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)

Pancreatic A cell response to arginine was measured in hedgehogs during the periods of lethargy and arousal and then during activity. Spontaneous plasma glucagon concentrations were lower during lethargy than during activity, and they increased during arousal. Arginine administration induced a slight, but significant delayed increase in plasma glucagon concentration in the lethargic hedgehog (body temperature: 6 degrees). During arousal, in vitro glucagon secretion was temperature dependent suggesting that body rewarming might, in itself, be an important stimulating factor of the A cells. In the presence of arginine, the glucagon output of the pancreas of lethargic hedgehogs was high at low temperatures. It decreased to a nadir at 19 degrees and increased up to 37 degrees. However, the basal or arginine-stimulated glucagon secretion of animals in lethargy was higher than that of animals in activity. These characteristics suggested the presence of a particular pool of cold-adapted enzymes in the A cells of lethargic hedgehogs.
Gen Comp Endocrinol 1983 Oct
PMID:Pancreatic A cell response to arginine in the hibernating hedgehog (Erinaceus europaeus). 635 39

The frontal ganglion of the adult forms of the tobacco hornworm, Manduca sexta, was investigated immunocytochemically for the occurrence of the gastro-entero-pancreatic (GEP) neurohormonal peptides, namely insulin, nerve growth factor, epidermal growth factor, insulin C-peptide, somatostatin, glucagon, glicentin, pancreatic polypeptide (PP), polypeptide YY (PYY), secretin, vasoactive intestinal peptide (VIP), gastric inhibitory peptide (GIP), gastrin, cholecystokinin (CCK), enkephalin, alpha- and beta-endorphins, substance P, neurotensin, bombesin, motilin, ACTH, serotonin, and calcitonin. Among all the antisera tested, positive immunostaining was obtained with anti-insulin B-chain serum only. The insulin B-chain immunoreactivity was localized in 4-6 large (30-40 microns) neurons, in the neuropile, and in the recurrent nerve. It is speculated that the insulin-like immunoreactive material may be transported to the neurohaemal organ (corpora cardiaca) through the nervi cardiaco-somatogastrici.
Gen Comp Endocrinol 1984 Apr
PMID:Immunocytochemical evidence for the occurrence of insulin in the frontal ganglion of a Lepidopteran insect, the tobacco hornworm moth, Manduca sexta L. 637 93

Frog liver adenylate cyclase was characterized with respect to divalent cation interaction and hormonally stimulated activities. The enzyme catalyzed the synthesis of cyclic [32P]3',5'-AMP from alpha-32P-labeled ATP. The activity of the enzyme was linear with time and protein concentration. The Km for ATP was 0.5 mM, in the presence or absence of stimulators. The temperature optimum was 25 degrees. GTP (10(-4) M) increased the stimulation of adenylate cyclase by epinephrine. Similar activities were obtained using 5 mM Mg2+ or Mn2+. At higher concentrations, both ions inhibited epinephrine-stimulated, but not basal or fluoride-stimulated activities. Approximately equivalent hormonal stimulation was obtained with maximal stimulating concentrations of epinephrine, isoproterenol, glucagon, and prostaglandin E1. Norepinephrine was less stimulatory. Only catecholamine-stimulated activities were inhibited by propranolol (10(-5) M). The data suggest that catecholamines stimulate frog liver adenylate cyclase through interactions with beta adrenergic receptors. The adenylate cyclase in frog liver differs from its mammalian counterpart in its response to temperature and maximally stimulatory concentrations of hormones.
Gen Comp Endocrinol 1983 Apr
PMID:Catecholamine and divalent cation effects on frog liver adenylate cyclase. 660 83

Adrenaline, arginine vasopressin, arginine vasotocin, and glucagon, all at 10(-6) M, stimulate glycogen breakdown and glucose release from hepatic tissue of Neoceratodus forsteri cultured in vitro. Adrenaline acts via a beta-adrenergic receptor in this species. Gluconeogenesis from 2 mM lactate occurred at a rate of 680 +/- 39 nmol/g liver/h. This rate of gluconeogenesis was unaffected by the addition of 10(-6) M adrenaline.
Gen Comp Endocrinol 1983 Sep
PMID:The role of hormones in regulation of carbohydrate metabolism in the Australian lungfish Neoceratodus forsteri. 662 65

1. The role of endogenous glucagon and insulin on the hypolipidemic and glycogenolytic effect of clofibrate was determined in the euthyroid and propylthiouracil (PTU)-induced hypothyroid mice. 2. PTU was fed in diet (0.15%) for 2 weeks and then clofibrate added to diet (0.25%) for 4 weeks. 3. Both PTU and clofibrate significantly increased liver weight but had no effect on kidney weight. PTU significantly decreased plasma triglycerides (TG) and increased cholesterol (Ch). 4. Clofibrate had a significant hypotriglyceridemic effect in both euthyroid and hypothyroid mice but did not affect plasma cholesterol. 5. Clofibrate decreased hepatic glycogen in euthyroid but not in hypothyroid mice. 6. Glucose-6-phosphatase activity was not affected by either PTU or clofibrate. 7. Neither PTU nor clofibrate affected hepatic TG or Ch. 8. Biliary lipid changes due to PTU treatment were reversed by clofibrate administration. 9. Since plasma insulin and glucagon levels were not affected by clofibrate in either euthyroid or hypothyroid mice, our results suggest that the hypotriglyceridemic and glycogenolytic effect of clofibrate is not mediated by changes in circulating insulin and glucagon ratio. 10. Moreover, while the glycogenolytic effect of clofibrate seems to be dependent, the hypotriglyceridemic effect seems to be independent of thyroid hormones.
Gen Pharmacol 1982
PMID:Hypolipidemic and glycogenolytic effect of clofibrate (CPIB) in hypothyroid mice: role of insulin and glucagon. 703 29

Stress induces a hypermetabolic state of increased urinary nitrogen loss and increased metabolic rate. The principal reason for such a response is the mobilization of amino acids and the production of glucose to provide energy for the cells involved in the host immune response and wound repair. The endocrine hormones, eg, cortisol, the catecholamines, and glucagon, are largely responsible for these effects. Insulin and growth hormone administration can produce anabolic effects to block the loss of body protein. Administration of specific amino acids, such as glutamine, also appears to be beneficial. However, the hypermetabolic state goes beyond derangement of endocrine hormone levels. Although the cytokines are also important mediators, it is not clear how these mediators, in concert with hormonal changes, produce all of the manifestations of the hypermetabolic state seen in stress.
Curr Opin Gen Surg 1993
PMID:Regulation of protein metabolism during stress. 758 15

Histology and immunohistochemical reactivity (IR) toward insulin, glucagon, somatostatin14, and pancreatic polypeptide were investigated in the pancreas and in other tissues of Bufo bufo during metamorphosis. Insulin IR cells appeared at the very beginning of metamorphosis among exocrine pancreatic cells rich in yolk platelets, not completely arranged in acini. Less than 1 week later, glucagon, somatostatin14, and pancreatic polypeptide IR cells also appeared. At metamorphic climax, both endocrine and exocrine tissues of the pancreas underwent extensive degeneration, mainly via apoptotic cellular death. At this time the number of IR cells and the intensity of immunohistochemical reactions decreased for all the hormones tested. Pancreatic reorganization began at the end of the climax.
Gen Comp Endocrinol 1995 Feb
PMID:Morphogenesis of the pancreas of Bufo bufo during metamorphosis. 762 18

The aim of this work was to develop an in vitro model suitable for studying insulin secretion in amphibians and for identifying agents capable of either blocking or stimulating such a process in this group. For this purpose, pancreases from the toad Bufo arenarum were incubated for 60 min at 25 degrees with several insulin secretagogues and blockers, and the immunoreactive insulin released into the medium was measured by radioimmunoassay. Under these experimental conditions, metabolic (glucose, ketoisocaproic acid, and arginine) and nonmetabolic (K+ and tolbutamide) agents as well as glucagon and acetylcholine significantly stimulated the release of immunoreactive insulin. Conversely, somatostatin and nifedipine blocked its secretion. All these agents exerted similar effects on the mammalian pancreas. These results prove that our model is a useful tool with which to study in vitro insulin secretion in amphibians and to identify agents which affect hormone release in this group.
Gen Comp Endocrinol 1995 May
PMID:An in vitro model suitable for studying insulin secretion in amphibians. 763 65

In organ cultures of liver tissue from the axolotl, Ambystoma mexicanum, 1 nmol/l arginine vasotocin (AVT) increased tissue cyclic AMP (cAMP) concentration, activated glycogen phosphorylase, and caused glycogen breakdown and glucose release. Addition of 10 nmol/l insulin had no effect on any of these parameters. Addition of glucagon together with AVT caused a further increase in tissue cAMP but not in glucose release. Ten nanomoles per liter of insulin added to the cultures 5 min before 1 nmol/liter AVT inhibited all the above actions of AVT. This inhibitory action of insulin was not apparent in the presence of the cAMP phosphodiesterase inhibitor isobutylmethylxanthine (IBMX), which indicates that insulin activates cAMP phosphodiesterase and so reduces the concentration of cAMP in the tissue. This cannot occur in the presence of IBMX. These findings confirm previous reports that AVT causes hepatic glycogenolysis in the axolotl via an increase in tissue cAMP level.
Gen Comp Endocrinol 1993 Feb
PMID:Insulin counters the glycogenolytic effect of arginine vasotocin in liver pieces from the axolotl, Ambystoma mexicanum, cultured in vitro. 768 Oct 19

1. The non-steroidal anti-inflammatory naproxen inhibited steady-state glycogenolysis stimulation caused by norepinephrine, phenylephrine (alpha 1-agonists) and methotrexate (not receptor mediated) in the isolated perfused rat liver. Stimulation of glycogenolysis caused by these agents is Ca(2+)-dependent. 2. Naproxen did not inhibit glycogenolysis stimulation caused by glucagon. 3. The action of naproxen depended on the extracellular Ca2+ concentration. At 0.25 mM extracellular Ca2+, the norepinephrine stimulated glycogenolysis was inhibited by 60% by 0.5 mM naproxen. At 3.5 mM Ca2+, inhibition was reduced to 25%. The inhibition degree correlated linearly with the extracellular Ca2+ concentration. 4. 45Ca2+ efflux stimulation caused by norepinephrine was not affected by naproxen, indicating that the mobilization of the intracellular Ca2+ pools was not significantly affected by naproxen. The initial increases in glycogenolysis caused by norepinephrine in the absence of extracellular Ca2+ (pre steady-state) were not affected by naproxen. These increases depend on intracellular Ca2+ mobilization. 5. It can be concluded that the action of naproxen is most probably related to the cytosolic Ca2+ concentration which, under steady-state conditions, depends on the extracellular one during the action of Ca(2+)-dependent glycogenolytic agents.
Gen Pharmacol 1995 Jan
PMID:Naproxen inhibits hepatic glycogenolysis induced by Ca(2+)-dependent agents. 771 62


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