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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 calcitonin (CT) and other hormones on the bile calcium excretion after a single intraperitoneal administration of calcium (4.0 mg/100 g BW) was investigated in thyroparathyroidectomized rats. Porcine, salmon, and synthetic eel CT (80 MRCmU/100 g BW, respectively) markedly increased the bile calcium excretion in comparison with that of calcium-administered rats. Tetragastrin (7.5 microgram/100 g BW), and insulin (50 mU/100 g BW) did not alter significantly the bile calcium excretion, while epinephrine (100 microgram/100 g BW), glucagon (50 microgram/100 g BW), and parathyroid hormone (25 U/100 g BW) increased significantly. The increasable effect of CT on the bile calcium excretion was significantly prevented by epinephrine (10 and 100 microgram/100 g BW). The present results suggest that the bile calcium excretion may be increased by the hormones which causes the elevation of cyclic AMP in the liver cells of rats.
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PMID:Effects of calcitonin and other hormones on bile calcium excretion in thyroparathyroidectomized rats. 43 94

To investigate a possible action of insulin on the glomerulus, the binding 125I-insulin to the isolated glomeruli prepared from rat kidney was examined. When incubated at 22 degrees C, 125I-insulin binding proceeded with time and reached a steady state at 45 min at which time nonspecific binding was less than 25% of total binding. A small fraction of 125I-insulin was degraded during incubation. This binding was specific to insulin in that it was inhibited by unlabeled porcine and beef insulins and to a lesser extent by porcine proinsulin and desalanine-desasparagine insulin, but not by glucagon, parathyroid hormone, vasopressin, calcitonin, and angiotensin II. Increasing concentrations of nonlabeled insulin displaced 125I-insulin binding in a dose-dependent fashion. Scatchard plot of the data was curvilinear consistent with either two classes of receptors with different affinities or a single class of receptors that demonstrate negative cooperativity. The addition of excess nonlabeled insulin to the glomeruli preincubated with 125I-insulin resulted in a rapid dissociation of approximately or equal to 70% of bound 125I-insulin. Insulin decreased the increments in glomerular cyclic AMP levels by epinephrine and by prostaglandin E2, but not those by histamine. These data showed the presence of specific insulin receptors in the glomeruli, and that insulin action may be, at least in part, through modulation of glomerular cyclic AMP concentrations. Such action of insulin may underlie the alteration in glomerular ultrafiltration and the glomerular ultrafiltration and the development of glomerular lesions in diabetes mellitus, a disease in which insulin deficiency or the tissue resistance to insulin exists.
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PMID:Binding of 125I-insulin to the isolated glomeruli of rat kidney. 50 Aug 16

1. In incubated tubule fragments from renal cortex of fed rats gluconeogenesis from pyruvate was stimulated by adrenaline (1mum optimum) and by the selective alpha-adrenergic agonists oxymetazoline and amidephrine. The selective beta-agonists isoproterenol and salbutamol were ineffective at concentrations up to 10mum. 2. Stimulation of gluconeogenesis by 1mum-adrenaline was almost completely blocked by 10mum-phentolamine (alpha-antagonist), partially blocked by 10mum-phenoxybenzamine (alpha-antagonist) and unaffected by 10mum-propranolol (beta-antagonist). 3. Adrenaline stimulation of gluconeogenesis was rapid and was sustained for at least 1h. 4. Oxymetazoline (alpha-agonist) was extremely potent in stimulation of gluconeogenesis. This compound stimulated glucose production from pyruvate, lactate and glutamate, but not from succinate or glycerol. 5. In the absence of Ca(2+) oxymetazoline was ineffective, whereas some stimulatory effect of adrenaline on gluconeogenesis was still observed. 6. Glucagon had no effect on gluconeogenesis from pyruvate in the presence of 1.27mm-Ca(2+) and inhibited the process in the presence of 0.25mm-Ca(2+). Parathyrin (parathyroid hormone) stimulated gluconeogenesis at 1.27mm-Ca(2+). 7. In short incubations of tubule fragments glucagon, papaverine and adrenaline significantly increased 3':5'-cyclic AMP. Adrenaline also slightly decreased 3':5'-cyclic GMP. Oxymetazoline had no effect on the amount of either cyclic nucleotide. 8. At all concentrations tested, theophylline and papaverine decreased gluconeogenesis from pyruvate. 9. It is concluded that renal gluconeogenesis may be increased by alpha- but not beta-adrenergic stimuli and that this is probably independent of changes in 3':5'-cyclic AMP or 3':5'-cyclic GMP. An involvement of Ca(2+) in the action of oxymetazoline appears likely, but this is less certain with adrenaline.
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PMID:Hormonal control of gluconeogenesis in tubule fragments from renal cortex of fed rats. Effects of alpha-adrenergic stimuli, glucagon, theophylline and papaverine. 59 61

Differences in metabolic homeostasis in 12 patients with initial vs. eight patients with repeated attacks of acute pancreatitis have been compared during the acute phase of the disease. As a group, subjects with a previous history of pancreatitis had significantly lower glucagon concentrations (P less than 0.002) for the over all 24-hour study period. Conversely, the serum concentrations of blood sugar, insulin, growth hormone, gastrin, cortisol, nonesterified fatty acids, triglycerides and cholesterol failed to distinguish between the two patient groups. Likewise, immunoreactive plasma parathyroid hormone and calcitonin levels were comparable in both patient populations. Of the measurements considered, it would appear therefore that plasma immunoreactive glucagon is the best indicator of previous pancreatic inflammation. Evaluation of parenchymal integrity during an episode of acute pancreatitis would be of prognostic and therapeutic value in this disease.
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PMID:First 24 hours of acute pancreatitis. A biochemical and endocrine evaluation of initial versus repeated attacks. 69 15

Dilute aqueous solutions of glucagon were investigated by high-resolution 1H nuclear magnetic resonance at 360 MHZ. Monomeric glucagon was found to adopt predominantly an extended flexible conformation which contains, however, a local non-random spatial structure involving the fragment--Phe-22--Val-23--Gln-24--Trp-25--. This local conformation is preserved in the partial sequence 22--26 and could thus be characterized in detail. Two interesting conclusions resulted from these experiments. One is that the local spatial structure in the fragment 22--25 of glucagon is identical to that observed in the fragment 20--23 of the human parathyroid hormone. Secondly, the backbone conformation in the C-terminal fragment of glucagon in solution must be different from the alpha-helical structure observed in single crystals of glucagon. These new structural data are analyzed with regard to relationships with glucagon binding to the target cells.
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PMID:1H nuclear-magnetic-resonance studies of the molecular conformation of monomeric glucagon in aqueous solution. 72 Mar 38

Plasma glucose, insulin, and alpha-cell glucagon profiles were examined in ten adults with uncomplicated primary hyperparathyroidism before and 8-12 week after surgical removal of a single parathyroid adenoma. Treatment restored abnormal serum calcium and phosphorus concentrations to a normal range and reduced serum parathyroid hormone levels from 47 +/- 4 to 16 +/- 4 mu 1 Eq/ml (normal = 0-40). Plasma glucose curves during 100-g oral glucose tolerance, 30 min intravenous glucose (1.5 g/min), or arginine infusions (1.0 g/min) did not differ before and after surgery. However, basal and peak insulin concentrations were higher before treatment during these tests (p less than 0.05). Basal glucagon levels were unaffected by hyperparathyroidism (72 +/- 7 versus 77 +/- 7 pg/ml). Peak 30 min values after arginine provocation were also similar before and after treatment as was maximal suppression of basal glucagon during glucose infusions. Four patients also received 400 g lean beef meals. Glucose and glucagon responses over 240-min periods were nearly identical before and after surgery despite higher insulin levels before treatment. It is concluded that elevated serum parathyroid hormone and plasma insulin concentrations in primary hyperparathyroidism do not relate to abnormalities of plasma alpha-cell glucagon in the basal state or after glucose, arginine, or protein administration.
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PMID:Plasma alpha-cell glucagon in primary hyperparathyroidism. 78 68

The relatives of 25 index patients with primary parathyroid hyperplasia were tested for hypercalcemia. At least 13 of these patients had one or more first degree relatives with hypercalcemia. Two familial syndromes each with autosomal dominant transmission were recognized. Two index patients were part of large kindreds categorized as having familial hypocalciuric hypercalcemia (FHH). Manifestations of multiple endocrine neoplasia type I were present in the kindreds of at least four other index patients (FMEN I). In seven other kindreds there were too few affected members to allow definitive classification. Differences between manifestations of FHH and FMEN I were described. Among offspring of affected persons in kindreds with FHH, as distinct from FMEN I, the prevalence of hypercalcemia approached the theoretic maximum of 50 per cent during the first two decades. In FHH, nephrolithiasis and peptic disease were unusual; moderate hypercalcemia occurred without hypercalciuria; and subtotal parathyroidectomy did not abolish hypercalcemia. Concentrations of peptide hormones other than parathyroid hormone (PTH) were normal in those with FHH; in FMEN I high concentrations of glucagon in plasma were found in five of six patients tested, and high concentrations of gastrin were found in three of 12 patients. Hypergastrinemia generally accompanied obvious peptic disease. Distinction of the two conditions is important since patients with FHH may not benefit from subtotal parathyroidectomy, but they generally have a better clinical prognosis than do patients with FMEN I.
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PMID:Family studies in patients with primary parathyroid hyperplasia. 87 Nov 27

Recent data on various environmental stressors and blood hormone patterns are presented for lactating cattle. Known stressor effects of such factors as environmental temperature, air pollution, and noise on the plasma thyroxine, growth hormone, cortisol, prolactin, progesterone, luteinzing hormone, epinephrine, and norepinephrine of lactating cattle are discussed. Information on stressor effects is lacking on glucagon, insulin, vasopressin, calcitonin, oxytocin, thyrotrophic hormone, follicle stimulating hormone, melatonin, parathyroid hormone, and estrogens in the lactating cow. The importance of evaluating both the effect of environmental stressor and of production or lactation intensity is emphasized in the overall interpretation of changes in hormone of plasma. The short and long term environmental heat effects on thyroxine, cortisol, and growth hormone are clear with initial increased due to acute stressors and a decline of amounts in plasma after prolonged exposure to stressors. The relationship of amounts in plasma of these hormones to milk production appears to be related directly for cortisol, growth hormone, and prolactin with an inverse relationship with thyroxine. Epinephrine and norepinephrine seem to be elevated with prolonged environmental heat stress. However, the influence of intensity of lactation has not been measured. Hormones in plasma as they relate to stressor effects and milk production are important as potential indicators of the physiological state of a cow and reflect the physiological compensations a cow undergoes at various lactation intensities and/or stress exposure.
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PMID:Effects of environmental and other stressors on blood hormone patterns in lactating animals. 98 81

1. A technique for indirectly labelling antibodies to polypeptide hormones, by combining them with radioactively labelled anti-(immunoglobulin G) is described. (a) 125I-labelled anti-(rabbit immunoglobulin G) and anti-(guinea-pig immunoglobulin G) antibodies with high specific radioactivity were prepared after purification of the antibodies on immunoadsorbents containing the respective antigens. (b) Rabbit immunoglobulin G antibodies to human growth hormone, porcine glucagon and guinea-pig immunoglobulin G antibodies to bovine insulin and bovine parathyroid hormone were combined with immunoadsorbents containing the respective polypeptide hormone antigen. (c) The immunoglobulin G antibodies to the polypeptide hormones were reacted with 125-I-labelled anti-(immunoglobulin G) antibodies directed against the appropriate species of immunoglobulin G,and the anti-hormone antibodies were combined with the hormone-containing immunoadsorbent. (d) 125I-labelled anti-(immunoglobulin G) antibodies and anti-hormone antibodies were simultaneously eluted from the hormone-containing immunoadsorbent by dilute HCl, pH 2.0. After elution the anti-(immunoglobulin G) antibodies and antihormone antibodies were allowed to recombine at pH 8.0 and 4 degrees C. 2. The resultant immunoglobulin G-anti-immunoglobulin G complex was used in immunoradiometric (labelled antibody) and two-site assays of the respective polypeptide hormone. 3. By using these immunoassays, concentrations down to 90pg of human growth hormone/ml, 100 pg of bovine insulin/ml, 80 pg of bovine parathyroid hormone/ml and 150 pg of glucagon/ml were readily detected. Assays of human plasma for growth hormone and insulin by these methods showed good agreement with results obtained by using a directly 125I-labelled anti-hormone antibody in an immunoradiometric assay of human growth hormone or by radioimmunoassay of human insulin. 4. The method described allows immunoradiometric or two-site assays to be performed starting with as little as 450 ng of polypeptide hormone-antibody protein. An additional advantage of the method is that a single iodination of the readily available antibodies to immunoglobulin G allows the establishemnt of several polypeptide hormone assays
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PMID:Immunoassay of serum polypeptide hormones by using 125I-labelled anti(-immunoglobulin G) antibodies. 108 Apr 19

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


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