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)

To clarify the impact of hypothermia on the hormonal control of glucose metabolism, rats were rendered hypothermic (25 C) after catheterization of the portal vein. Glucose, insulin, glucagon, and catecholamine concentrations were serially monitored, and the regional blood flows were measured, allowing the estimation of hormone outputs. Hypothermia reduced the portal blood flow by 50% without changing arterial blood pressure, blood gases, or pH. Portal plasma insulin secretion dropped (0.05 +/- 0.01 vs. 0.23 +/- 0.04 mU/min), and glucagon secretion increased (0.81 +/- 0.18 vs. 0.38 +/- 0.10 ng/min). The B cell responses to glucose, arginine, and glucagon were abolished, while the A cell response to arginine was not significantly affected. Glucose intolerance was apparent after iv glucose or arginine loads. Haloperidol and to a lesser extent phentolamine suppressed the cold-induced glucagon rise. Phentolamine and to a lesser extent haloperidol alleviated the cold-induced suppression of insulin release. Propranolol, naloxone, and atropine were relatively inactive. The cold-induced glucose intolerance was not corrected by phentolamine treatment. A marked resistance to iv insulin was apparent in these rats, which is in contrast to a normal sensitivity to iv glucagon.
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PMID:Glucagon and insulin secretion and their biological activities in hypothermic rats. 643 6

Hyperthyroid patients in the postabsorptive state have elevated levels of blood glycerol and ketone bodies (KB): this is believed to be due to increased lipolysis and ketogenesis. These increased glycerol and KB levels return toward normal after oral propranolol administration. In order to investigate the mechanism of action of propranolol in hyperthyroid patients, we compared the effects of the oral administration of propranolol with those of timolol, propylthiouracil (PTU), and a placebo. The placebo had no effect. The free thyroxine index, immunoreactive insulin level and glucagon level were not modified by propranolol, timolol, or PTU. Propranolol decreased the pulse rate (P less than 0.01) and the levels of serum triiodothyronine (T3; P less than 0.05), blood glycerol (P less than 0.01), and KB (P less than 0.01). Like propranolol, timolol decreased the pulse rate (P less than 0.01) but had no effect on the T3, glycerol, or KB levels. Propylthiouracil did not modify the pulse rate, but like propranolol, it decreased the T3 (P less than 0.05), glycerol (P less than 0.01) and KB (P less than 0.01) levels. These results suggest that the metabolic actions of propranolol are not caused by its hemodynamic effects nor its beta-blocking properties but are mediated by the decrease of the T3 level.
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PMID:Reduction of increased levels of blood glycerol and ketone bodies by propranolol in human hyperthyroidism: role of the fall of the triiodothyronine level. 650 8

The effects of epinephrine (E) on plasma norepinephrine (NE) concentrations and cardiovascular responses before and after beta-blockade were studied in 36 patients with essential hypertension and 10 age-matched normal controls. The resting plasma NE and E were significantly higher in the borderline hypertensives (251 +/- 21 (SE) pg/ml, p less than 0.005; 57 +/- 5, p less than 0.05) than in normal controls (127 +/- 18; 38 +/- 7). An immediate rise in plasma E and NE was observed after one bolus intravenous administration of glucagon (1 mg). Then, plasma E fell rapidly to the baseline, whereas plasma NE declined much slowly. Propranolol did not affect the plasma E response to glucagon, but eliminated a prolonged rise of plasma NE. Exogenous E infusion (1.25-1.50 micrograms/min) for 30 min caused a definite rise in both plasma NE and blood pressures and lasted more than 30 min after termination of the infusion. Propranolol did not alter the time course of plasma E, but again inhibited a prolonged rise in both plasma NE and blood pressures. These findings support the view that plasma E can act physiologically as a sustained stimulator to the presynaptic beta-adrenoceptors, leading to an enhancement of NE release and a rise in blood pressure in man.
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PMID:The role of epinephrine in essential hypertension. 663 77

Xylazine was administered intravenously (0.16 mg/kg) to sheep. This was associated with a transient hyperglucagonaemia, hypoinsulinaemia and hyperglycaemia. The rate of glucose appearance as determined by isotope dilution techniques was increased three to four fold during the first 20 minutes after xylazine administration. Phentolamine prevented the xylazine-induced increase in the rate of appearance of glucose, and in concentrations of glucose and glucagon in plasma. The insulin response was not altered by phentolamine. Propranolol had no effect on the glucose and hormonal responses due to xylazine. The xylazine-induced effects on glucose metabolism and secretion by glucagon and insulin appear to be mediated by the alpha-adrenoceptors.
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PMID:Effect of adrenergic drugs on glucose and plasma glucagon and insulin responses to xylazine in sheep. 675 74

The effectiveness of cold exposure on the secretion of insulin and glucagon were examined using five adult sheep. Endocrine responses were studied in a warm environment and after cold exposure (0 C) from 4-19 days. Compared to levels at room temperature, basal plasma glucose levels were elevated during cold exposure, but basal levels of plasma insulin and glucagon were unchanged. Cold exposure significantly decreased the early insulin response to a primed iv infusion of glucose. Plasma glucose and glucagon levels during glucose infusion were unaffected by cold exposure. The decrease in plasma glucose after iv insulin injection (0.2 U/kg BW) was greater during cold exposure than at room temperature. Butyrate injection (0.625 mmol/kg, iv) resulted in a significantly lower secretion of both insulin and glucagon in the cold than in the warm environment. The glucagon response to arginine infusion (0.5 g/kg over 30 min, iv) was elevated by cold exposure, whereas the insulin response to arginine tended to be reduced. Propranolol infusion (20 micrograms/kg . min, iv) caused a slight inhibition of insulin secretion in the cold environment, but did not affect glucagon levels in either the cold or warm environment. Phentolamine infusion (20 micrograms/kg . min, iv) inhibited glucagon secretion, particularly in the cold environment, and caused a markedly greater stimulation of insulin secretion in the cold. It is concluded that cold exposure insufficient to cause hypothermia decreases insulin secretion in response to a variety of stimuli. Effects of cold on glucagon secretion depend upon the stimulating agent used.
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PMID:Effects of cold exposure on insulin and glucagon secretion in sheep. 675 53

To assess the functional maturity of adrenergic modulation of plasma concentration of glucose, as well as immunoreactive glucagon (IRG) and immunoreactive insulin (IRI) secretion in utero, adrenergic agonists with or without beta (propranolol) or alpha (phentolamine) antagonists were infused to the chronically catheterized sheep fetus (n = 35) late in the third trimester. Mean +/- S.E. days at study was 129.5 +/- 1.5; term is 150 days. In 9 separate studies at gestational age 129 +/- 1 days, the infusion of saline for 3 hr was not associated with significant changes in the basal levels of glucose, IRG, or IRI. With epinephrine, 6 microgram/min (n = 6) glucose rose from 16.7 +/- 3.6 to 41.9 +/- 9.7 mg/dl, IRG rose from 75 +/- 8 to 219 +/- 45 pg/ml, and IRI fell from 22.6 +/- 1.7 to 12.7 +/- 3.5 microunits/ml (P less than 0.05 for each). Propranolol alone (n = 4) did not alter basal glucose or IRG but significantly suppressed IRI. Propranolol did, however, markedly attentuate the rise in glucose and IRG while exaggerating the fall in IRI during epinephrine infusion. Qualitatively similar but smaller responses were obtained with epinephrine, 0.4 microgram/min (n = 10). Similarly, elevation of glucose and suppression of IRI was obtained with norepinephrine, 2 microgram/min (n = 5), but IRG levels did not rise significantly. Alpha-Adrenergic blockade alone augmented IRI from 18 +/- 3 to 38 +/- 5 microunits/ml without affecting glucose or IRG concentrations; during alpha blockade, norepinephrine infusion failed to induce the rise in glucose, IRG remained unchanged, and IRI remained elevated (n = 5). 2-Deoxy-D-glucose, 200 mg IV over 30 min, did not affect glucose, IRG, or IRI (n = 5). Thus, appropriate adrenergic modulation of plasma concentrations of glucose, and of IRG and IRI secretion is established in the third trimester.
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PMID:Adrenergic modulation of pancreatic hormone secretion in utero: studies in fetal sheep. 699 82

To test for a possible role of adrenergic mechanisms in the altered glucagon secretion in the spontaneously diabetic "BB" rat, the responses of glucose, insulin, and glucagon to adrenergic blocking agents in diabetic and normal rats were compared at rest and during 2 h of immobilization stress. In unstressed normal rats, phentolamine alone caused a 20 mg/dl fall in glycemia, 1.2 ng/ml rise in insulin (IRI), and no change in glucagon (IRG), whereas the only effect of propranolol was a minor rise in glycemia. Stress caused increments in glycemia of 72 mg/dl and in IRG of 94 pg/ml, and no change in IRI. Phentolamine significantly attenuated the stress-related increments, and IRI increased by the same amount as in the unstressed state. Propranolol exhibited no statistically significant effects on the response to stress. These findings are consistent with alpha-adrenergic stimulation of IRG and suppression of IRI secretion. In unstressed diabetic rats (mean time 0 glycemia, 431 mg/dl), propranolol caused only a small rise in glycemia, whereas phentolamine induced marked increments of glycemia (131 mg/dl) and IRG (116 pg/ml). Stress alone did likewise (189 mg/dl, 122 pg/ml) as did stress with the phentolamine (271 mg/dl, 144 pg/ml). However propranolol significantly attenuated the stress-induced increments in glycemia (88 mg/dl) and IRG (82 pg/ml). Thus both alpha- and beta-adrenergic receptors influence IRG secretion in the diabetic rats. An in vivo model for elucidating neural control of glucoregulation has been developed that is independent of cardiovascular fitness.
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PMID:Adrenergic regulation of glucagon and insulin secretion during immobilization stress in normal and spontaneously diabetic BB rats. 701 96

Atenolol, Pindolol and Propranolol in single daily doses administered to 18 selected patients with mild essential hypertension achieved adequate control of blood pressure. Chlorothiazide had been initially administered twice a day without full control of blood pressure and this diuretic therapy was continued unaltered throughout the study. Methacholine challenge testing of respiratory function was performed during the placebo phase and with each beta adrenoreceptor-blocking drug. In the 18 non-asthmatic patients, the reduction in FEV1, was significant only for propranolol therapy when compared to placebo. Each beta adrenoreceptor-blocking drug was associated with small, but significant, increases in fasting plasma triglyceride concentrations and suppression of fasting immuno-reactive glucagon concentrations.
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PMID:Beta adrenoreceptor-blocking drugs once daily in essential hypertension: a comparison of propranolol, pindolol and atenolol. 701 82

The interrelationships of glucagon and insulin with the sympathetic system on glucose turnover during exercise were examined in sheep. Six sheep were run for 45 min on a treadmill with and without alpha- and/or beta-adrenergic blockade. The exercise-induced increase in glucose appearance, as assessed by infusion of [2-3H]glucose, was reduced during the first 25 min of exercise by phentolamine administration. The metabolic clearance rate of glucose also was greater during exercise with phentolamine treatment than without. Phentolamine was associated with a rise in insulin concentrations and appeared to delay the exercise-induced rise in glucagon. Propranolol administration had no effect on glucose turnover and plasma glucagon and insulin. Nor did it have any effect on the changes in glucose, insulin, or glucagon induced by phentolamine administration. These observations are consistent with the alpha-adrenergic mediation of the sympathetic influences on insulin and glucagon secretion, which may account in part for the glucose adaptations to exercise in sheep. However, direct affects of circulating catecholamines on and increased stimulation of sympathetic innervation to the liver cannot be ruled out.
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PMID:Glucose, glucagon, and insulin during adrenergic blockade in exercising sheep. 703 12

In order to characterize the adrenergic control of the pancreatic A cell the effect on glucagon secretion of three sympathomimetic substances - epinephrine, isoproterenol and phenylephrine - and two adrenergic blocking agents - propranolol and phentolamine - were tested separately in the basal state and during glucagon hypersecretion induced by arginine infusion or glucopenia, using the isolated perfused rat pancreas. Epinephrine and isoproterenol infusion caused a prompt and sustained glucagon release in the basal state and potentiated glucagon response to metabolic stimuli. Insulin secretion was suppressed by epinephrine and slightly stimulated by isoproterenol. The stimulatory effect on glucagon secretion observed during phenylephrine infusion was abolished by concomitant propranolol infusion and potentiated by phentolamine. Insulin secretion was markedly depressed by phenylephrine: this effect was reserved by concomitant phentolamine infusion, while no effect was observed by concomitant propranolol infusion. Propranolol caused a suppression of both glucagon and insulin secretion, while phentolamine slightly enhanced glucagon and insulin production. In conclusion, beta-adrenergic receptor stimulation markedly increased pancreatic glucagon secretion and slightly enhanced pancreatic beta-cell activity; conversely, alpha-adrenergic agents markedly depressed insulin secretion while scarcely influencing glucagon production.
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PMID:Characterization of adrenergic control of glucagon secretion from isolated perfused rat pancreas. 716 May 20


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