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 stress response in humans commonly includes elevations in plasma concentrations of glucocorticoids, catecholamines, glucagon, growth hormone, aldosterone, and renin, resulting in alterations in the metabolism of glucose and other energy substrates, and in increased sodium and water retention. In severe illness, triiodothyronine and sometimes thyroxine are decreased without evidence of clinical hypothyroidism. Antidiuretic hormone may be elevated in bacterial meningitis and other central nervous system disorders, as well as in acute asthma, chronic ventilator therapy, pneumothorax, atelectasis, and postoperatively. Increased ADH concentration can lead to significant hypoosmolality and hyponatremia with adverse effects on the patient. In the setting of severe intracerebral insults, ADH may be inappropriately low, resulting in diabetes insipidus. Insulin concentrations may be inappropriately low for serum glucose concentration, or insulin may have diminished receptor responsiveness in seriously stressed patients. Either situation leads to hyperglycemia. Disturbances in calcium, phosphorus, and magnesium homeostasis may occur relatively frequently in the critically ill patient in response to therapeutic interventions, or illness-induced altered metabolism. It is not always clear when an altered metabolic or hormonal state is an appropriate response to a stress, or represents decompensation of the body's mechanisms for coping with that stress. It is important, however to recognize the common responses of the organism to severe illness, and to monitor for treatable abnormalities which occur.
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PMID:Endocrine manifestations of critical illness in the child. 354 20

Fifteen male Holstein X Frisian calves, weighing 65 +/- 3 kg and fed a milk replacer twice daily were fitted with a return cannula loop, chronically implanted at 10 days of age in the pancreatic duct, were used. In six successive experiments we have observed the influence of an intravenous infusion of secretin, cholecystokinin pancreozymin (CCK-PZ), vasoactive intestinal peptide (VIP), glucagon, gastrin and somatostatin on pancreatic juice flow rate, and on the excretion of proteins, calcium, inorganic phosphorus, zinc and amylase activity of pancreatic juice. In two other experiments, we have studied the interaction of secretin (or CCK-PZ) with somatostatin (SRIF). Each experiment was performed 5 h after calves feeding and no milk was given to the animals during the time of sampling. Our results indicate that the endocrine regulation of the exocrine pancreas in young calves is similar to that described in other mammals. Secretin and CCK-PZ increased significantly excretion of water, calcium, magnesium, inorganic phosphorus, zinc, proteins and amylase activity. Somatostatin and glucagon inhibited effects observed with two precedent hormones. Gastrin increased pancreatic juice flow rate but excretion of protein and amylase activity do not varied significantly. VIP showed no significant effect on pancreatic excretion of water, minerals, proteins and amylase activity. However, our animals seem to be characterized by a more intense excretion of proteins and amylase in the pancreatic juice following secretin than after CCK-PZ infusion.
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PMID:The endocrine regulation of exocrine pancreas in preruminant milk-fed calves. 610 15

The effects of sustained fiber ingestion on gastric emptying glucose tolerance, hormone responses, and jejunal absorption of glucose and lysine were studied in healthy volunteers. Subjects were placed on a low-fiber (3 g) diet for 2 wk, followed by 4 wk of an isocaloric diet supplemented with 20 g/day of either apple pectin (7 subjects) or alpha-cellulose (6 subjects). At the conclusion of each dietary period subjects ingested a low-fiber breakfast surface-labeled with 99mtechnetium sulfur-colloid. Gastric emptying half-time, plasma glucose, calcium, phosphorus, insulin, glucagon, gastrin, human pancreatic polypeptide, and motilin were determined. Gastric emptying half-time was prolonged approximately twofold after pectin supplementation (p less than 0.005) and returned to normal 3 wk after discontinuing pectin supplementation. Cellulose supplementation did not alter the gastric emptying rate. Plasma glucose, calcium, phosphorus, and hormonal responses to the meal were unchanged after either pectin or cellulose supplementation. Pectin ingestion did not impair intestinal absorption of glucose or lysine. In contrast to sustained cellulose ingestion, sustained pectin ingestion slows the gastric emptying rate; the mechanism underlying this adaptive effect is unknown.
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PMID:Sustained pectin ingestion delays gastric emptying. 628 2

Blood glucose, insulin, calcium (Ca), phosphorus (P), parathyroid hormone (PTH) and calcitonin (CT) were evaluated in 8 normal children, aged 17-41 months, during an oral glucose load; in 7 normal children, aged 15-42 months, during i.v. glucose infusion; and in 6 normal children, aged 19-40 months, during glucagon administration. During the oral glucose tolerance tests the mean maximum decline of Ca (8.63%) and p (12.66%) was at 120 min, while PTH and CT significantly increased from basal values of 1.36 ng/ml +/- 0.21 and 97 pg/ml +/- 14 to 2.20 ng/ml +/- 0.22 and 140 pg/ml +/- 13, respectively, at 45 min. During i.v. glucagon administration the mean maximum decline of Ca (9.64%) and P (12.28%) was at 30 min. PTH levels rose significantly from basal values of 1.2 mg/ml +/- 0.22 to 2.1 ng/ml +/- 0.32 at 45 min, while CT increased rapidly from basal levels of 90 pg/ml +/- 14 to 127 pg/ml at 15 min. In conclusion, increases in glucose and insulin due to ingestion or infusion of glucose, or to glucagon injection, are therefore not only associated with a fall in serum Ca and P but also with rises in PTH and CT.
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PMID:Parathyroid hormone and calcitonin in glucose regulation. 700 78

To study the relationship between islet hormonal secretion and intracellular content of five elements, a rat islet perifusion technique was used in 24 paired experiments. Control and experimental chambers each containing 100 islets, received 2.8 and 16.7 mM D-glucose, respectively. Effluent was collected frequently for hormone measurements. At eight different time intervals form 0--30 min islets were fixed and prepared for scanning electron microscopy. Over 900 unobscured alpha and beta cells were selected by size and shape criteria. Energy dispersive x-ray analysis was applied to each single cell to determine relative content of calcium (Ca), potassium (K), sodium (Na), chlorine (Cl), and phosphorus (P). Experimental chambers exhibited typical acute (0--9 min) and second phase (10--30 min) insulin secretion in association with suppression of glucagon release after 10 min. At 2 min an abrupt upward K spike in both alpha and beta cells was followed at 3--4 min with a 1.5- to 2-fold rise of Ca and a reciprocal decrease in K, Na, Cl, and P. From 3 to 30 min biphasic insulin secretion. Reduced alpha cell calcium after 6 min preceded suppression of glucagon secretion. After 2 min K related inversely to Ca content in both alpha and beta cells. These results could not be reproduced when D-galactose was substituted for D-glucose. We conclude that sequential changes of Ca content that are reciprocally related to K are predictive of beta cell insulin release and suppression of alpha cell glucagon secretion.
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PMID:Fluctuations of calcium, phosphorus, sodium, potassium, and chlorine in single alpha and beta cells during glucose perifusion of rat islets. 702 94

Plasma and urine phosphate concentrations were improved in 21 patients with diabetes mellitus during "optimal" metabolic control as compared with "suboptimal" control. During the "suboptimal" control phase the daily insulin dosage averaged 38 +/- 22 (SD) U/day and the mean plasma glucose levels averaged 17.1 +/- 1.8 mmol/l, while during the "optimal" control phase the daily insulin dosage averaged 84 +/- 59 U/day and the mean plasma glucose level was 6.2 +/- 1.4 mmol/l. The institution of rigid diabetic control over 4-10 days significantly raised serum phosphorus from 1.12 +/- 0.16 to 1.26 +/- 0.19 mmol/l (p less than 0.001), and decreased urinary phosphorus excretion from 686 +/- 125 to 588 +/- 88 mg/day (p less than 0.001). These changes were associated with significant reductions in urinary calcium, urinary glucose, plasma immunoreactive glucagon and serum parathyroid hormone. This diminution in urinary phosphorus loss may have been due to diminished glycosuria but equally could have been influenced by a direct action of insulin on the renal tubule or suppression of glucagon and parathyroid hormone secretion. Under the conditions of this study, reduced urinary phosphorus may have been sufficient to cause a rise in serum phosphorus despite the known effects of insulin on the cellular influx of phosphorus.
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PMID:The effect of chronic insulin therapy on phosphate metabolism in diabetes mellitus. 702 29

The effect of intramuscular administration of glucagon (Glg) and calcitonin (Ct) on the pattern of serum calcium (Ca), in organic phosphorus (P), blood glucose (BS), immunoreactive insulin (IRI) and growth hormone (GH) was investigate in 14 patients after total thyroid ablation during replacement therapy. In seven patients the pattern of Ct after Glg administration was assessed in the same conditions. Both hormones induced a prompt and marked decrease of Ca with out any differences between effect of Glg and Ct. The decline of P due to Glg is more rapid and marked than the due to Ct, the difference being significant from 60 to 120 min. Glg caused a rapid and marked rise of BS and IRI with a tendency toward normalization up to 180 min, GH rose significantly from 120 to 180 min. The changes of BS and IRI due to Ct were slow and less marked, but prolonged: level of BS increased and that of IRI decreased. No effect of Ct administration on GH was recorded. In general, neither the effects of Glg nor those of Ct were influenced by hypothyroidism. This fact may be of importance for use of Glg in testing GH reserve in hypothyroidism. Ct after Glg administration in athyroid patients failed to exhibit any significant changes. Thus our results support the assumption about similar and independent action of Glg and Ct on calcium and phosphate homeostasis and different effects of both hormones on glucose metabolism.
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PMID:Comparison of metabolic effects of glucagon and calcitonin and assessment of direct effect of glucagon on calcitonin level in athyroid man. 703 Sep

The effect of 25(OH)vitamin D3 [25(OH)D3] on the phosphaturic action of glucagon was studied using clearance techniques in the following groups of rats: group 1, parathyroidectomized (PTX) glucagon-infused rats receiving intravenous 25(OH)D3; group 2, PTX 25(OH)D3-pretreated rats receiving intravenous glucagon; and group 3, the thyroparathyroidectomized glucagon-infused rats receiving intravenous 25(OH)D3. The effect of 25(OH)D3 on glucagon-induced increase of cAMP in kidney slices and glucagon-activated adenylate cyclase (AC) in kidney membrane fractions was studied in vitro. In group 1, 25(OH)D3 suppressed the glucagon-induced phosphaturia by reducing fractional excretion of phosphorus (CP/CIn) from 0.175 +/- 0.02 (mean +/- SE) to 0.112 +/- 0.12 (P less than 0.05); this was associated with a reduction of urinary cAMP from 1,830 +/- 230 to 660 +/- 120 pmol/min (P less than 0.01). In group 2, pretreatment with 25(OH)D3 reduced CP/CIn from 0.221 +/- 0.025 to 0.108 +/- 0.012 (P less than 0.005). In group 3, 25(OH)D3 reduced CP/CIn from 0.165 +/- 0.012 to 0.075 +/- 0.011 (P less than 0.005). In vitro, 25(OH)D3 blunted the glucagon-induced activation of the AC/cAMP system by reducing AC from 570 +/- 30 to 325 +/- 28 pmol cAMP.mg protein-1.h-1 (P less than 0.01) and the cAMP level from 11.2 +/- 0.9 to 8.5 +/- 0.7 pmol cAMP/g wet tissue (P less than 0.05). These results show that 25(OH)D3 blunts the phosphaturic action of glucagon and suggest that this response may be mediated through suppression of the AC/cAMP system.
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PMID:Evidence for interference of 25(OH)vitamin D3 with phosphaturic action of glucagon. 722 86

Following previous work showing that i.v. arginine induces a fall in blood phosphorus and an increase in blood potassium in normal subjects, investigation of the mechanism underlying these metabolic changes was extended to a group of 14 insulin-dependent diabetics and a further 6 normal volunteers. In the diabetics, arginine (0.5 g/kg body weight) in 30 min caused a slight, but significant fall in blood phosphorus (delta = -0.40 +/- 0.04 mg/ml p less than 0.01). This was well below the fall noted in the normal subjects, which, as demonstrated in the earlier study, is to a great extent mediated by insulin. The increase in blood potassium was much more marked than in the normal subjects (delta = + 1.42 +/- 0.15 mEq /l; p less than 0.001) and rose to pathological levels (5.6 to 6.5. mEg/l) in 9 out of 14 patients. There were no significant changes in blood pH, plasma osmolality, or plasma aldosterone. Inhibition of the glucagon response to arginine by means of a priming dose of 250 micrograms somatostatin, followed by infusion of 1,500 micrograms/hr, did not abolish the rise in blood potassium. These findings indicate that insulin protect against arginine-induced hyperkalaemia and that this metabolic alteration does not depend on glucagon, acidosis, enhance plasma osmolality, nor the suppression of aldosterone secretion. Persons with low insulin secretion due, for example, to stress or diabetes, run the risk of pathological hyperkalaemia if subjected to i.v. infusion of arginine.
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PMID:The risk of pronounced hyperkalaemia after arginine infusion in the diabetic subject. 731 14

Calcium and phosphorus metabolism is mainly regulated by PTH through its actions on kidney and bone. PTHrP, which is associated with the hypercalcemia of malignancy syndrome, binds to and activates the same receptor that PTH does. cDNA clones of PTH/PTHrP receptors from rat osteosarcoma (ROS 17/2.8) and opossum kidney (OK) cells are highly homologous and are members of a novel G protein-linked receptor family that includes calcitonin, glucagon, GLP-1, GHRH, VIP, and secretin receptors. Analysis of the protein sequence predicts a receptor with 7 transmembrane domains, a 155 amino acids (aa) extracellular (EC) N-terminal, and 130aa intracellular C-terminal domaina. The extracellular domain has 6 conserved cysteines and 4 potential glycosylation sites. When transfected in COS cells, both receptors are able to bind PTH and PTHrP active fragments with equal affinity. Likewise, agonists activate both adenylate cyclase and phospholipase C efficiently. The N-terminal EC domain and the first EC loop seem to determine the receptor binding capacity with the agonists. Activation of adenylate cyclase and phospholipase C might involve multiple sites between the 3rd helix and the C-terminal tail. Partial characterization of the rat PTH/PTHrP receptor gene demonstrates the existence of at least 15 exons. The first six transmembrane domains are encoded by separated exons. The PTH/PTHrP receptor mRNA is expressed mainly in kidney and bone, and also is widely expressed in many tissues, but not all. A major 2.3-2.5 kb transcript is observed in all these tissues. Nevertheless, 2 larger transcripts are observed in kidney and liver, and multiple smaller mRNA species are observed in kidney, skin, and testis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mode of action of parathyroid hormone (PTH) and PTH-related peptide (PTHrP) in target organs]. 785 77


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