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)

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

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

Short-term desensitization to hormone-induced cAMP accumulation was investigated in the medullary (MTAL) and the cortical (CTAL) thick ascending limbs of Henle's loop isolated by microdissection from the rat kidney. The following agonists were studied: vasopressin, glucagon and human calcitonin in the MTAL, and vasopressin, glucagon, human calcitonin, parathyroid hormone (PTH) and the beta-adrenergic agonist isoproterenol in the CTAL. Isolated tubules were preincubated in vitro for 60 min in the presence or absence of a maximal concentration of one of the five agonists (vasopressin 10 nM, glucagon 10 nM, calcitonin 100 nM, PTH 10 nM, isoproterenol 1 microM). Desensitization induced by each agent to its own action was then quantified by measuring the amount of cAMP accumulating in the presence of the phosphodiesterase inhibitor isobutylmethylxanthine and the same agonist concentration as that used during preincubation. In the MTAL, as previously reported, preincubation with vasopressin led to a marked (80%-85%) desensitization to this hormone. A significant hormone self-induced desensitization of about 45% was also obtained with glucagon, but not with calcitonin. In the CTAL, the following order of potency to elicit desensitization was observed: vasopressin (80%) greater than isoproterenol (50%) greater than glucagon (30%) greater than PTH (20%, NS) greater than calcitonin (10%, NS). Thus, the magnitude of desensitization varied greatly from one hormone to another, but for a given hormone, was of roughly similar extent in both MTAL and CTAL.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential short-term desensitization to vasopressin, isoproterenol, glucagon, parathyroid hormone and calcitonin in the thick ascending limb of rat kidney. 131 67

We show that osteoclasts bind parathyroid hormone (PTH) in a manner that displays the properties of receptor-dependent hormone binding, that is, saturability, time dependence, temperature dependence, and hormone specificity. Osteoclasts were isolated from the endosteum of 2 to 3 week chick tibiae and maintained in culture for 4-6 days. Bovine PTH-(1-84) was biotinylated with N-hydroxysuccinimidobiotin. Biotinyl-PTH (btPTH, 10(-5)-10(-11) M) was added to the cultured osteoclasts for 2-20 minutes. After rinsing away unbound btPTH, fluorescein isothiocyanate-labeled avidin (FITC-avidin) at a concentration of 66 micrograms/ml was applied. Receptor binding characteristics were assessed: (1) saturation occurred at around 10(-6) M btPTH; (2) competition of excess unlabeled PTH was found, namely, a 10-fold excess abolished fluorescence; (3) specificity was shown by adding other polypeptide hormones (insulin, glucagon, and calcitonin) in 10- to 100-fold excess--no effect on PTH binding was observed; and (4) affinity of btPTH for its binding site was indicated by half-maximal binding approximately equal to 10(-7) M for both osteoclasts and osteoblasts. Biotin (10(-5) M) or FITC-avidin (66 micrograms/ml) alone did not cause fluorescence. The time course of btPTH on the cell exterior was short: at 2 and 5 minutes dots of fluorescence were randomly dispersed over the cell surface, by 10 minutes most of the fluorescence was clustered in one region of the membrane, and by 20 minutes most of the hormone was no longer present on the surface of the cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Specific binding of parathyroid hormone to living osteoclasts. 131 66

Glucagon-like peptide 1 (GLP-1) is a hormone derived from the preproglucagon molecule and is secreted by intestinal L cells. It is the most potent stimulator of glucose-induced insulin secretion and also suppresses in vivo acid secretion by gastric glands. A cDNA for the GLP-1 receptor was isolated by transient expression of a rat pancreatic islet cDNA library into COS cells; this was followed by binding of radiolabeled GLP-1 and screening by photographic emulsion autoradiography. The receptor transfected into COS cells binds GLP-1 with high affinity and is coupled to activation of adenylate cyclase. The receptor binds specifically GLP-1 and does not bind peptides of related structure and similar function, such as glucagon, gastric inhibitory peptide, vasoactive intestinal peptide, or secretin. The receptor is 463 amino acids long and contains seven transmembrane domains. Sequence homology is found only with the receptors for secretin, calcitonin, and parathyroid hormone, which form a newly characterized family of G-coupled receptors.
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PMID:Expression cloning of the pancreatic beta cell receptor for the gluco-incretin hormone glucagon-like peptide 1. 132 60

Identification of hormone target sites in the nephron has been achieved in part using autoradiography, and largely with microdissection and microanalysis techniques that permit quantitative measurements of hormone binding or postbinding effects in discrete nephron segments. The nephron target sites of hormones whose intracellular second messenger is known have been located by measuring their stimulatory effect on cyclic AMP or GMP production along the nephron. These hormones include arginine vasopressin, parathyroid hormone, calcitonin, and beta-adrenergic catecholamines. In contrast, the action sites of hormones whose cellular mediators are less well understood have been identified using micro modifications of conventional binding techniques scaled down to the minute (less than or equal to 1 microgram protein) amount of tissue available. In this group are aldosterone, corticosterone, insulin, angiotensin II, alpha-adrenergic catecholamines and dopamine. Atrial natriuretic peptides and glucagon have been studied with both methods. The precise localization of hormone receptors and sites of action in the functionally heterogeneous nephron is critical for understanding the interactions between the kidney and the endocrine system in fluid volume homeostasis, blood pressure control, and in biochemical and metabolic regulation.
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PMID:Hormone receptors and sites of action in the kidney. 132 67

A number of regulatory peptides were investigated for their ability to elevate plasma cAMP. Pituitary adenylate cyclase activating peptide (PACAP)-27, PACAP-38, helodermin, helospectin I and II, vasoactive intestinal peptide (VIP), glucagon, parathyroid hormone (PTH), calcitonin and calcitonin gene-related peptide were among the peptides that were highly effective in raising plasma cAMP when given intravenously in equimolar doses to conscious mice. PACAP-27 and -38 were more effective than any of the other peptides. PACAP 16-38, secretin, gastrin-17, galanin, somatostatin, cholecystokinin-8s, pancreatic polypeptide, substance P, peptide YY and neuropeptide Y were inactive and also did not interfere with the PACAP-27-evoked rise in plasma cAMP levels. Repeated injections of PACAP-27 every 30 min caused a progressive reduction in the plasma cAMP response (measured 5 min after each injection). Forskolin, an activator of adenylate cyclase, dose-dependently raised the plasma concentration of cAMP and displayed a synergistic effect when given in a low dose concurrently with PTH or PACAP-38. The phosphodiesterase inhibitor rolipram dose-dependently raised the plasma concentration of cAMP. Combined treatment with PACAP-27 and a threshold dose of rolipram resulted in an exaggerated plasma cAMP response. Kidney hilus ligation suppressed the responses to PACAP-38, PTH, helodermin, helospectin, VIP, glucagon and calcitonin. Hepatectomy suppressed the response to glucagon but was without effect on the response to the other peptides. Pancreatectomy and spleenectomy reduced the response to VIP, but was without effect on the response to the other peptides. PACAP-27 stimulated cAMP efflux from the isolated rat tail vein. Hence, it cannot be excluded that blood vessels contribute to the peptide evoked plasma cAMP response in vivo.
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PMID:Neuropeptides of the vasoactive intestinal peptide/helodermin/pituitary adenylate cyclase activating peptide family elevate plasma cAMP in mice: comparison with a range of other regulatory peptides. 133 41

The inner medullary collecting duct (IMCD) of the rat consists of two structurally and functionally distinct segments, i.e., the initial and the terminal IMCD. To identify factors that may regulate the transport function in the IMCD segments, we assessed whether catecholamines, carbachol, prostaglandin E2 (PGE2), bradykinin, glucagon, calcitonin, parathyroid hormone, or epidermal growth factor affects adenosine 3',5'-cyclic monophosphate (cAMP) production in microdissected tubules in the presence and absence of arginine vasopressin (AVP, 0.1 nM). All experiments were performed in the presence of 3-isobutyl-1-methylxanthine, and cAMP was measured by radioimmunoassay. Epinephrine (greater than or equal to 50 nM) and clonidine (greater than or equal to 1 microM) markedly decreased AVP-induced cAMP levels in both IMCD segments. However, phenylephrine did not show an effect. The inhibitory effect of epinephrine was blocked by yohimbine (50 nM) but not by prazosin (50 nM). In isolated perfused terminal IMCDs, epinephrine inhibited AVP-stimulated urea permeability. Isoproterenol (1 microM), in the absence of AVP, caused a significant increase in cAMP level only in the initial IMCD. Propranolol (1 microM) inhibited this isoproterenol effect, but atenolol did not. Dopamine (less than or equal to 1 microM) had no effect on cAMP levels in either IMCD segment. Carbachol, PGE2, and the various peptide hormones had no effect on cAMP levels (+/- AVP) in either IMCD segment. We conclude that an adrenergic beta 2-receptor is present only in the initial IMCD, where its occupation increases cAMP production. We conclude also that an adrenergic alpha 2-receptor is present in both IMCD segments, where its occupation inhibits AVP-induced cAMP production.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hormone and autacoid regulation of cAMP production in rat IMCD subsegments. 135 41

We measured changes in serum insulin-like growth factor-1 (IGF-1), calcitriol, parathyroid hormone (PTH), thyroid hormones, insulin, and plasma glucagon in response to seven days of treatment with a pharmacological dosage of recombinant human growth hormone (r-hGH) (0.1 IU/kg sc twice daily) or placebo in 20 normal male volunteers to evaluate whether the effect of r-hGH on biochemical bone markers could be attributed to changes in these hormones. Serum IGF-1 (p < 0.001) and vitamin D-binding protein (p < 0.001) increased steadily during treatment returning to baseline at day 14. Total calcitriol (p < 0.01) and free calcitriol index (p < 0.001) increased transiently at day 4. Furthermore, serum insulin (p < 0.001) and both total (p < 0.001) and free triiodothyronine (p < 0.02) increased during treatment, while serum PTH and plasma glucagon remained unchanged. In conclusion, pharmacological doses of r-hGH increased not only IGF-1 but also free-calcitriol index, insulin, and free T3. The increase in these hormones may be co-responsible for some of the observed effects of r-hGH on bone turnover and calcium homeostasis.
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PMID:Effects of short-term growth hormone treatment on PTH, calcitriol, thyroid hormones, insulin and glucagon. 144 44

Basal adenosine 3',5'-cyclic monophosphate (cAMP) content and the modulation of its production were studied in the frog's semicircular canal epithelium. This epithelium secretes endolymph, a K(+)-rich, positively polarized fluid. The basal cAMP content measured by microradioimmunoassay was 244 +/- 14.2 fmol/structure per 5 min (n = 30). This content was increased about 8 times by 10(-5) M forskolin. Vasotocin, the frog antidiuretic hormone, increased the cAMP production by factors of 1.3 and 3.3 at concentrations of 10(-8) M and 10(-7) M, respectively. This stimulatory effect of vasotocin was blunted by the addition of alpha 2-adrenergic agonists, such as 10(-8) M-10(-5) M norepinephrine, in the presence of 10(-5) M propranolol, or 10(-5) M clonidine. Prostaglandin E2 at a concentration of 10(-8) M, which did not affect the cAMP production, did not modify the response to vasotocin. Glucagon (10(-6) M), calcitonin (10(-6) M), and parathyroid hormone (10 units/ml) did not affect the cAMP content. Prostaglandin E2 (10(-7) M) and the beta-adrenergic agonist isoproterenol (10(-6) M) stimulated the cAMP production by a factor of 1.6. These results indicate that the frog semicircular canal is a target of both vasotocin and catecholamines and that catecholamines through alpha 2-receptors modulate vasotocin-induced cAMP generation. Further, this interaction might be of physiological relevance in the modulation of ion transport in this structure.
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PMID:Antidiuretic hormone stimulation of adenylate cyclase in semicircular canal epithelium. 167 38


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