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)

Gluconeogenesis from lactate, pyruvate, fructose, alanine, and other substrates was accelerated by glucagon or epinephrine in hepatocytes isolated from rat liver. Glucagon and epinephrine also increased cyclic AMP accumulation by rat hepatocytes. Isoproterenol increased cyclic AMP but not gluconeogenesis, while phenylephrine accelerated gluconeogenesis. The activation of gluconeogenesis by epinephrine was unaffected by propranolol but blocked by dihydroergotamine. Dibutyryl cyclic AMP added to hepatocytes stimulated gluconeogenesis at concentrations as low as 1 muM. Exogenous cyclic GMP (0.1- muM) inhibited gluconeogenesis due to either glucagon or epinephrine without affecting basal gluconeogenesis. However, carbamylcholine did not affect gluconeogenesis by hepatocytes. Basal gluconeogenesis and the increases due to all agents were inhibited by removal of extracellular calcium or the presence of A-23187, D-600, or tetracaine. In contrast, added 0.1 muM cyclic GMP, 2 mM NH-4-Cl, and 10 muM phenethylbiguanide inhibited glucagon- or epinephrine-stimulated gluconeogenesis without affecting basal values. Studies with hepatocytes indicate that the hormonal activation of gluconeogenesis is not limited to substrates entering prior to triose phosphate formation. Glucagon may act by increasing cyclic AMP which acts via unknown mechanisms to increase gluconeogenesis. In contrast, epinephrine acts via a cyclic AMP-independent mechamism which does not appear to involve cyclic GMP, Ca-2+ flux, of K+ flux.
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PMID:Cyclic nucleotides and gluconeogenesis by rat liver cells. 16 60

1. Hydrocortisone increases in vivo incorporation of [14C] glucose into fetal liver glycogen in the last days of gestation, whereas in glucagon-treated fetuses, a slight decrease in the incorporation rate was found. 2. Hydrocortisone increases total synthetase activity as that of synthetase a but was without effect on fetal liver glycogen phosphorylase. 3. Glucagon causes a slight increase in phosphorylase a activity on days 19-21, and was without effect on the activities of synthetase a and total synthetase. 4. Dibutyryl cyclic AMP had no effect on the key enzymes of glycogen metabolism 1 h after injection in utero, whereas after 6 h an increase in phosphorylase a activity was found without any change in synthetase a activity.
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PMID:Effect of hydrocortisone and glucagon on glycogen metabolism in the fetal rat liver. 17 42

Insulin and glucagon stimulate amino acid transport in freshly prepared suspensions of isolated rat hepatocytes. The kinetic properties of alpha-amino[1-14C]isobutyric acid (AIB) transport were investigated in isolated hepatocytes following stimulation by either hormone in vitro. In nonhormonally treated cells (i.e. basal state), saturable transport occurred mainly through a low affinity (Km approximately equal to 40 mM) component. In insulin or glucagon-treated hepatocytes, saturable transport occurred through both a low affinity component (similar to that observed in the basal state) and a high affinity (Km approximately equal to 1 mM) component. At low AIB concentrations (less than 0.5 mM), insulin and glucagon at maximally stimulating doses increased AIB uptake about 2-fold and 5-fold, respectively. The high affinity component induced by either hormone exhibited the properties of the A (alanine preferring) mediation of amino acid transport. This component required 2 to 3 h for maximal expression, and its emergence was completely prevented by cycloheximide. Half-maximal stimulation was elicited by insulin at about 3 nM and by glucagon at about 1 nM. Dibutyryl cyclic AMP mimicked the glucagon effect and was not additive to it at maximal stimulation. Maximal effects of insulin and glucagon, or insulin and dibutyryl cyclic AMP, were additive. We conclude that insulin and glucagon can modulate amino acid entry in hepatocytes through the synthesis of a high affinity transport component.
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PMID:Insulin and glucagon stimulation of amino acid transport in isolated rat hepatocytes. Synthesis of a high affinity component of transport. 48 5

Glucagon stimulated the incorporation of Na2H32PO4 and L-(14C)serine into phosphatidylserine in heart muscle slices. The increase above control was about 2-fold at ten minutes and 6-fold at thirty minutes for (32P) and 12-fold as early as three minutes for (14C)serine. Although a smaller, but significant, incorporation of (32P) into phosphatidylethanolamine was also observed, glucagon did not stimulate the incorporation of (14C)serine into phosphatidylethanolamine. Glucagon did not significantly augment the incorporation of either tracer into phosphatidylcholine, lysophosphatidylcholine, phosphatidylinositol, cardiolipin, phosphatidic acid, or sphingomyelin. Dibutyryl cyclic 3',5'-AMP did not increase the incorporation of (32P) or (14C)serine into phosphatidylserine. Since phosphatidylserine appears to serve a critical role in coupling the glucagon receptor to the catalytic moiety of adenylate cyclase, the data suggest that the hormone may initially increase the amount of its own coupler.
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PMID:Glucagon-mediated stimulation of (32P) orthophosphate and (14C) serine incorporation into phosphatidylserine in cardiac muscle slices. 124 47

1. Differences in responses to lipolytic agents have been investigated in vitro in abdominal adipose tissue from lines of broiler chickens selected for body weight (GL, a 'fat' line) or for food efficiency (FC, a 'lean' line). 2. Dibutyryl cyclic adenosine monophosphate stimulated in vitro lipolysis, as measured by the glycerol release, by adipose tissue from GL or from FC chickens to the same extent. 3. Glucagon stimulated glycerol release from adipose tissue from FC chickens, but not from GL chickens. 4. Adipose tissue from GL chickens was much more sensitive to chicken growth hormone (GH) compared to FC chickens. 5. It is concluded that the selection criteria applied influenced the number of adipose GH and glucagon receptors, the number of adipose GH receptors being lower and of glucagon receptors being higher in FC chickens compared to GL chickens.
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PMID:Abdominal adipose tissue from broiler chickens selected for body weight or for food efficiency differ in in vitro lipolytic sensitivity to glucagon and to chicken growth hormone, but not to dibutyryl cAMP. 133 3

The rates of de novo purine and protein synthesis were assessed in vivo in rat liver after bolus administration of glucagon. The specific activity of hepatic purines and the specific activity ratio of hepatic purine/protein were used as an index of the rate of de novo purine synthesis and the rate relative to protein. Glucagon at doses of 0.01 mg to 0.1 mg/200 g body weight (BW), administered as an intravenous bolus, inhibited dose-dependently the rate of de novo purine synthesis and the rate relative to protein although it increased dose-dependently the hepatic concentration of 5-phosphoribosyl 1-pyrophosphate (PRPP). The inhibition of the rate of de novo purine synthesis recovered to control levels during the period between 60 and 90 minutes after glucagon administration. Dibutyryl cyclic AMP (Bt2 cAMP) partially mimicked this effect of glucagon in that it did not increase the rate of de novo purine synthesis in spite of increased concentrations of PRPP. These results suggest that an intravenous bolus of glucagon inhibits the rate of de novo purine synthesis through increasing cAMP concentration. The data are consistent with inhibition of amidophosphoribosyltransferase (ATase) in spite of increased PRPP concentrations.
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PMID:In vivo inhibition of the rate of de novo purine synthesis in rat liver by glucagon. 242 58

Ginsenosides Rb2, Rc and Rg1 suppressed corticotropin-induced, dibutyryl cyclic AMP-induced and epinephrine-induced lipolysis with the relative potencies Rb2 greater than Rc greater than Rg1. The inhibition of corticotropin-induced lipolysis by ginsenoside Rg1 could not be overcome by increasing the dose of the lipolytic hormone while that of ginsenosides Rc and Rb2 was nearly abolished by corticotropin at a dose of 40 nM which by itself produced maximal lipolysis. Dibutyryl cyclic AMP-stimulated lipolysis was also inhibited. Only ginsenoside Rb2 suppressed glucagon-induced lipolysis. All three ginsenosides did not inhibit basal lipolysis or basal incorporation of D-[3-3H]glucose into lipids. Insulin-stimulated lipogenesis was diminished by ginsenosides Rg1 and Rc but not by ginsenoside Rb2.
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PMID:Effect of ginsenosides Rg1, Rc and Rb2 on hormone-induced lipolysis and lipogenesis in rat epididymal fat cells. 301 81

Protein degradation in Reuber H35 hepatoma monolayers was measured as release of radioactive trichloroacetic acid-soluble material from intracellular protein labelled with [3H]leucine for 16 hr followed by 3-hr chase period. Proteolysis in this system was stimulated by physiological concentration of glucagon reaching a maximum at 10(-7) M with an increase of 30%. Dibutyryl cyclic AMP also had a stimulatory effect. When both glucagon and dibutyryl cyclic AMP were present at optimal concentrations, their effects were not additive suggesting that glucagon may act via the formation of cyclic AMP. In the presence of protein synthesis inhibitor, cycloheximide or puromycin, proteolysis remained responsive to glucagon. Glucagon counteracted the inhibitory effect of insulin on proteolysis.
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PMID:Stimulation by glucagon and adenosine-3',5'-cyclic monophosphate of protein degradation in Reuber H35 hepatoma monolayers. 303 17

Freshly isolated hearts of fetal mice of gestational ages ranging between 12 and 22 days (term) were exposed to several concentrations of a variety of chronotropic agents. Acetylcholine (10(-4)-10(-2) M) caused marked bradycardia in all hearts, even after only 12-14 days' gestation (i.e., even before cardiac innervation had occurred), and the intensity of the response increased steadily with advancing age throughout gestation. Responsiveness to norepinephrine was present but minimal at 12-14 days, so that mean atrial rate rose by < 10% with a maximal concentration of the drug (10(-5) M); responsiveness became more marked by 15-16 days (just after the time atrial innervation is thought to begin) and still greater effects appeared just before term. Glucagon had no effect in hearts of < 17 days' gestational age, but caused tachycardia thereafter, indicating that cardiac responsiveness to glucagon differentiates later than does responsiveness to norepinephrine. Responses to theophyl-line in 12-14 day hearts exceeded those to norepinephrine, indicating that the drug can affect heart rate independently of its ability to cause release of endogenous catecholamines. In contrast, tyramine caused no response until 21-22 days, well after the time the beta-receptor has differentiated and after innervation is fairly well developed, suggesting that the drug's primary sympathomimetic effect is indirect rather than direct. Dibutyryl cyclic AMP did not cause tachycardia at any fetal age. It is concluded that maturation of responsiveness of the mouse heart to cardioactive drugs develops in specific patterns for different agents. The identification of differential patterns of maturation for various drugs may provide valuable means for characterizing the differentiation of specific receptors and for investigating possible mechanisms of action of the drugs.
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PMID:Maturation of responsiveness to cardioactive drugs. Differential effects of acetylcholine, norepinephrine, theophylline, tyramine, glucagon, and dibutyryl cyclic AMP on atrial rate in hearts of fetal mice. 435 75

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


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