Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of various hormonal and pharmacological manipulations on somatostatin distribution were investigated to elucidate the physiological significance of somatostatin in the hypothalamus and the other regions of the rat brain. Immunoreactive somatostatin (IRS) was measured by radioimmunoassay newly developed. Insulin induced an increase of hypothalamic IRS and a decrease of plasma RGH, while glucose administration resulted in the opposite responses, which were not significant. Insulin also increased IRS in the thalamus and the brain stem. The insulin-induced increase of hypothalamic IRS was reduced by hyperglycemia. Glucagon reduced IRS initially and then increased it with an elevation plasma RGH. L-dopa did not affect hypothalamic IRS, although it decreased plasma RPRL. Phentolamine slightly increased plasma RGH and decreased IRS in most regions of the rat brain, while propranolol increased IRS in these regions. Pretreatment with propranolol significantly increased plasma RGH 120 min after insulin administration, and hypothalamic IRS decreased initially by pretreatment with propranolol, and then it increased significantly. When pretreated with propranolol, glucagon markedly increased plasma RGH and decreased IRS significantly. From these findings it is concluded that hypothalamic IRS may participate in the hormonal regulatory system in correlation to plasma RGH, as observed in studies on plasma GH and hypothalamic IRS following insulin, glucose, propranolol or phentolamine administration, but IRS in other regions of the brain may have some other actions as a neurotransmitter or a modulator, because of no significant correlation between plasma GH or PRL and IRS in these regions following various stimuli. In addition, glucose homeostasis and adrenergic mechanism may be important factors in regulating IRS in the rat brain.
 ...
PMID:Immunoreactive somatostatin in the hypothalamus and other regions of the rat brain: effects of insulin, glucose, alpha- or beta-blocker and L-dopa. 3 44

Serotonin (5HT) (5 mg/kg-25 mg/kg; i.p.) induced a dose-related increase of plasma glucagon (IRG) (using 30K antibody) 3 to 60 min after administration to overnight fasted rats. Blood glucose (BS) also increased as early as 10 min post-injection whereas plasma insulin (IRI) increased in a non dose-related (30 min to onset) manner. Adreno-demedullation prevented the rise of BS and IRI, but not IRG. Pretreatment with reserpine (5 mg/kg; i.p.; 24 hr earlier) did not prevent the actions of 5HT. Pretreatment with the alpha-adrenergic antagonist phentolamine (3 mg/kg-6 mg/kg; i.p.) reduced but did not prevent the subsequent rise of IRG, whereas beta-adrenergic blockade with propranolol (5 mg/kg-10 mg/kg; i.p.) was without effect. Phentolamine and the lower dose of propranolol (5 mg/kg) reduced the 5HT-induced hyperglycemia; whereas the higher dose (10 mg/kg) prevented the hyperglycemia. Phentolamine potentiated and propranolol prevented (5 mg/kg) or reversed (10 mg/kg) the 5HT-induced IRI rise. Pretreatment with the 5HT-antagonist, methysergide, prevented all the effects of 5HT. Precursor loading with 5HTP (5 mg/kg-50 mg/kg; i.p.) also resulted in a dose-related increase of IRG and a slight increase of IRI. Blockade of the conversion of 5HTP to 5HT with Ro-4-4602 (an L-aromatic acid decarboxylase inhibitor) blocked the subsequent rise of IRG. These results suggest that the 5HT-induced changes in BS and IRI may be secondary to a release of epinephrine and/or norepinephrine, but that the effects of 5HT on the release of IRG cannot be explained solely by this mechanism.
 ...
PMID:The acute pharmacologic effects of serotonin on the release of insulin and glucagon in the intact rat. 31 Jun 65

The effects of glucagon injection on temperature regulation and some metabolic parameters were studied in the pigeon. Glucagon (100 microng/kg) always inhibited shivering and caused a fall in the oxygen consumption and body temperature of the unanesthetized pigeon at + 6 degrees C. At + 34 degrees C, the same dose of glucagon had no effect on these parameters. At 22 degrees C, glucagon produced an elevation in plasma free fatty acid (FFA) and blood glucose levels. The rise in FFA at 22 degrees C coincided with the suppression of shivering at 6 degrees C. The glucagon-mediated rise in plasma FFA, but not glucose level, was potentiated by cold ambient temperature. Adrenergic blocking agents given prior to glucagon did not abolish its effects. Phentolamine even prolonged the absence and accelerated the suppression of shivering. A dissociation in the mechanisms by which catecholamines and glucagon suppress shivering is suggested. Although mobilizing energy reserves, glucagon does not seem to be calorigenic in the pigeon at this dose. The interpretation of the changes in plasma FFA levels is discussed in relation to fuel consumption during shivering.
 ...
PMID:Effect of glucagon on thermogenesis in the pigeon. 86 Jul 58

Radiodiagnostic potential of intra-arterially injected vasodialting agents was investigated by their effect on total and segmenal resistances (VR) of mesenteric vasculature, blood flow in superior mesenteric artery and its bleeding branch; heart rate and ventricular and systemic blood pressure. Dipyridamole, isoxsuprine, protricular and systemic blood pressure. Dipyridamole, isoxsuprine, prochlorperazine, lidocaine, meglumine diatrizoate and carbon dioxide were poor dilators. Phentolamine produced hypotension; glucagon and serpasil an extremely long dilation. A large and short vasodilation was produced with tolazoline and nylidrin, but both agents increased VR of the postcapillary segment and caused transient hypotension and arrhythmias, nylidrin's side effects were smaller. Oxygen produced large and long vasodilation and minimal systemic effects. It is concluded that oxygen or possibly nylidrin are suitable agents should an intermittently bleeding mesenteric artery be dilated for diagnostic purposes prior to angiography.
 ...
PMID:Vasocilators in the canine mesenteric circulation. Evaluation of a potential aid in the diagnosis of gastrointestinal bleeding. 108 28

In man, epinephrine induces increases in plasma levels of glucagon, a lipolytic and hyperglycemic hormone. To determine glucagon's contribution to this hyperglycemia and lipolysis, the effects of inhibition of pancreatic alpha-cell responses to epinephrine were investigated with somatostatin and adrenergic receptor blockade. To avoid ambiguities that might result from concomitant changes in endogenous insulin secretion, these studies were performed in juvenile-type, insulin-deficient diabetic subjects. Compared with normal subjects, the diabetics had excessive glucagon responses to epinephrine, which had been infused to attain circulating levels within the range found in man in severe stress. Both somatostatin and propranolol completely prevented glucagon responses and diminished the glycemic response to epinephrine by 40 to 50 per cent. Free fatty acid responses to epinephrine were completely prevented by propranolol but unaffected with somatostatin. Phentolamine had no effect on glucose, free fatty acid, or glucagon responses to epinephrine. These studies demonstrate that epinephrine, via a beta-adrenergic receptor mechanism, causes excessive plasma glucagon elevation in human diabetes mellitus and indicate that this hyperglucagonemia participates in the hyperglycemic, but not the lipolytic, response to epinephrine. Catecholamine-induced hyperglucagonemia may thus provide an additional explantation for the deterioration in carbohydrate tolerance associated with stress.
 ...
PMID:Studies on the mechanism of epinephrine-induced hyperglycemia in man. Evidence for participation of pancreatic glucagon secretion. 110 95

In experiments with rabbits, glucagon prolonged the half-period of absorption of sodium iodide 125J in the left ventricular myocardium. Regitine prevented acceleration of the heart rate and impairment of capillary flow after glucagon. In healthy rabbits hippurate 125J clearance was unaffected by glucagon. After injury of the heart muscle by injection of silver nitrate solution into the left ventricular wall and depression of blood pressure, glucagon partly normalized renal clearance of hippurate 125J.
 ...
PMID:The influence of glucagon on the blood supply of the heart and kidneys in rabbits. 121 13

The present study was designed to clarify the mechanism of adrenergic modulation of pancreatic glucagon secretion in rats under physiological conditions by 1) epinephrine infusion alone or together with adrenergic blockers and 2) administration of adrenergic agonists. Intravenous infusion of epinephrine alone (1 microgram/kg/min, equal to 0.7 nmol/kg/min) caused a significant increase in glucagon secretion. Phentolamine (an alpha blocker) or yohimbine (an alpha 2 blocker) administration completely inhibited the increase of glucagon secretion caused by epinephrine infusion, but neither the administration of bunazosin (an alpha 1 blocker) nor beta blockers inhibited it. Infusion of clonidine (an alpha 2 agonist) caused significant increase of glucagon secretion even at a low dose of 0.5 nmol/kg/min, although infusion of neither an alpha 1 nor a beta 2 agonist caused it even at the high dose of 40.0 nmol/kg/min. It is concluded that the alpha 2 receptor mechanism plays the most important role in the adrenergic modulation of glucagon secretion in rats under physiological conditions.
 ...
PMID:Alpha 2-adrenergic modulation of pancreatic glucagon secretion in rats. 135 30

The present study was conducted to examine the roles of hormonal factors in plasma potassium alterations in acute respiratory acidosis. Respiratory acidosis (pH, 7.07-7.10) induced by the inhalation of 10% CO2, 20% O2 and 70% N2 mixed gas caused an increase in the plasma potassium concentration beyond that of the control of 3.44 +/- 0.12 (mean +/- SE) to 4.36 +/- 0.07 mEq/l (p less than 0.01) within 180 min. The plasma norepinephrine concentration was also noted to significantly increase at the same time. Phentolamine (40 micrograms/kg/min i.v.) did not affect the degree of acidosis or acidosis-induced hyperkalemia. No significant changes in the plasma levels of epinephrine, insulin, glucagon, cortisol or aldosterone could be detected. Hormonal factors would thus appear not to be essential to potassium movement from intracellular to extracellular compartments in acute respiratory acidosis.
 ...
PMID:Roles of hormones in plasma potassium alteration in acute respiratory acidosis in dogs. 140 6

To study the regulation of islet hormone secretion in exercise-stress, we developed a swimming mouse model. Mice swam for 2, 6, or 10 minutes whereafter blood was sampled for analysis of plasma levels of insulin, glucagon, and glucose. Plasma insulin levels, which were not different from resting controls after 2 or 6 minutes of swimming, were slightly lower after 10 minutes of swimming (P less than .05). Plasma glucagon levels were increased after 2, 6, and 10 minutes of swimming (P less than .001), and plasma glucose levels were lower after 6 and 10 minutes of swimming (P less than .05). Glucose (5.6 mmol/kg)-stimulated insulin secretion was inhibited by 52% +/- 9% by the swimming (P less than .001). The mechanisms behind this inhibition of glucose-stimulated insulin secretion and the increase in basal plasma glucagon levels induced during 2 minutes of swimming were investigated by the use of autonomic receptor antagonists, administered intraperitoneally 20 minutes before the swimming period. The ganglionic antagonist hexamethonium (56 mumols/kg) prevented the swimming-induced inhibition of glucose-stimulated insulin secretion, indicating involvement of nerves in the inhibition. Also the nonselective alpha-adrenoceptor antagonist phentolamine (6.0 mumols/kg) and the alpha 2-adrenoceptor antagonist yohimbine (3.6 mumols/kg) prevented the inhibition of glucose-stimulated insulin secretion induced by swimming, whereas the beta-adrenoceptor antagonist L-propranolol (9.6 mumols/kg) had no effect. The swimming-induced increase in plasma glucagon levels was partially inhibited by hexamethonium by (58% +/- 24%, P less than .05). Phentolamine and yohimbine totally prevented the increase in plasma glucagon levels, whereas L-propranolol had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Insulin and glucagon secretion in swimming mice: effects of autonomic receptor antagonism. 197 57

In man, a decrease in plasma glucose concentration results in a compensatory increase in hepatic glucose release. Studies in vitro have suggested that a low glucose concentration per se may directly stimulate hepatic glucose release, an effect often referred to as autoregulation. Whether autoregulation occurs in man in response to a physiologic decrement in blood glucose is not known. Therefore, seven healthy, nonobese subjects were studied on two occasions to determine the role of autoregulation in mediating the increase in glucose production that accompanies a physiologic decrement in plasma glucose concentration. On both occasions, plasma glucose concentrations were clamped successively at 95, 65, and 95 mg/dl for 2 h each. Insulin (approximately 14 microU/ml) and glucagon (approximately 70 pg/ml) were maintained constant on both occasions by an infusion of somatostatin and insulin. Phentolamine and propranolol also were infused on one occasion to produce combined alpha- and beta-adrenergic blockade. In the absence of adrenergic blockade, glucose production increased by approximately 1.3 mg/kg X min when the plasma glucose concentration was decreased from 95 to 65 mg/dl and decreased by approximately 1.5 mg/kg X min when glucose was increased from 65 to 95 mg/dl. In the presence of adrenergic blockade, the increase and decrease in glucose production averaged 0 and 0.5 mg/kg X min, respectively, representing 70-100% inhibition. We conclude that, in the presence of low physiologic insulin concentrations, autoregulation is not a major contributor to the hepatic response to a physiologic decrement in plasma glucose concentration in man.
 ...
PMID:The role of autoregulation of the hepatic glucose production in man. Response to a physiologic decrement in plasma glucose. 286 44


1 2 3 4 Next >>