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)

Basal adenyl cyclase activity and its response to epinephrine and glucagon were studied in isolated adipocyte ghosts obtained from fed, starved, refed, and fat-diet-adapted rats. Epinephrine stimulation of adenyl cyclase was significantly increased in fasted rats, but the glucagon response did not change. Rats fasted for 48 hr and refed a high carbohydrate, low fat diet for 48 or 96 hr showed no differences from chow-fed animals in either basal or hormone-stimulated adenyl cyclase activity. Rats adapted to a high fat, low carbohydrate diet showed an initial and transitory increase in basal activity but a progressive loss of epinephrine- and glucagon-stimulated enzyme activities. The loss in hormone responsiveness correlated well with a decrease in hormone-stimulated lipolysis of fat pads and was associated with a significant increase in fat cell diameter.
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PMID:Effects of starvation, refeeding, and fat feeding on adipocyte ghost adenyl cyclase activity. 433 99

The present studies were undertaken to determine the role, if any, of cyclic 3',5'-adenosine monophosphate (cyclic AMP) as a chemical inducer of rat liver alkaline phosphatase. Cholera enterotoxin, given intravenously to rats, led to a rapid rise in the activity of hepatic adenyl cyclase that was 7(1/2) times greater than control values in 6 h. Cyclic AMP levels were also significantly increased above control values while the activity of cyclic nucleotide phosphodiesterase was unchanged. Hepatic alkaline phosphatase activity was increased 5(1/2) times above control in 12 h, but its rise followed that of adenyl cyclase and cyclic AMP by several hours. Cycloheximide inhibited the rise of hepatic alkaline phosphatase but not that of adenyl cyclase. The administration of glucagon, a known stimulator of hepatic adenyl cyclase, and of dibutyryl cyclic AMP, led to similar striking increases in hepatic alkaline phosphatase activity. This alkaline phosphatase increase was blocked by the prior administration of cycloheximide. Bile duct ligation, a known stimulator of hepatic alkaline phosphatase activity, failed to produce any significant changes in adenyl cyclase or cyclic AMP. Concomitant treatment of rats with bile duct ligation and cholera enterotoxin or bile duct ligation and glucagon, had no additive effect on the increase in hepatic alkaline phosphatase activity, although the increase occurred earlier. These results suggest that: (a) cyclic AMP may act as an inducer of hepatic alkaline phosphatase: (b) the stimulation of hepatic alkaline phosphatase by cholera enterotoxin is mediated by cyclic AMP; (c) the rise in hepatic alkaline phosphatase following bile duct ligation is not mediated by cyclic AMP; (d) the same alkaline phosphatase in rat liver may be induced by two (or more) mechanisms, only one of which requires cyclic AMP.
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PMID:Alkaline phosphatase. Possible induction by cyclic AMP after cholera enterotoxin administration. 435 3

1. Intracellular recordings of membrane potential were made from superficial cells of isolated mouse liver segments superfused with physiological salt solutions.2. The mean resting cell membrane potential was -39.4 mV.3. Glucagon caused a dose-dependent membrane hyperpolarization which was detectable at 10(-9)M and maximal (7 mV) at 10(-7)M. The hyperpolarization started within half a minute after exposure to glucagon. Secretion (2 x 10(-7)M) had no effect on the membrane potential.4. Adrenaline (10(-6)M) and isoprenaline (10(-6)M) also caused membrane hyperpolarization (4-6 mV). The effect of isoprenaline, but not that of adrenaline, was blocked by propranolol (5 x 10(-6)M).5. Dibutyryl adenosine 3',5'-monophosphate (10(-3)M) caused a membrane hyperpolarization of 4-8 mV.6. In the absence of extracellular K or the presence of Strophanthin-G (10(-3)M) the resting potential was decreased and the response to glucagon reduced. During exposure to a solution containing 20 mM-K the resting potential was slightly enhanced and the amplitude of the glucagon-induced hyperpolarization reduced compared with control conditions.7. It is concluded that the effect of glucagon on the membrane potential is due to an interaction with specific membrane receptors probably leading to activation of the membrane-bound adenyl cyclase. It is probable that the hyperpolarization is mediated by cyclic AMP. The hyperpolarization induced by glucagon is dependent on a normal function of the membrane Na-K pump.
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PMID:The effect of glucagon on the liver cell membrane potential. 436 92

We have shown that two unrelated prostaglandin antagonists block both thyrotropin (TSH) and prostaglandins E (PGE(1), PGE(2)) stimulation of thyroidal adenyl cyclase activation and cyclic 3',5'-adenosine monophosphate (cAMP) formation, suggesting that prostaglandins play an important role in regulating thyroid function. To further explore this postulate, we measured prostaglandin content by radioimmunoassay in homogeneous bovine thyroid cell preparations in the presence and absence of TSH. Antibodies to albumin-conjugated PGE(1) and PGF(2alpha) showed specificity for prostaglandins E and F, respectively, but reacted, albeit far less effectively, with heterologous prostaglandins. A double antibody system was used to separate free from antibody-bound PGE(1)-(3)H and PGF(2alpha)-(3)H. Thyroid cells were extracted with ethanol/ethyl acetate and the various prostaglandins separated on silicic acid columns. Recoveries of added PGE(1)-(3)H and PGF(2alpha)-(3)H through the extraction and separation procedures ranged from 50-80%. The sensitivity of the method was 10-50 pg. Basal thyroid cell content of PGE(1) and PGF(2alpha) "equivalents" varied between cell preparations (range = 2-6 ng/0.2 ml cell suspension) but, in each instance, remained constant during 5-30-min incubations at 37 degrees C. TSH, 10-100 mU/ml, increased the levels of cell PGE(1) and PGF(2alpha) "equivalents" 30-80% above basal during 5-15-min incubations. The stimulatory effect was specific for TSH, no increase in PGE(1) or PGF(2alpha) "equivalent" levels being seen with luteinizing hormone (LH), human growth hormone (HGH), adrenocorticotropic hormone (ACTH), or glucagon. These data support the thesis that prostaglandins may mediate TSH effects on thyroid.
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PMID:Thyrotropin increases prostaglandin levels in isolated thyroid cells. 462 70

An electron microscopic procedure has been developed, using rat liver, for the localization of hormone-sensitive adenyl cyclase. Isoproterenol-sensitive adenyl cyclase is located almost exclusively in the parenchymal cells. In contrast, glucagon-sensitive adenyl cyclase is located primarily in the reticulo-endothelial cells but is also present in parenchymal cells. Sodium fluoride-sensitive adenyl cyclase is found in both cell types.
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PMID:Hormone-sensitive adenyl cyclase: cytochemical localization in rat liver. 543 97

Although glucagon exerts positive inotropic effects in patients with no or mild impairment of cardiac function, similar effects are not consistently observed in patients with chronic heart failure. Accordingly, the inotropic effects of glucagon on papillary muscles from normal cats and cats in which right ventricular failure had been produced for 4-145 days by pulmonary artery banding were compared. At the peak of the concentration-response curve, glucagon increased peak isometric tension (T) in normal muscles from 4.4+/-0.4 to 6.6+/-0.5 g/mm(2) (P <0.001), and maximum rate of tension development (dT/dt) from 16.9+/-0.9 to 25.1+/-1.6 g/sec per mm(2) (P < 0.001). In contrast, glucagon produced no significant increases in T or dT/dt in failure muscles. The percentage increases in T and dT/dt caused by norepinephrine were the same in muscles from normal and failing hearts. Since the cardiac effects of glucagon and norepinephrine may be mediated by adenyl cyclase, responsiveness of adenyl cyclase was determined in particulate fractions of the right ventricle. Glucagon activated adenyl cyclase in normal, but had no effect in failure preparations. Norepinephrine-induced activation of adenyl cyclase, however, was unaltered by failure. Thus, in contrast to norepinephrine, glucagon loses the capacity to augment myocardial contractility and activate adenyl cyclase in hearts derived from cats in chronic failure.
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PMID:Effects of experimental heart failure on the capacity of glucagon to augment myocardial contractility and activate adenyl cyclase. 544 51

Vasoactive intestinal peptide (VIP) has been shown to be steroidogenic in monolayer cultures of a murine adrenal tumor but must be present at concentrations about 100-fold greater than ACTH to elicit the same degree of stimulation. Both peptides enhanced cAMP synthesis, although there was again a difference of 2 orders of magnitude in the dose-response curves. In contrast, VIP stimulated adenyl cyclase activity of tumor membranes in the same concentration range as ACTH. Maximum activity with VIP was less than that with ACTH in the absence or presence of a saturating amount of guanylyl imido-diphosphate. Saturating amounts of both peptides stimulated activity to levels greater than that with either ACTH or VIP alone, but the activity was not fully additive. An o-nitrophenyl sulfenyl derivative of ACTH inhibited ACTH-stimulated adenyl cyclase activity but not VIP-stimulated activity. Low concentrations of calcium potentiated the ability of submaximal doses of ACTH to stimulate adenyl cyclase but had no effect on the response to VIP. Concentrations of secretin or glucagon comparable to that of VIP did not stimulate steroidogenesis in intact cells. These data suggest that VIP may bind to a unique receptor which may be distinct from that of ACTH.
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PMID:Vasoactive intestinal peptide- and adrenocorticotropin-stimulated adenyl cyclase in cultured adrenal tumor cells: evidence for a specific vasoactive intestinal peptide receptor. 624 49

Alanine-2-oxoglutarate aminotransferase activity in mouse liver is stimulated by the intravenous injection of glucagon. The stimulation is abolished by pretreatment with actinomycin D indicating that the increased activity is probably due to new enzyme formation. Administration of dibutyryl cyclic AMP, isoproterenol, an activator of adenyl cyclase and theophylline, an inhibitor of phosphodiesterase also increases the enzyme activity suggesting the involvement of cyclic AMP in glucagon-mediated increase of enzyme activity.
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PMID:Effect of glucagon on alanine 2-oxoglutarate aminotransferase. 631 82

Previous studies have shown that sympathetic factors and blood glucose are of importance in the development of seizures and lung damage from OHP. In the present study we examined the influence of beta sympathetic agonists and blocking agents and glucagon on OHP toxicity. Rats were exposed to 6 ATA OHP and examined for time-to-seizure and lung damage. Pretreatment with propranolol increased the time-to-seizure by 70% and practolol by 50% without altering gross lung appearance or lung wet wt/dry wt. Propranolol and practolol also prevented brain glycogen depletion prior to seizure which otherwise occurred in subconvulsive exposure to OHP. Isoproterenol and glucagon pretreatment had no effect on time-to-seizure but isoproterenol did increase lung injury. Both practolol and propranolol block the beta-receptor influence on adenyl cyclase-stimulated second messenger production, while both isoproterenol and glucagon activate adenyl cyclase to produce second messenger. Our results may suggest a possible role for second messenger in mediating some of the acute toxic effects of OHP on the CNS.
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PMID:Beta adrenergic receptors and glucagon in seizures from exposure to oxygen at high pressure (OHP). 631 53

The effects of 10(-10) to 10(-7) M glucagon on cAMP, phosphorylase a, cell calcium, and glucose production, and glucagon interactions with epinephrine were studied in isolated hepatocytes from adult male and female rats. At physiological concentrations (10(-10) - 10(-9) M), glucagon activated phosphorylase by increasing cAMP and not by raising the cytosolic free calcium. At supra-physiologic concentrations (and in the male only), glucagon slightly increased the cytosolic free calcium, the fractional efflux of calcium, and, after 2 h, decreased the cell calcium content. Exposure of hepatocytes to the simultaneous administration of 10(-9) M glucagon and 10(-7) M epinephrine resulted in a prolongation of the activation of phosphorylase a and a greater release of glucose from glycogen stores than exposure to either agonist alone. In the male, the effects of low concentrations of the two hormones on phosphorylase a activity were additive. Cytosolic free calcium was increased by 10(-6) M epinephrine from 280 to 500 nM while physiological concentrations of glucagon did not change it. In these intact cells, there was no evidence of an alpha 2-adrenergic inhibition of adenyl cyclase and no indication that cAMP depresses the rise in cell calcium induced by alpha-adrenergic stimuli.
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PMID:Regulation of hepatic glycogenolysis by glucagon in male and female rats. Role of cAMP and Ca2+ and interactions between epinephrine and glucagon. 632 32


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