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 role of Ca2+ in the secretion of insulin and glucagon was investigated by studying the effects of Ca2+ ionophores on hormone secretion from isolated perifused islets of Langerhans. Ionophore X537A (100 muM), which binds alkaline earth cations and also complexes some univalent cations, caused a rapid transient increase in insulin and glucagon secretion which was not dependent on the presence of Ca2+ in the perifusion medium. Ionophore A23187 (100 muM), which specifically binds bivalent cations at neutral pH values, similarly increased insulin secretion in complete and Ca2+-free medium, but only stimulated glucagon release in the presence of extracellular Ca2+. Since the stimulatory effects of both ionophores were associated with an increased Ca2+ flux in the islets, these experiments support the hypothesis that Ca2+ may trigger the release of insulin and suggest that it is also involved in the secretion of glucagon. The basal rate of both insulin and glucagon release was significantly increased when Ca2+ was omitted from the perifusion medium, but it is proposed that this finding may be due to adverse effects on cell-membrane function under these conditions.
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PMID:Insulin and glucagon secretion from isolated islets of Langerhans. The effects of calcium ionophores. 110 4

An abrupt reduction of medium osmolarity by as little as 20 mosM evoked a discrete short-lived insulin secretory response from perifused chopped pancreas or isolated islets. The insulin response occurred earlier than that induced by either glucose or tolbutamide. None of the usual modifiers of insulin secretion significantly altered this secretory response. Glycolytic inhibitors, adrenergic agonists and blocking agents, cholinergic blocking agents, mitotic spindle inhibitors, and agents influencing sodium pump activity failed to alter hyposmolar-induced insulin secretion. Manipulation of the perifusion medium calcium concentration was the only procedure tested that influenced the secretory response. Perturbations of medium calcium concentration that increased the tissue-to-medium calcium gradient augmented the hyposmolar-induced insulin response and those that decreased tissue-to-medium calcium gradient greatly inhibited the response. The precise cause of the insulin response to a decrease in bathing fluid osmolarity remains undefined; however, the stimulus is not specific for insulin because increases in glucagon and amylase were also elicited by the hyposmolar stimulus.
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PMID:An effect of hyposmolarity on insulin release in vitro. 111 35

Plasma calcitonin, glucagon and parathyroid hormone were measured in patients with acute pancreatitis. Plasma calcitonin was not detectable in 6 specimens obtained from the hypocalcaemic patients. Plasma glucagon values were similar in patients with acute pancreatitis and control subjects and were unrelated to hypocalcaemia, which was not even induced by glucagon infusion. High or rising parathyroid hormone levels were noted in association with hypo-and normocalcaemia, suggesting that parathyroid hormone rises and maintains plasma calcium within normal limits. Plasma parathyroid hormone was, however, undetectable in 8 patients with prolonged hypocalcaemia. Deficiency of parathyroid hormone due to its destruction by proteolytic enzymes or because of parathyroid gland exhaustion is suggested as the major factor inducing persistent hypocalcaemia in acute pancreatitis. Administration of parathyroid hormone should, therefore, be considered in patients with acute pancreatitis when hypocalcaemia does not respond to intravenous calcium therapy.
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PMID:The aetiology of hypocalcaemia in acute pancreatitis. 111 72

We compared the maximal calcitonin secretion produced by pentagastrin, calcium, and glucagon for preoperative detection of medullary thyroid carcinoma in four subjects with normal or slightly increased plasma immunoreactive calcitonin (iCT) levels. In each case, pentagastrin administration produced higher peak iCT levels (5- to 36-fold increases over basal) than did calcium infusion (by 1.9- to 10.3-fold) and glucagon administration (by 3.6- to 27.4-fold). These preliminary studies suggest that pentagastrin is an effective agent for use in rapid stimulation tests designed to detectmedullary thyroid carcinoma in asymptomatic patients who have normal basal iCT concentrations.
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PMID:Stimulation tests for diagnosis of medullary thyroid carcinoma. 111 54

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

Variables of calcium metabolism were measured in 11 patients with clearly documented acute pancreatitis. Total and ionized calcium levels were either low or in the low-normal range as were phosphorus and total magnesium levels. Parathyroid hormone levels were high, and there was a significant inverse correlation with ionized calcium. Gastrin levels were normal, calcitonin values were uniformly below the detection limit of the assay, and pancreatic glucagon levels were elevated. The hypocalcemia of acute pancreatitis was probably not caused by abnormalities of glucagon, calcitonin, or gastrin secretion. Furthermore, parathyroid hormone secretion was apparently not impaired. Hypomagnesemia possibly played a minor role. This study suggests that the hypocalcemia of acute pancreatitis is secondary to extraskeletal calcium sequestration or an as yet unidentified defect of bone metabolism, or both.
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PMID:The hypocalcemia of acute pancreatitis. 114 52

COOH-terminal octapeptide of cholecystokinin (CCK-octapeptide) and the cholinergic agent carbamylcholine each produced a fourfold stimulation of calcium outflux in guinea pig isolated pancreatic acinar cells. Neither agent altered calcium influx. Stimulation of calcium outflux was rapid and specific, was abolished by reducing the incubation temperature to 4 degrees C, and was a saturable function of the secretagogue concentration. The concentrations of CCK-octapeptide and carbamylcholine that produced half-maximal stimulation of calcium outflux were 3.1 x 10(-10) M and 4.9 x 10(-5) M, respectively. The cholinergic antagonist antropine competitively inhibited carbamylcholine stimulation of calcium outflux but did not alter stimulation produced by CCK-octapeptide. Stimulation of calcium outflux by maximal concentrations of carbamycholine plus CCK-octapeptide was the same as that produced by a maximal concentration of either agent alone.Calcium outflux became refractory to stimulation by secretagogues, and incubation with either CCK-ostapeptide or carbamylcholine produced a refractoriness to both agents. The relative potencies with CCK and its related fragments stimulated calcium outflux were CCK-octapeptide greater than heptapeptide greater than CCK greater than hexapeptide = gastrin. Secretin, glucagon, and vasoactive intestinal peptide, at concentrations as high as 10(-5) M, failed to alter calcium outflux and did not affect stimulation by CCK-octapeptide or by carbamycholine.
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PMID:Action of cholecystokinin and cholinergic agents on calcium transport in isolated pancreatic acinar cells. 115 Aug 77

Plasma concentrations of calcium, phosphate, citrate, albumin, and parathyroid hormone (PTH) were measured during and after exchange transfusion of infants suffering from haemolytic disease using blood anticoagulated with acid-citrate and dextrose (ACD) or heparin. Pretransfusion plasma PTH and phosphate both correlated positively with postnatal age but not with each other. Transfusion with ACD blood caused a twelvefold rise in plasma citrate levels but no significant change in plasma calcium, phosphate, or PTH of the infant, despite the concentration of these substances being lower in the donor blood. The concentration of calcium, phosphate, and albumin was higher in heparinized than in ACD donor blood, and infants transfused with heparinized blood showed no change in the plasma concentration of any substance measured during transfusion. The addition of 50 mug glucagon to ACD donor blood had no effect on PTH secretion. 3 hours after transfusion there was a rise in the plasma PTH infants who had received ACD blood but not in those given heparinized blood. Transfusion with ACD blood caused a net loss of calcium, phosphate and albumin from the infant, whereas transfusion with heparin blood did not. Both types of transfusion caused a net loss of PTH but this was significantly greater in those given ACD blood. These results show that transfusion with ACD blood results in increased secretion of PTH, probably due to the fall in ionized calcium concentration caused by the citrate load.
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PMID:Parathyroid hormone secretion during exchange transfusion. 117 Aug 13

Thyrocalcitonin release mediated by glucagon secreted from the acutely inflamed pancreas has been postulated as a possible mechanism for hypocalcemia in acute pancreatitis. To test this hypothesis, hemorrhagic pancreatitis was induced in a group of thyroidectomized pigs. No source of thyrocalcitonin other than the thyroid has been described in the pig. Their subsequent serum calcium concentrations were compared with those in a group of thyroid intact pigs also given hemorrhagic pancreatitis. The results indicate that the hypocalcemia observed during the first 24 hours following induction of pancreatitis is not related to the presence of an intact thyroid. Differences observed in the degree of hypocalcemia between the two groups 30 to 48 hours after pancreatitis developed may be of significance but could be explained by dilutional differences alone. Thyrocalcitonin apparently has little if any role in the hypocalcemia observed during the course of acute pancreatitis.
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PMID:Mechanisms of hypocalcemia in acute hemorrhagic pancreatitis. 119 6

This study was designed to investigate changes in cardiac performance during hypoglycemia produced by the administration of insulin in the newborn piglet. With heart rate, aortic pressure, and aortic flow held constant, the treated group demonstrated a pronounced positive inotropic response manifested by an increase of dP/dt max to 138% of control values. Central nervous system function and beta adrenergic activity were excluded from the preparation by ligation of the brachiocephalic vessels and administration of practolol. For reasons discussed, it is unlikely that the findings can be ascribed to glucagon contamination. Therefore, the increase in contractility presumably resulted from a direct effect of insulin upon the myocardium. Clinical and laboratory data suggest that the resistance of the neonate to hypoxia is modified by glycogen stores. Insulin is known to increase glycogen synthesis, and this effect might be expected to augment myocardial resistance to hypoxia. Under the conditions of these experiments, however, pretreatment with insulin had no demonstrable influence on the rate of deterioration of cardiac function during hypoxia. The mechanism of cardiac stimulation by insulin is unknown but may involve calcium fluxes.
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PMID:Positive inotropic action of insulin on piglet heart. 121 Mar 41


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