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)

Norepinephrine (NOR) is a potent activator of carbohydrate metabolism in isolated hepatocytes from copper rockfish (Sebastes caurinus), increasing rates of glycogenolysis fourfold with an EC50 of 6.3 nM. Nanomolar concentrations of NOR also enhance gluconeogenesis. Epinephrine (EPI) activates both pathways to a smaller extent; the corresponding EC50 for glycogenolysis is 320 nM. There is no significant difference between the magnitude of glucose production in response to comparable doses of NOR, bovine glucagon, and catfish glucagon-like peptide. Experiments with an adrenergic agonist (isoproterenol) and antagonists (propranolol, prazosin, atenolol) indicate that NOR effects are mediated through beta-adrenoceptors. Catecholamine-activated glycogenolysis measured at 100 nM EPI or NOR is poorly correlated with a 30-50% rise in intracellular cAMP. Glucose production following catecholamine administration is not linear: 50% of the hourly glucose output is released within the first 17 min (NOR) and 5 min (EPI), respectively. During hepatocyte incubation (60 min at 15 degrees), added NOR and EPI (100 nM) were not degraded to any significant extent. In the absence of added hormones, rockfish hepatocytes produce 7.41 +/- 0.89 mumol glucose x g-1 packed cells x hr-1 at 15 degrees, with gluconeogenesis accounting for 35.0% of the total production. The rate of glucose output, which is linear for at least 60 min, is not correlated with the initial hepatocyte glycogen level.
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PMID:Norepinephrine: a potent activator of glycogenolysis and gluconeogenesis in rockfish hepatocytes. 197 May 44

To establish the role of hepatic nerves in hepatic glycogenolytic and gluconeogenic regulation during exercise, dogs underwent a laparotomy during which the hepatic nerves were either left intact (C; n = 8) or cut (DN; n = 5). At least 17 days after surgery, dogs were studied during 150 min of treadmill exercise (12% grade, 100 m/min). Glucose production (Ra) and gluconeogenesis (GNG) were assessed by combining [3-3H]glucose, [U-14C]alanine, and indocyanine green infusions with arterial, portal vein, and hepatic vein sampling. Glucagon and insulin were similar at rest and exercise in both groups. Norepinephrine rose from 145 +/- 10 to 242 +/- 32 pg/ml by 150 min of exercise in C and from 150 +/- 25 to 333 +/- 83 pg/ml in DN. Epinephrine rose from 66 +/- 7 pg/ml at rest to 108 +/- 10 and 148 +/- 24 pg/ml after 30 and 150 min of exercise in C and from 90 +/- 15 pg/ml at rest to 185 +/- 33 (P less than 0.05 compared with C) and 194 +/- 36 pg/ml after 30 and 150 min of exercise in DN. Plasma glucose fell gradually from 108 +/- 2 and 106 +/- 3 mg/dl at rest to 96 +/- 4 and 92 +/- 8 by the end of exercise in C and DN, respectively. Ra was similar in C and DN rising from 3.2 +/- 0.2 to 8.7 +/- 0.6 and 2.6 +/- 0.2 to 7.5 +/- 1.1 mg.kg-1.min-1, respectively, by the end of exercise. Minimum and maximum rates of GNG from alanine, glycerol, and lactate were elevated in DN compared with C during rest and exercise. However, the exercise-induced changes in GNG were similar in both groups. In conclusion, nerves to the liver are not essential to the increased Ra and glucose homeostasis during moderate-intensity exercise.
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PMID:Hepatic nerves are not essential to the increase in hepatic glucose production during muscular work. 220 Feb 75

Vasoactive intestinal polypeptide (VIP) has been shown to stimulate melatonin synthesis in mammalian pineal; however, a regulatory role for VIP in the avian pineal has not been explored. Immunocytochemical and physiological response experiments were performed to investigate whether 1) immunoreactive VIP fibers innervated the avian pineal gland; 2) VIP had a specific effect on melatonin release that was mediated by cAMP stimulation; and 3) alpha 2-adrenergic signal transduction was associated with a reduction in cAMP levels. Immunocytochemical experiments demonstrated the presence of both tyrosine hydroxylase- and VIP-immunoreactive fibers in the avian pineal gland. Treatment of dispersed chick pineal cell cultures with VIP stimulated melatonin release (maximum 6-fold increase; EC50 = 1.8 nM) when administered during the 12-h light period of a 12-h light, 12-h dark cycle. Of the other four peptides tested [porcine VIP-(10-28), porcine peptide histidine isoleucine, porcine secretin, and human glucagon), only peptide histidine isoleucine stimulated melatonin release (EC50 = 30 nM). The effect of VIP was mediated by a time- and dose-dependent increase in cAMP accumulation (maximum 4-fold increase). The specific alpha 2-agonist UK-14,304 reduced cAMP accumulation (maximum 43% reduction) and inhibited melatonin release (EC50 = 19 nM) in the presence of 3 X 10(-8) M VIP. Norepinephrine-induced inhibition of nocturnal melatonin release was blocked by the elevation of cAMP achieved through the administration of forskolin (EC50 = 0.2 microM), isobutylmethylxanthine (EC50 = 112 microM), or 8-bromo-cAMP (EC50 = 166 microM). Collectively, these results demonstrate the presence and functional significance of VIP in the avian pineal gland, and the interaction of VIP and norepinephrine at the level of cAMP in the regulation of melatonin biosynthesis.
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PMID:Vasoactive intestinal polypeptide and alpha 2-adrenoceptor agonists regulate adenosine 3',5'-monophosphate accumulation and melatonin release in chick pineal cell cultures. 247 31

This study compared the metabolic responses to parenteral nutrition in five septic and six nonseptic individuals. Oxygen uptake (VO2) was measured for 1 h preinfusion and during the first 2 h of parenteral nutrition infusion. While baseline VO2 was 19% higher in the septic compared with nonseptic patients (p less than 0.01), both groups responded similarly to nutrition: VO2 increased 25% and 27% above baseline in the nonseptic and septic groups, respectively (NS between groups). Respiratory quotient increased 9% in the nonseptic (p less than 0.01) and 5% in the septic (p less than 0.05) patients during infusion. Plasma glucose and insulin increased identically in both groups. Cortisol was consistently higher in the septic patients whereas glucagon decreased similarly in both groups with feeding. Norepinephrine increased 25% in response to the nutrition and remained elevated in the nonseptic group. The results illustrate the effect nutrient-induced thermogenesis may have in the energy balance of parenterally fed patients.
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PMID:Thermic effect of parenteral nutrition in septic and nonseptic individuals. 250 61

The effect of plasma noradrenaline concentrations within the physiological range (less than 5-6 nM) on the endocrine pancreas was investigated in 9 nondiabetic volunteers. Noradrenaline significantly inhibited plasma insulin levels but did not change plasma glucagon and somatostatin concentrations.
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PMID:Effects of physiological increases in plasma noradrenaline on the human endocrine pancreas. 257 94

We compared the effects of electrical stimulation of the splanchnic nerves and infusions of neuropeptide Y, noradrenaline or a combination of the two on pancreatic vascular resistance and exocrine and endocrine secretion. For these studies we used isolated perfused pig pancreas with preserved splanchnic nerve supply. The exocrine secretion was stimulated with physiological concentrations of secretin and cholecystokinin octapeptide. Noradrenaline and NPY at 10(-8) M both increased pancreatic perfusion pressure. Their effects were additive and similar in magnitude to that of electrical stimulation of the splanchnic nerves at 4-8 Hz. Nerve stimulation as well as NPY and noradrenaline infusions inhibited exocrine secretion, but an additive effect could not be demonstrated. Neither NPY nor noradrenaline could reproduce the stimulatory effect of nerve stimulation on glucagon secretion, nor the weak inhibitory effect on somatostatin secretion. NPY alone had no effect on insulin secretion and did not influence the inhibitory effect of noradrenaline. It is concluded that NPY is likely to cooperate with noradrenaline in the control of pancreatic blood flow, whereas its role in the control of pancreatic secretion is likely to be of minor importance, if any.
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PMID:On the regulatory functions of neuropeptide Y (NPY) with respect to vascular resistance and exocrine and endocrine secretion in the pig pancreas. 267 36

Brown adipose tissue (BAT) glucagon level was higher in cold-acclimated rats (CA) than in warm controls (WC). Noradrenaline (NA) injection increased BAT glucagon levels in both WC and CA with increases in plasma glucagon levels. The magnitude of increase was significantly greater in CA for plasma glucagon, while it did not differ for BAT between groups. However, BAT glucagon was kept at a higher level in CA after NA injection than in WC.
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PMID:Noradrenaline-induced changes in rat brown adipose tissue glucagon. 276 Nov 24

To examine the beta-adrenergic effects of the catecholamines in poorly controlled diabetes, we have studied insulin-deprived alloxan-diabetic (A-D) dogs during 90 min of moderate exercise (100 m/min, 10-12 degrees) alone (C) or with propranolol (5 micrograms . kg-1 . min-1) (P) or combined P and somatostatin infusion (0.5 microgram . kg-1 . min-1) (P + St). In P, in contrast to C, immunoreactive glucagon (IRG) rose only after 50 min of exercise. However, hepatic glucose production (Ra) rose normally. In P + St, IRG fell 50% below basal, and the Ra response to exercise was abolished. Interestingly, in P and P + St, glucose metabolic clearance rate (MCR) rose by 400% above the inadequate MCR response to exercise in C, despite 30% lower insulin levels. Compared with C, free fatty acids (FFA) and lactate were sharply reduced during P and P + St. Plasma glucose (G) did not change in C, but due to elevated glucose uptake, G fell over 120 mg/dl in P, and due to diminished Ra, G fell 170 mg/dl in P + St. Norepinephrine was similar in all groups. Epinephrine and cortisol were higher in P + St by 90 min of exercise, perhaps as a result of hypoglycemia. In summary, during exercise in poorly controlled A-D dogs, beta-blockade does not appear to affect Ra; beta-blockade leads to diminished mobilization of extrahepatic substrate as evidenced by reduced FFA and lactate levels; beta-blockade increases MCR to levels seen in normal dogs during exercise alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of beta-adrenergic mechanisms during exercise in poorly controlled diabetes. 286 46

The role of Ca2+ in stimulation of the malate-aspartate shuttle by norepinephrine and vasopressin was studied in perfused rat liver. Shuttle capacity was indexed by measuring the changes in both the rate of production of glucose from sorbitol and the ratio of lactate to pyruvate during the oxidation of ethanol. (T. Sugano et al. (1986) Amer. J. Physiol. 251, E385-E392). Asparagine (0.5 mM), but not alanine (0.5 mM) decreased the ethanol-induced responses. Norepinephrine and vasopressin had no effect on the ethanol-induced responses when the liver was perfused with sorbitol or glycerol. In the presence of 0.25 mM alanine, norepinephrine, vasopressin, and A23187 decreased the ethanol-induced responses that occurred with the increase of flux of Ca2+. In liver perfused with Ca2+-free medium, asparagine also decreased the ethanol-induced responses, but norepinephrine and vasopressin had no effect. Aminooxyacetate inhibited the effects of norepinephrine, A23187, and asparagine. Regardless of the presence or absence of perfusate Ca2+, the combination of glucagon and alanine had no effect on the ethanol-induced responses. Norepinephrine caused a decrease in levels of alpha-ketoglutarate, aspartate, and glutamate in hepatocytes incubated with Ca2+. The present data suggest that the redistribution of cellular Ca2+ may activate the efflux of aspartate from mitochondria in rat liver, resulting in an increase in the capacity of the malate-aspartate shuttle.
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PMID:Ca2+-dependent activation of the malate-aspartate shuttle by norepinephrine and vasopressin in perfused rat liver. 289 18

We investigated the direct pancreatic effects of noradrenaline in vivo on the secretion of insulin, glucagon, and somatostatin from the in situ pancreas in halothane-anaesthetized dogs. Noradrenaline was infused into the superior pancreatic artery at 12 ng min-1, a rate that did not alter systemic glucose or noradrenaline levels nor heart rate or blood pressure. This pancreatic infusion of noradrenaline did not affect the basal pancreatic output of insulin, yet did markedly inhibit arginine-stimulated insulin secretion. The acute insulin response (AIR) to an intravenous injection of arginine (2.5 g), which was 4293 +/- 1260 microM min-1 under control conditions, was reduced to 1054 +/- 396 microU min-1 by noradrenaline (P less than 0.01). Noradrenaline increased basal pancreatic glucagon output from 321 +/- 130 pg min-1 to 876 +/- 309 pg min-1 after 20 min of infusion (P less than 0.05) and the acute glucagon response (AGR) to arginine, being 1033 +/- 203 pg min-1 under control conditions and 1746 +/- 249 pg min-1 during noradrenaline infusion (P less than 0.05). The basal output of somatostatin did not change during noradrenaline infusion, but arginine-stimulated somatostatin secretion was impaired. The acute somatostatin response (ASLIR) to arginine was 473 +/- 124 fmol min-1 under control conditions and was decreased to 140 +/- 80 fmol min-1 by noradrenaline (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of pancreatic noradrenaline infusion on basal and stimulated islet hormone secretion in the dog. 290 99


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