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)

Secretory protein-I (SP-I) of parathyroid glands and chromogranin A ( CGA ) of adrenal medullary chromaffin cells are chemically similar if not identical proteins. Both proteins are contained within secretory granules and appear to be cosecreted with granule contents, for example, in the parathyroid with PTH and in the adrenal with epinephrine and dopamine beta-hydroxylase. Antisera to bovine SP-I and porcine CGA , together with antisera to a variety of peptide hormones, were used in an immunofluorescence study of rat tissues in order to determine the probable distribution and cellular localization of these proteins. In addition to their previously demonstrated presence in parathyroid and adrenal cells, the SP-I/ CGA protein family was detected in cells of the thyroid that contained calcitonin and often SRIF but not thyroglobulin; in cells of the anterior pituitary staining for the alpha-subunit of TSH/FSH/LH but not in cells staining for GH, PRL, ACTH, or beta-endorphin; in pancreatic islet cells staining for SRIF and pancreatic polypeptide-related peptides, but not for insulin or glucagon; in the celiac and mesenteric ganglia in cells some of which contained SRIF; and in the gastric antrum in cells containing SRIF, but not gastrin. SP-I/ CGA was not detected in cells of the liver, kidney, parotid gland, or acinar pancreas or in the intermediate or posterior lobes of the pituitary. These results suggest that this protein family enjoys a widespread but highly restricted distribution in many different endocrine-peptide cells of the rat, many that are believed to be of the APUD cell series. The possibility is raised that SP-I/ CGA plays some physiological role in the secretory process or exerts an effect of its own in the periphery after secretion.
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PMID:Selective localization of the parathyroid secretory protein-I/adrenal medulla chromogranin A protein family in a wide variety of endocrine cells of the rat. 623 31

The concentration of cyclic AMP which is known as an intracellular mediator of hormone action increased in the plasma of patients with chronic renal failure (CRF). In the present study, the plasma concentration of cyclic AMP significantly correlated not only with serum, creatinine, and urea levels, but also with plasma PTH and glucagon in patients with CRF. Furthermore, plasma concentrations of PTH and glucagon correlated with the serum creatinine concentration to a significant extent. To discuss the cause of the increased cyclic AMP concentration in plasma of patients with CRF, multivariate analyses were carried out on the obtained clinical data from patients and normal subjects. In the factor analysis on the clinical data from 61 subjects, cyclic AMP, creatinine and BUN correlated with the first factor and PTH correlated with the second factor. The cumulative contribution ratio by the second factor was 76%. The results of the cluster analysis indicated that cyclic AMP, creatinine, and BUN formed a cluster and PTH glucagon made another cluster. These results suggest that the elevated plasma concentration of cyclic AMP in patients with CRF was mainly introduced not by overproduction but by the retention of cyclic AMP due to the decreased renal function.
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PMID:A multivariate factor analysis of the high plasma concentration of cyclic AMP in patients with chronic renal failure. 624 11

Although more and more is known about the nature of neuropeptides, there are two basic questions which need to be looked at in order for the neurophysiologists and the neuropharmacologists to have all the tools necessary for their studies. The first question is the site of biosynthesis of neuropeptides and the second is their biosynthetic pathway. We believe and propose that all neuropeptides will be formed from a larger molecular weight precursor similar to beta-LPH for beta-endorphin. All models of peptide hormones (pro-insulin, pro-PTH, pro-glucagon, beta-lipotropin etc.,) show the same characteristic preferential site of cleavage made of a double basic residue. This is also the type of cleavage recently described by Nakanishi et al. (1979). Using the rat pars intermedia, we showed that this tissue preferentially makes alpha-MSH and beta-endorphin from a large precursor, while beta-LPH and ACTH are short lived intermediates. All products of maturation were identified by chemical analyses leaving no doubt about their nature and identity. We strongly believe that the brain will biosynthesize beta-endorphin and possibly alpha-MSH in similar fashion. We also predict that our results will apply to the other neuropeptides which wil be formed from large precursors. These studies could be very useful in the interpretation of the intricate relationship between neuropeptides and behavioral effects.
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PMID:New perspectives in neuropeptides. Biosynthesis from large precursors. The pro-opio-melanocortin model in the pars intermedia. 626 51

Using the single tubule adenylate cyclase microassay, we investigated in vitro in three different segments of the rat nephron whether the effects of various hormones are additive when these hormones are tested in combination. In the cortical portion of the thick ascending limb (CAL), no additivity of the effects of glucagon, calcitonin, and PTH was observed. In the medullary portion of the thick ascending limb (MAL), the effects of vasopressin and glucagon were only partly additive, and the effects of vasopressin and calcitonin were fully additive. In the cortical collecting tubule (CCT), the effects of calcitonin and vasopressin were nonadditive in the kidneys in which vasopressin alone induced a high cyclase stimulation, whereas they were fully additive when vasopressin induced a low cyclase stimulation. The data suggest that in each segment, the hormones tested stimulated the same cells: no additivity was observed when cyclase Vmax acted as the limiting factor of the response; partial or full additivity was observed when the number of hormone receptors acted as the limiting factor of the response. As a consequence, calcitonin, glucagon, and PTH should induce the same effects in CAL; vasopressin, glucagon, and calcitonin, the same effects in MAL; and vasopressin and calcitonin, the same effects in CCT.
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PMID:Multiple hormonal control of adenylate cyclase in distal segments of the rat kidney. 628 98

The effects of Tramadol-N2O-anaesthesia on the per- and postoperative change in blood concentrations of cortisol, prolactin, thyroxine, triiodothyronine, cyclic AMP, glucagon, antidiuretic hormone, PTH-peptide (44-68), glucose, lactate, pyruvate and free fatty acids (FFA) were investigated in connection with elective orthopaedic surgery. Anaesthesia in man with Tramadol and nitrous oxide were found to be associated with a significant elevation of plasma cortisol and plasma prolactin in man. However, cortisol secretion during anaesthesia is associated with an inhibition in T4-T3 conversion. No significant alterations in plasma glucagon concentrations were observed. Generally, surgical trauma induced a significant increase in plasma cyclic AMP with intraoperative levels between 26.4 and 34.3 pmol/ml. At the end of surgery a significant fall in plasma PTH-peptide (44-68) occurred. There was also a significant change in plasma ADH levels following induction of anaesthesia. During surgery we found plasma ADH levels up to 56 pg/ml. In addition stress and surgical trauma increased blood glucose and FFA while plasma pyruvate and plasma lactate nearly remained unchanged. The data would suggest that the non-specific stress response attributed to anaesthesia may in fact be reflecting a response to relatively light anaesthesia.
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PMID:[Endocrine reaction pattern in the course of a one-phase tramadol-N2O combination anesthesia]. 629 29

We examined the relationship between PTH binding and stimulation of cAMP formation in a cell line derived from opossum kidney (OK). In the presence of isobutylmethylxanthine (1 mM) bovine PTH(1-34) [bPTH(1-34)] (244 nM) stimulated cAMP accumulation in confluent cultures up to 40-fold over basal; this response to PTH was stable for 35 passages. The concentration of bPTH(1-34) required to raise cell cAMP levels half-maximally was 5-12 nM. Binding of [125I]bPTH(1-34) to OK cells was saturable; Scatchard analysis of competitive binding data yielded a dissociation constant (KD) = 6 +/- 2 nM, with 1.0 pmol binding sites/mg cell protein. Under steady state binding conditions 89% of labeled PTH remained precipitable by 10% trichloroacetic acid, suggesting minimal metabolism of the hormone. The PTH antagonist (8Nle, 18Nle, 34Tyr)bPTH(3-34)amide competed for [125I]bPTH(1-34) binding sites and inhibited the action of bPTH(1-34) to raise cAMP levels. The intact PTH molecule, bPTH(1-84), and the weak agonist hPTH(1-34) synthesized by Brewer were both less potent than bPTH(1-34) (6 times and 30 times, respectively) with regard to binding and cAMP production. Calcitonin and arginine vasopressin did not bind to PTH receptors but raised cAMP levels in OK cell cultures 3- and 10-fold, respectively; neither glucagon nor ACTH(1-24) influenced PTH binding of cAMP in OK cells. Varying the extracellular calcium concentration in the medium bathing cells did not influence basal or PTH-stimulated cAMP generation. These data suggest that PTH receptors in OK cells are of high affinity, are selective for PTH, and are coupled to adenylate cyclase. This established epithelial cell line provides a model in which to study the mechanism of action of PTH in the kidney.
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PMID:Parathyroid hormone receptors coupled to cyclic adenosine monophosphate formation in an established renal cell line. 632 Nov 47

A case of a 65-year-old woman with a pancreatic tumor secreting insulin, glucagon, and associated with high PTH levels and hypercalcemia is reported. The patient underwent two Streptozotocin (STZ) treatments (1 g iv/week for 10 weeks) after liver metastases were found. Hormonal and metabolic parameters were monitorized . Before the first STZ treatment insulin levels ranged between 78 and 132 microU/ml. After STZ administration insulin decreased and then remained lower (8-48 microU/ml) until the death of the patient. Pre-treatment glucagon levels ranged between 1.3 and 3.9 ng/ml. STZ induced a decrease of glucagon to 0.5 ng/ml. Glucagon chromatography revealed the prevalence of high molecular weight (greater than 6,000 mol wt) immunoreactive glucagon (0.9 ng/ml) drastically reduced by STZ treatment (0.15 ng/ml). Hypoaminoacidemia was observed before STZ administration, but at the end of the therapy plasma amino acid concentrations were normal. Hypercalcemia too was sensitive to STZ, but not PTH value, which remained high. The second STZ treatment performed a year later was less effective and so a chemotherapeutic protocol was started. Our findings suggest a cytolitic effect of STZ on malignant A-cell, with reduction of glucagon levels and restoration of amino acid metabolism. This effect would be useful for medical treatment of non-operable glucagon secreting tumors.
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PMID:Effect of streptozotocin in a case of glucagon-secreting malignant islets-cell tumor. 632 96

An incubation of uremic human serum with normal rat adipose tissue will make the subsequently isolated adipocytes less responsive to insulin. To examine the extent of insulin resistance, we obtained sera from nondiabetic, uremic patients, who had not undergone dialysis therapy. The sera were then dialyzed (3500 molecular-weight cutoff) for 18 hr against a defined culture medium to eliminate possible in vitro effects of altered levels of end-product metabolites, electrolytes, and metabolic substrates. After an incubation of epididymal fat tissue from normal rats, for 3 hr with the dialyzed sera (50% vol/vol), cells were isolated and washed. The insulin stimulation of 14C-glucose (0.2 mM) incorporation to 14CO2 and total lipids was significantly reduced in the adipocytes pretreated with sera from 19 of the 29 uremic patients. Although elevated in the uremic patients, the sera levels of insulin, and parathyroid and growth hormones were not correlated to insulin resistant activity. Furthermore, incubation of adipose tissue for 3 hr with insulin, glucagon, or PTH did not produce resistance. The uremic sera reduced glucose utilization equally at 0.2 and 50 mM glucose, suggesting that the insulin resistance was induced additionally at a site distal to the glucose transport system. However, the concentration of insulin (22 microunits/ml) required for half-maximal stimulation of glucose metabolism was not altered by pretreatment with uremic serum. Also, neither the isoproterenol-stimulated lipolysis nor the inhibition of this cellular event was influenced by pretreatment with uremic sera.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Induction of insulin resistance in normal adipose tissue by uremic human serum. 637 54

Most of the clinical problems experienced by the IDM in the immediate neonatal period are manifestations of abnormal fetal developmental physiology that occur in response to an increased flux of glucose from mother to fetus. The principal fetal responses are hyperglycemia, hyperinsulinemia, increased metabolic rate, and hypoxemia. Those fetal responses very likely lead to a redistribution of cardiac output, increased release of norepinephrine, and blunted release of glucagon. More fat is stored in adipocytes; more glycogen is stored in the liver; the heart may develop asymmetric septal hypertrophy; and lung metabolism is altered to delay the appearance of mature surfactant. At birth, the macrosomic IDM develops hypoglycemia that has a multifactorial basis (hyperinsulinemia, hypoglucagonemia, and probably diminished gluconeogenic and cortisol production rates). The IDM may experience respiratory symptoms from one of three causes: IRDS, persistent pulmonary hypertension, or congestive heart failure. Hyperbilirubinemia may occur because of increased rate of hemolysis; hypocalcemia and hypomagnesemia are likely within the first 3 days in association with a sluggish PTH response; and abnormal levels of inhibitors of fibrinolysis and platelet prostaglandin E-like substances may stimulate abnormal thrombosis.
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PMID:Infants of diabetic mothers. Fetal and neonatal pathophysiology. 638 22

In exceptional cases, acromegaly develops as the clinical expression of an ectopic secretion of Growth Hormone (GH) or Growth Hormone-Releasing Factor (GRF), tumorous in origin. In the present report, we describe an instance of acromegaly caused by the secretion of GRF from a voluminous pancreatic tumor. The resection of this tumor resulted in a temporary disappearance of the biological and clinical symptoms of acromegaly, which then reappeared in conjunction with a rise in plasma GRF. From this pancreatic tumor, substances displaying a potent GRF activity were isolated and characterized. Amino acid analyses revealed that they were related to 3 peptides containing respectively 44, 40 and 37 aminoacids. The largest (hp GRF (1-44)-NH2) referred as hp GRF or somatocrinin is considered to be the primary molecule. The pancreatic tumor was multisecreting as proved by high plasma levels of somatostatin, pancreatic polypeptide and glucagon, normalized after the tumor removal, taken together with the immunocytochemical demonstration of the presence of these peptides in the tissue and with the isolation of somatostatin. In contrast hypercalcemia associated with an elevated plasma level of IR-PTH was unmodified by tumor removal. Diagnosis of acromegaly as ectopic endocrine syndrome will probably be facilitated by plasma GRF radioimmunoassay, as a result of production of anti synthetic GRF antibodies.
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PMID:[Acromegaly, clinical expression of the production of growth hormone releasing factor in pancreatic tumors]. 643 Feb 7


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