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)

Successive epinephrine infusions were used as a partial model to examine hormonal and metabolic responses to repeated stress stimuli. As both the endogenous opiates and epinephrine are released in response to stress, we have also studied interactions between epinephrine and B-endorphin. Epinephrine (0.1 microgram/kg . min) was infused for 60 min, followed by a 60-min recovery, in nine normal, conscious dogs. In a similar study, B-endorphin (0.06 microgram/kg . min) was given 30 min before epinephrine, then continuously infused throughout the study (N = 4 dogs). When epinephrine was infused, levels rose to 600-800 pg/ml. The changes in glucagon, B-endorphin, FFA, and hepatic glucose production were similar during both epinephrine infusions, but there was a diminished insulin response, a greater decrease in glucose metabolic clearance, and a greater increase in plasma glucose with the second epinephrine infusion. When B-endorphin was given, plasma levels increased to 5.3 ng/ml. Compared with the infusion of epinephrine alone, there was a much greater rise in plasma glucose due to greater suppression of glucose metabolic clearance. With the second epinephrine infusion, however, the changes in glucose concentration were not substantially different from those seen during the second infusion of epinephrine alone, as both hepatic glucose production and glucose metabolic clearance were suppressed. B-endorphin diminished the insulin and glucagon responses during the first epinephrine infusion and abolished them during the second, but did not alter the FFA, ACTH, or cortisol responses to epinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beta-endorphin modulation of the glucoregulatory effects of repeated epinephrine infusion in normal dogs. 299 13

3T3-L1 adipocytes were used to test the hypothesis that hormone-sensitive lipolysis and lipoprotein lipase activity might be regulated in a reciprocal manner. Intracellular lipolysis was stimulated by catecholamine, dibutyryl cAMP, and ACTH, but not by glucagon. The effects of epinephrine on lipolysis were blocked by the beta-antagonist propanolol but not by the alpha-antagonist phentolamine. Hormone-stimulated lipolysis was not changed by acute (45 min) or chronic (2 days) treatment of the cells with insulin whereas the latter treatment augmented lipoprotein lipase activity about fivefold. Epinephrine did not affect the lipoprotein lipase activity of insulin-stimulated cells. Withdrawal of glucose from the medium decreased lipoprotein lipase activity and the effect of epinephrine on lipolysis. Effects of lipolytic agents on activity of lipoprotein lipase were variable and concentration-dependent. Lipoprotein lipase activity was decreased only by concentrations of epinephrine greater than those inducing maximal intracellular lipolysis, and the decrease in activity occurred about 30 min after the increase in glycerol release. There seems to be no relationship between the level of activity of lipoprotein lipase and the maximal rate of hormone-stimulated lipolysis in 3T3-L1 cells. Unlike in adipose tissue and adipocytes of rats, hormone-stimulated lipolysis and lipoprotein lipase activity in murine 3T3-L1 adipocytes appear to be regulated independently.
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PMID:Effect of epinephrine and other lipolytic agents on intracellular lipolysis and lipoprotein lipase activity in 3T3-L1 adipocytes. 301 31

To characterize beta-receptors which affect pancreatic A-cell activity, the effects of propranolol (beta non-selective blockade) and metoprolol (beta 1 selective blockade) were evaluated on epinephrine modulated insulin (IRI) and glucagon (IRG) release both in basal state and during metabolic stimulus (arginine 20 mM). The isolated perfused rat pancreas model with the exclusion of stomach and duodenum was used. Epinephrine infusion (at 10(-7) M) caused a prompt and sustained increase in basal IRG secretion and significantly potentiated glucagon release in response to metabolic stimulus. Insulin secretion was markedly suppressed by epinephrine both in basal conditions and during metabolic stimulus. Propranolol (at 10(-7) M) and metoprolol (at 10(-7) M) infusion clearly and similarly counteracted epinephrine stimulatory effects on IRG secretion but failed to elicit any significant effect on the epinephrine inhibited IRI release either in basal state or during the metabolic stimulus. These results suggest that, at least in the rat, the adrenergic stimulation of IRG release is mediated through a beta 1 receptor.
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PMID:Effects of beta non-selective and beta 1 selective adrenergic blocking agents on glucagon secretion from isolated perfused rat pancreas. 302 Jan 14

The aim of the present work is to investigate a possible interaction on glucagon secretion between adenosine, a compound released by tissues in energy-deficient states, and epinephrine, the hormone of stress largely implicated in such conditions. The study was performed using the isolated perfused rat pancreas in presence of a physiological glucose concentration (5 mM). Epinephrine administered at a low concentration (0.01 microM) was ineffective on glucagon secretion, and adenosine at 1.65 microM was previously shown to be moderately stimulating. This nucleoside alone induced a transient increase of glucagon secretion rate that peaked at 300% of basal value at 2 min; in presence of epinephrine (ineffective per se) the rise induced by the nucleoside alone was doubled. This potentiating effect was not observed with the neurotransmitter norepinephrine at the dose tested. Propranolol (1 microM) did not alter the potentiating effect of epinephrine but this effect was completely suppressed by the alpha-blocker, phenoxybenzamine (6 microM). In conclusion epinephrine potentiates an adenosine-stimulating effect on glucagon secretion; this effect seems more specific for the adrenal medulla hormone epinephrine, since norepinephrine at the same dose is ineffective; it is mediated via alpha-adrenergic receptors. It is attractive to speculate that epinephrine and adenosine act in potentiating synergism on glucagon secretion; this might be of physiological importance during stressful energy-deficient situations.
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PMID:Epinephrine potentiates adenosine-stimulating effect on glucagon secretion. 303 Jan 34

Acute hormonal regulation of liver carbohydrate metabolism mainly involves changes in the cytosolic levels of cAMP and Ca2+. Epinephrine, acting through beta 2-adrenergic receptors, and glucagon activate adenylate cyclase in the liver plasma membrane through a mechanism involving a guanine nucleotide-binding protein that is stimulatory to the enzyme. The resulting accumulation of cAMP leads to activation of cAMP-dependent protein kinase, which, in turn, phosphorylates many intracellular enzymes involved in the regulation of glycogen metabolism, gluconeogenesis, and glycolysis. These are (1) phosphorylase b kinase, which is activated and, in turn, phosphorylates and activates phosphorylase, the rate-limiting enzyme for glycogen breakdown; (2) glycogen synthase, which is inactivated and is rate-controlling for glycogen synthesis; (3) pyruvate kinase, which is inactivated and is an important regulatory enzyme for glycolysis; and (4) the 6-phosphofructo-2-kinase/fructose 2,6-bisphosphatase bifunctional enzyme, phosphorylation of which leads to decreased formation of fructose 2,6-P2, which is an activator of 6-phosphofructo-1-kinase and an inhibitor of fructose 1,6-bisphosphatase, both of which are important regulatory enzymes for glycolysis and gluconeogenesis. In addition to rapid effects of glucagon and beta-adrenergic agonists to increase hepatic glucose output by stimulating glycogenolysis and gluconeogenesis and inhibiting glycogen synthesis and glycolysis, these agents produce longer-term stimulatory effects on gluconeogenesis through altered synthesis of certain enzymes of gluconeogenesis/glycolysis and amino acid metabolism. For example, P-enolpyruvate carboxykinase is induced through an effect at the level of transcription mediated by cAMP-dependent protein kinase. Tyrosine amino-transferase, serine dehydratase, tryptophan oxygenase, and glucokinase are also regulated by cAMP, in part at the level of specific messenger RNA synthesis. The sympathetic nervous system and its neurohumoral agonists epinephrine and norepinephrine also rapidly alter hepatic glycogen metabolism and gluconeogenesis acting through alpha 1-adrenergic receptors. The primary response to these agonists is the phosphodiesterase-mediated breakdown of the plasma membrane polyphosphoinositide phosphatidylinositol 4,5-P2 to inositol 1,4,5-P3 and 1,2-diacylglycerol. This involves a guanine nucleotide-binding protein that is different from those involved in the regulation of adenylate cyclase. Inositol 1,4,5-P3 acts as an intracellular messenger for Ca2+ mobilization by releasing Ca2+ from the endoplasmic reticulum.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Mechanisms of hormonal regulation of hepatic glucose metabolism. 303 41

The effects of epinephrine, glucagon and insulin on the activity and degree of phosphorylation of fructose-1,6-bisphosphatase in isolated hepatocytes maintained in cell culture for 24 h were investigated. Epinephrine caused a rapid decrease in the apparent Km monitored as the activity ratio between the activity at 12.5 and 83 microM fructose-1,6-bisphosphate, reaching a maximum after 5 min. Glucagon caused a slower and less pronounced activation, and insulin caused an equally slow increase in Km. The effect of epinephrine and glucagon was completely reciprocated by insulin and the action of insulin was totally erased by the other two. Glucagon stimulated the incorporation of [32P]phosphate into fructose-1,6-bisphosphatase from about 2.5 to 4.2 mol/mol enzyme and epinephrine to 3.5 mol/mol. The effect of the two hormones acting together was cumulative. Insulin brought about a decrease in the degree of phosphorylation to 2.0 mol/mol. The effect of epinephrine was shown to be caused by the beta-receptors, since it was completely blocked by propanolol (a beta-antagonist) and remained unaffected by the presence of phentolamine (an alpha-antagonist).
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PMID:Effects of epinephrine, glucagon and insulin on the activity and degree of phosphorylation of fructose-1,6-bisphosphatase in cultured hepatocytes. 303 99

The 2-aminoisobutyric acid transport in hepatocytes isolated from 3- and 24-month-old rats was studied and some age-related differences were observed. The basal uptake appeared to be almost constant in cells from old animals during the incubation time, while, in the cells from adults, it showed a progressive increase, interpreted as being due to a derepression mechanism. Epinephrine and glucagon increased the transport in hepatocytes from animals of both ages, even if with a slightly different pattern; the hormones increased the Vmax, while the Km was unchanged at each age tested. However, the glucagon-induced increase in Vmax was lower in the older animals. The mechanism of hormonal action appeared to be similar in adult and old rats. In fact the uptake stimulation by glucagon and epinephrine showed a dependence on protein synthesis. The epinephrine effect was mediated by alpha-adrenergic receptors. No effect was exerted by extracellular amino acids on hepatocytes from 24-month-old animals, suggesting a loss of adaptative regulation mechanism with aging. This behaviour was reflected in the kinetic parameters; in fact the Vmax was not modified by extracellular amino acids at 24 months of age, while it appeared to be strongly decreased in the adult.
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PMID:Regulation of amino acid transport in hepatocytes isolated from adult and old rats. 322 58

Epinephrine responses to hypoglycemia and to identical relative work loads have been shown to be higher in endurance-trained athletes than in untrained subjects. To test the hypothesis that training increases the adrenal medullary secretory capacity, we studied the effects of glucagon (1 mg/70 kg iv), acute hypercapnia (inspired O2 fraction = 7%), and acute hypobaric hypoxia (inspired Po2 = 87 Torr), respectively, on the epinephrine concentration in arterialized hand vein blood in eight endurance-trained athletes [T, O2 uptake = 66 (62-70) ml.min-1.kg-1] and seven sedentary males [C, O2 uptake = 46 (41-50)]. In response to identical increments in glucagon concentrations, plasma epinephrine increased more in T than in C subjects [0.87 +/- 0.11 vs. 0.38 +/- 0.14 (SE) nmol/l, P less than 0.05]. In response to hypercapnia [arterial PCO2 = 56 +/- 0.7 Torr (T) and 55 +/- 0.4 (C), P greater than 0.05], the increment in epinephrine was significant in T (0.38 +/- 0.11 nmol/l) but not (P less than 0.1) in C subjects (0.22 +/- 0.11). Hypoxia [arterial PO2 = 42 +/- 2 Torr (T) and 41 +/- 2 (C), P greater than 0.05] increased epinephrine in T (0.22 +/- 0.10 nmol/l, P less than 0.05) but not in C subjects (0.01 +/- 0.07). The plasma norepinephrine concentration never changed, whereas heart rate always increased, the increase being higher (P less than 0.05) in T than in C subjects only during hypercapnia. The results indicate that training increases the capacity to secrete epinephrine.
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PMID:Effect of physical training on the capacity to secrete epinephrine. 328 27

Cytoplasmic Ca2+ (Ca2+i) was monitored in single guinea-pig pancreatic alpha 2-cells exposed to modulators of glucagon release. The stimulatory amino acid arginine raised Ca2+i from 62 to 160 nM, whereas the inhibitor glucose reduced both the latter concentration and basal Ca2+i by 30%. Epinephrine which potentiates arginine-stimulated secretion by increasing cAMP, does so without affecting Ca2+i. The results indicate that glucagon secretion is positively modulated by Ca2+i. It is suggested that glucose-induced lowering of Ca2+i is a fundamental effect in cells where the sugar is readily metabolized.
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PMID:The actions of arginine and glucose on glucagon secretion are mediated by opposite effects on cytoplasmic Ca2+. 330 74

Eleven trained men (aged 34.5 +/- 2 yrs) were studied during a 16.1 km run in the heat (Ta = 30.2 degrees C). Fasting blood samples were taken prior to the run and at 6.4, 12.9, and 16.1 km, and 3 h recovery. Serum or plasma glucose, insulin, glucagon, glycerol, and catecholamines were measured. Mean values were: exercise intensity, 80% of VO2max; final rectal temperature, 39.9 degrees C; and weight loss, 4.0%. Glucose increased 61% by 6.4 km, then decreased significantly by 16.1 km. Glycerol increased by 415% at 6.4 km, and continued to increase throughout the run. Epinephrine increased progressively during the run, but norepinephrine increased at 6.4 km, and did not change further during the exercise. Insulin increased slightly at 6.4 km, then decreased significantly from 6.4-16.1 km. Glucagon increased from 6.4-12.9 km and remained elevated at 3 h recovery. Hormone and substrate measurements obtained only before and after prolonged exercise may not reflect changes that occur during the course of the exercise. The observed insulin-glucagon relationships vary from previous findings in nontrained subjects at lower exercise intensities.
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PMID:Hormone and energy substrate changes during prolonged exercise in the heat. 354 75


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