess the effect of excess calmodulin on beta-cell function we have isolated pancreatic islets from transgenic animals. Transgenic islets from 6- to 8-day-old mice used 40% less glucose than normal islets and contained 58% of the normal insulin content, 90% of the normal glucagon content, and 5-fold higher levels of calmodulin than islets from control mice of the same age. Parallel perifusions of normal and transgenic islets confirmed that excess calmodulin inhibited glucose-stimulated insulin secretion; first phase secretion was reduced by 60%, and second phase secretion was essentially absent. Static assays were performed to assess the response to other secretagogues. All fuel secretagogues tested were ineffective in stimulating insulin secretion from transgenic islets. Secretion in response to depolarizing levels of potassium was also severely impaired. The phosphodiesterase inhibitor 3-isobutyl-1-methyl-xanthine increased transgenic secretion, but not to the level obtained in normal islets. Of the compounds examined, only phorbol 12-myristate 13-acetate and carbachol, two substances thought to act in beta-cells by stimulation of protein kinase-C, produced equivalent secretion in normal and transgenic islets. Phorbol 12-myristate 13-acetate also appeared to restore second phase secretion in transgenic islets. These results indicate that the initial period of calmodulin-induced diabetes is due to a secretory defect. This defect appears to be distal to membrane depolarization and is selective for the second phase of insulin secretion.
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PMID:Elevated beta-cell calmodulin produces a unique insulin secretory defect in transgenic mice. 137 47

The present study was conducted to examine the roles of hormonal factors in plasma potassium alterations in acute respiratory acidosis. Respiratory acidosis (pH, 7.07-7.10) induced by the inhalation of 10% CO2, 20% O2 and 70% N2 mixed gas caused an increase in the plasma potassium concentration beyond that of the control of 3.44 +/- 0.12 (mean +/- SE) to 4.36 +/- 0.07 mEq/l (p less than 0.01) within 180 min. The plasma norepinephrine concentration was also noted to significantly increase at the same time. Phentolamine (40 micrograms/kg/min i.v.) did not affect the degree of acidosis or acidosis-induced hyperkalemia. No significant changes in the plasma levels of epinephrine, insulin, glucagon, cortisol or aldosterone could be detected. Hormonal factors would thus appear not to be essential to potassium movement from intracellular to extracellular compartments in acute respiratory acidosis.
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PMID:Roles of hormones in plasma potassium alteration in acute respiratory acidosis in dogs. 140 6

It has been speculated that glucoregulatory hormones and/or renal autacoids mediate the increase in glomerular filtration rate (GFR) induced by the administration of protein or amino acids. Because infusion of a mixture of amino acids (AA mix), but not of branched-chain amino acids (BCAA) alone, increases GFR, we performed a crossover study in seven normal subjects in which the glomerular hemodynamic effects of separate 3-h infusions of these two amino acid solutions were compared with changes in potential mediators of this response, i.e., glucoregulatory hormones, renin, vasodilatory prostaglandins (PGs), and guanosine 3',5'-cyclic monophosphate (cGMP). As expected, infusion of the AA mix but not BCAA resulted in a prompt and sustained increase in GFR. Both infusions caused a significant increase in plasma insulin, whereas glucagon increased only with the AA mix. Plasma growth hormone was initially unchanged with both infusions but increased after 2 h of BCAA. Neither infusion significantly increased the urinary excretion of PGE2, 6-keto-PGF1 alpha, or cGMP. Both infusions resulted in a small but significant decrease in plasma renin activity. Infusion of BCAA but not the AA mix resulted in a progressive decrease in plasma glucose and potassium concentrations and an increase in renal sodium reabsorption that may have resulted from stimulation of insulin secretion that was not counterbalanced by a simultaneous increase in glucagon. Thus only changes in glucagon exhibited a significant temporal relationship with changes in GFR, lending further support to a role for glucagon as a mediator of amino acid-induced glomerular hyperfiltration.
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PMID:Hormonal mediators of amino acid-induced glomerular hyperfiltration in humans. 164 85

The acute effects of i.v. somatostatin (250 mcg bolus followed by 250 mcg/h continuous infusion for two hours) on renal hemodynamics, renal electrolyte and water handling, and urinary excretion of catecholamines and prostaglandins, as well as on plasma concentrations of arginine vasopressin, atrial natriuretic factor, norepinephrine, epinephrine, dopamine, glucagon, and plasma renin activity were studied in seven normal subjects. Somatostatin decreased effective renal plasma flow and glomerular filtration rate, osmotic and free water clearances, urine volume, and sodium and potassium excretion, while urinary osmolality, fractional excretion of sodium, and phosphate excretion increased significantly. Plasma concentrations of arginine vasopressin, atrial natriuretic factor, norepinephrine, epinephrine, and dopamine remained unchanged, while plasma renin activity (3.0 +/- 0.25 vs 2.4 +/- 0.2 ng AngI/ml/h; p less than 0.01) and glucagon levels (40 +/- 11 vs 20 +/- 16 pg/ml; p less than 0.01) decreased. Urinary excretion of norepinephrine, epinephrine, dopamine, PGE2, and PGF2 alpha was suppressed under somatostatin. A significant positive correlation was found between urinary dopamine and sodium excretion (r = 0.7; p less than 0.001) and urinary prostaglandin E2 and glomerular filtration (r = 0.52; p less than 0.01). Without accompanying changes in plasma osmolality and vasopressin concentration significant antidiuresis occurred, suggesting a direct tubular effect of somatostatin. However, the hormone-induced changes are due mainly to the decrease in renal plasma flow. The results demonstrate that somatostatin at supraphysiological doses exerts significant effects on the kidney.
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PMID:Effect of somatostatin on kidney function and vasoactive hormone systems in health subjects. 168 Nov 32

The renal effect of cyclic somatostatin was studied on healthy subjects. The somatostatin was used at therapeutical dose in intravenous infusion. Somatostatin decreases the renal plasma flow, glomerular filtration rate, osmotic and free water clearances, sodium and potassium excretion and the tubular reabsorption of phosphorus while urinary osmolality increases. Under somatostatin infusion the urinary excretion of catecholamines, PGE2, PGF2 alfa and the plasma renin activity and the plasma concentration of glucagon and growth hormone decrease. The antidiuretic activity of somatostatin is due to a) a direct haemodinamic effect, b) an influence on the renal tubular transport as well and also c) because of change the water handling in the collecting ducts.
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PMID:[Effect of somatostatin on kidney function]. 168 89

The present studies demonstrate that the beta-cell line RINr1046-38 (RIN-38) retains the capability to secrete insulin in response to glucose. The maximal effect of glucose was a 5- to 9-fold stimulation of insulin secretion from RIN-38 cells. This glucose-induced insulin secretion was maximal at 0.6 mM and was modulated by other secretagogues. Potassium concentrations of 10 mM, adenylate cyclase activators (glucagon-like peptide-1 and forskolin), and a phosphodiesterase inhibitor (isobutylmethylxanthine) potentiated glucose-induced insulin secretion, but had little or no effect on insulin secretion in the absence of glucose. Potassium concentrations of 20 mM or more, glibenclamide, and carbachol (Cch) stimulated insulin secretion 8- to 12-fold in the absence of glucose, while only Cch potentiated the effect of glucose on insulin secretion. Amino acids (alanine, arginine, leucine, and ketoisocaproate) also stimulated insulin secretion. The alpha 2-adrenergic agonist clonidine (1 microM), low extracellular calcium (less than or equal to 0.5 mM), and extended culture of RIN-38 cells at low glucose concentrations (0.33 mM) inhibited the stimulatory effect of glucose on insulin secretion. Insulin secretion was retained in RIN-38 cells for up to 98 passages. However, extended passage was associated with a decline in cellular insulin content (83% decline over 89 passages). In addition, high passage cells lost the ability to secrete insulin in response to glucose, but continued to respond to other secretagogues (K+, alanine, and carbachol). In fact, in the absence of glucose the effect of Cch on insulin secretion was well maintained in high passage cells (8- and 9.9-fold increase in insulin secretion, passages 9 and 70, respectively). Thus, low passage RIN-38 cells secrete insulin in response to glucose and other insulin secretagogues. High passage cells do not respond to glucose, but continue to respond to other secretagogues. Based on these results we propose that high and low passage RIN-38 cells provide a model for examining molecular mechanisms of glucose-induced insulin secretion. In addition, these findings emphasize that passage information is essential for interpretation of secretion studies with RIN cell lines.
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PMID:Modulation of glucose-induced insulin secretion from a rat clonal beta-cell line. 170 Nov 27

The aim of the present study was to compare the degree of hypoglycaemia, the hypoglycaemic symptom score and counterregulatory responses to equimolar amounts of intravenously administered porcine and semisynthetic human insulin in a double-blind crossover study in insulin-dependent diabetic patients. After overnight stabilization of blood glucose to approximately 6 mmol l-1, insulin was infused from 06.00 hours at such a rate as to keep the blood glucose concentration constant at 6 mmol l-1. At 09.00 hours hypoglycaemia was induced by increasing the infusion rate to give a blood glucose level of 2 mmol l-1 within about 60 min. The individual infusion rate from the first test was repeated in the second test, 1 week later. Blood glucose minimum levels were 2.1 (range, 1.3-2.9) and 2.1 (1.3-2.8) mmol l-1 for porcine and human insulin, respectively. The insulin concentrations at blood nadirs were 107 (66-180) and 107 (56-184) pmol l-1, respectively, for porcine compared to human insulin (NS). Symptom scores at minimum blood glucose concentrations were 43 and 46, respectively, with a maximal difference in intensity of 1 point in each patient. There were no statistical differences in the counterregulatory responses of glucagon, epinephrine, norepinephrine, cortisol, growth hormone, prolactin, beta-endorphine or in serum-potassium decreases. Patients were unable to discriminate between the two forms of insulin. It is concluded that there are no differences between porcine and semisynthetic insulin with regard to glucose fall, hormonal counterregulation or symptom scores, when the two forms of insulin are administered intravenously in equimolar amounts.
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PMID:Counterregulatory hormonal response to insulin-induced hypoglycaemia in insulin-dependent diabetic patients: a comparison of equimolar amounts of porcine and semisynthetic human insulin. 200 48

Studies were performed on previously nephrectomized dogs to examine roles of hormonal factors in plasma potassium alterations in acute alkalosis. Respiratory and metabolic alkalosis were induced by hyperventilation and intravenous NaHCO3 or tris(hydroxymethyl)aminomethane (Tris) infusion, respectively. Respiratory and NaHCO3-induced alkalosis provoked decreases in plasma potassium from the control value of 5.12 +/- 0.68 (SE) to 4.21 +/- 0.55 meq/l (P less than 0.01) and from 4.65 +/- 0.26 to 3.91 +/- 0.16 meq/l (P less than 0.01) within 180 min, respectively. In contrast, Tris-induced alkalosis elicited an increase in plasma potassium from the control value of 4.56 +/- 0.30 to 5.31 +/- 0.30 meq/l (P less than 0.01). Hypokalemia in respiratory alkalosis was associated with a decrease in the plasma norepinephrine concentration from the control level of 377 +/- 104 to 155 +/- 41 pg/ml (P less than 0.05) but not with changes in plasma levels of epinephrine, insulin, glucagon, cortisol, and aldosterone. However, this hypokalemia was not affected by phentolamine. Also, somatostatin did not modify the hypokalemic response. NaHCO3-induced hypokalemia was associated with a decline in the plasma aldosterone and norepinephrine concentrations. The decline in plasma norepinephrine in NaHCO3-induced alkalosis followed the decrease in plasma potassium. In Tris-induced alkalosis, plasma insulin increased but norepinephrine decreased. The findings do not suggest fundamental roles of the hormonal factors in the plasma potassium alterations in bilaterally nephrectomized dogs with acute alkalosis.
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PMID:Role of hormonal factors in plasma K alterations in acute respiratory and metabolic alkalosis in dogs. 215 37


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