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)

In conscious dogs, phentolamine infusion significantly increased fasting portal vein insulin, glucagon, and decreased net hepatic glucose output and plasma glucose. Propranolol significantly decreased portal vein insulin, portal flow, and increased hepatic glucose production and plasma glucose. Phentolamine, propranolol, and combined blockade reduced glucose absorption after oral glucose. alpha, beta, and combined blockade abolished the augmented fractional hepatic insulin extraction after oral glucose. Despite different absolute amounts of glucose absorbed and different amounts of insulin reaching the liver, the percent of the absorbed glucose retained by the liver was similar for control and with alpha- or beta blockade, but markedly decreased with combined blockade. Our conclusions are: (a) phentolamine and propranolol effects on basal hepatic glucose production may predominantly reflect their action on insulin and glucagon secretion; (b) after oral glucose, alpha- and beta-blockers separately or combined decrease glucose release into the portal system; (c) net hepatic glucose uptake is predominantly determined by hyperglycemia but can be modulated by insulin and glucagon; (d) direct correlation does not exist between hepatic delivery and uptake of insulin and net hepatic glucose uptake; (e) alterations in oral glucose tolerance due to adrenergic blockers, beyond their effects on glucose absorption, can be, to a large extent, mediated by their effects on insulin and glucagon secretion reflecting both hepatic and peripheral glucose metabolism.
 ...
PMID:Effects of alpha and beta adrenergic blockade on hepatic glucose balance before and after oral glucose. Role of insulin and glucagon. 287 78

Using a new in vitro procedure of the isolated perfused rat pancreas with vagal innervation, electrical vagal stimulation produced an increase in both insulin and glucagon secretion in proportion to the pulse frequency, but an inhibition in somatostatin release. When atropine was infused, both insulin and glucagon responses to vagal stimulation were partially suppressed, whereas somatostatin release was enhanced. In the presence of hexamethonium, vagal stimulation failed to affect insulin, glucagon, or somatostatin secretion. Propranolol partially blocked both insulin and glucagon responses but did not influence somatostatin response. Phentolamine had no significant effect on release of hormones. Simultaneous administration of propranolol and phentolamine tended to inhibit both insulin and glucagon responses to vagal stimulation. These findings suggest that not only a cholinergic but also a noncholinergic neuron may be involved in vagal regulation of pancreatic hormone secretion and that these neurons may be under the control of preganglionic vagal fibers via nicotinic receptors.
 ...
PMID:Vagal regulation of insulin, glucagon, and somatostatin secretion in vitro in the rat. 288 48

This study examined the relationship between postnatal metabolic and hormonal changes and the accompanying rapid increase in mitochondrial adenine nucleotide content (ATP + ADP + AMP) in rabbit liver. The cytosolic NAD+/NADH concentration ratio, calculated from tissue pyruvate and lactate values, increased linearly 6.6-fold during the 1st postnatal h. The mitochondrial NAD+/NADH concentration ratio, calculated from tissue acetoacetate and beta-hydroxybutyrate values, increased 28-fold by 30 min postnatal. These changes in NAD+/NADH suggest that tissue oxygenation occurs rapidly and that oxygen supply rather than substrate supply is limiting for mitochondrial respiration in the immediate postnatal period. The normal increase in mitochondrial adenine nucleotide content that occurs within 2 h after birth was inhibited by hypoxia (5% O2). Glucagon stimulated the postnatal increase in mitochondrial adenine nucleotides but had no effect in combination with hypoxia. Both glucose and somatostatin injections inhibited the increase in mitochondrial adenine nucleotides and increased the insulin-to-glucagon ratio. Isoproterenol or dibutyryl cAMP stimulated, but propranolol did not inhibit, the normal increase in mitochondrial adenine nucleotide content. Phentolamine did not stimulate the postnatal accumulation of adenine nucleotides. In summary, the results show that the insulin-to-glucagon ratio is probably the most important hormone regulator of the rapid recompartmentation of adenine nucleotides into the mitochondrial matrix and that tissue oxygenation is strictly permissive for this hormone effect in the first 2 h after birth.
 ...
PMID:Regulation of mitochondrial adenine nucleotide content in newborn rabbit liver. 289 2

Glucagon secretion is known to be stimulated by activation of the alpha-adrenoceptors. In this study, we investigated whether alpha-adrenoceptor blockade by phentolamine affects basal and stimulated glucagon secretion in the mouse. Phentolamine was injected intraperitoneally to mice at dose levels varying from 2.6 to 260 mumol/kg. It was found that, while decreasing plasma glucose levels, phentolamine did not over this wide dose range affect basal glucagon concentrations indicating an inhibition of the hypoglycaemia-induced glucagon secretion. Further, phentolamine clearly inhibited the glucagon secretory response to beta-adrenergic or cholinergic stimulation. Thus, phentolamine (2.6 mumol/kg), impaired the glucagon secretory response to the beta 2-adrenoceptor agonist terbutaline by 51% (P less than 0.01), and to the cholinergic agonist carbachol by 44% (P less than 0.02). We conclude that alpha-adrenoceptor blockade by phentolamine inhibits the glucagon secretion following hypoglycaemia or stimulation by beta-adrenergic and cholinergic agonists. Thus, the alpha-adrenoceptors seem to be of great importance for glucagon secretion in the mouse.
 ...
PMID:Alpha-adrenoceptor blockade by phentolamine inhibits beta-adrenergically and cholinergically induced glucagon secretion in the mouse. 289 39

To determine whether the autonomic nervous system has a direct effect on GIP secretion, six normal subjects received a 4-hr intraduodenal perfusion of glucose (225 mg/min) and polyethylene glycol on four successive days. During the latter 2 hr, either normal saline, propranolol, phentolamine, or atropine were infused intravenously. Glucose absorption was calculated by measuring glucose and polyethylene glycol following luminal aspiration distal to the perfusion site. Basal and peak or nadir values in the saline study of plasma glucose, insulin, glucagon, and GIP were similar to the other three studies prior to autonomic blockade. During the latter 2 hr of the glucose perfusion, the plasma glucose and glucagon responses to saline did not differ from responses to the three blocking agents. Phentolamine but not atropine or propranolol resulted in a greater insulin response compared to saline (3247 +/- 762 vs 1348 +/- 388 microU/ml/120 min, P less than 0.01). GIP was not significantly affected by phentolamine (18,146 +/- 4574), propranolol (7585 +/- 5854), or atropine (15,797 +/- 6297) compared to saline (11,717 +/- 5204 pg/ml/120 min). Glucose absorption was unaffected by infusions of saline, phentolamine, and propranolol, but was increased following atropine infusion (5841 +/- 1120 vs 1044 +/- 808 mg/120 min, P less than 0.02). There appears to be no direct effect of the autonomic nervous system on glucose-induced secretion of GIP.
 ...
PMID:Lack of a direct effect of the autonomic nervous system on glucose-stimulated gastric inhibitory polypeptide (GIP) secretion in man. 352 48

The nervous control of hepatic urea and glutamine release and of ammonia uptake was studied in the rat liver perfused in situ. Electrical stimulation of the nerve bundles around the hepatic artery and the portal vein resulted in a reduction of urea release, of glutamine output and of ammonia uptake. At the same time, as observed before [Hartmann et al. (1982) Eur. J. Biochem. 123, 521-526], nerve stimulation led to a decrease of portal flow as well as to an increase of glucose release and a shift of lactate uptake to output. Noradrenaline infusion mimicked the nerve-dependent metabolic and hemodynamic changes in a first approximation only at the highly unphysiological concentration of 0.1 microM. It was without effect at 0.01 microM, which might be reached in the sinusoids as a result of overflow from the vasculature. In the presence of sodium nitroprusside nerve stimulation no longer reduced urea output, glutamine release and ammonia uptake or portal flow, yet it still increased glucose and lactate release. Phentolamine clearly reduced the alterations after nervous stimulation of urea output, ammonia uptake and portal flow, while propranolol was essentially not effective. The nerve-stimulation-dependent reduction of glutamine release was almost abolished in the presence of phentolamine and lowered to 50% by propranolol. Glucagon stimulated urea output but had no influence on glutamine release, ammonia uptake and portal flow. Nerve stimulation antagonized the glucagon-stimulated urea release. The present results suggest that in the perfused liver alpha-sympathetic hepatic nerves regulate urea release, glutamine output and ammonia uptake predominantly by an indirect mechanism via hemodynamic alterations, but glucose release by a direct mechanism also in the absence of circulatory changes.
 ...
PMID:Control of urea production, glutamine release and ammonia uptake in the perfused rat liver by the sympathetic innervation. 373 64

The effects of adrenergic stimulation and suppression on somatostatin (SS), insulin, and glucagon release were studied in intact dogs. Isoproterenol, a beta-adrenergic agonist, significantly increased portal venous and arterial levels of SS and arterial levels of insulin and glucagon. Propranolol, a beta-adrenergic antagonist, significantly decreased portal venous SS and suppressed the isoproterenol-stimulated increases in the levels of SS, insulin, and glucagon. alpha-Adrenergic stimulation (propranolol plus epinephrine) decreased portal venous SS and arterial insulin. Phentolamine, and alpha-adrenergic antagonist, increased portal venous and arterial SS and arterial glucagon. These data suggest that in intact dogs, stimulation of beta-adrenergic receptors enhances the release of SS, insulin, and glucagon, while stimulation of alpha-adrenergic receptors inhibits the release of SS and insulin without having a definitive effect on glucagon.
 ...
PMID:Adrenergic control of somatostatin release. 612 51

Somatostatin-like-immunoreactivity (SLI), immunoreactive insulin (IRI), glucagon (IRG) and catecholamine concentrations were measured in rat portal plasma during electrical stimulation of the vagus and splanchnic nerves, and during experimentally-induced hypovolaemia and hypoxaemia. Blood pressure, arterial gases and pH were monitored and hepatic blood flow was estimated (EHBF). Stimulation of the vagus nerves induced an increase in IRG and IRI concentrations, but had different influences on SLI level according to the concomitant experimental conditions. Stimulation of the left splanchnic nerve induced a sharp rise in SLI, IRG and catecholamine concentrations, whereas IRI level decreased hypovolaemia and hypoxaemia. Phentolamine treatment augmented the basal IRI, IRG and SLI concentrations. It did not suppress the hypovolaemia-induced rise of IRG and SLI concentrations, but unmasked a strong IRI release. By contrast, propranolol and atropine reduced significantly the A and D cell responses to acute hypovolaemia. These results are consistent with a profound influence of pancreatic nerves on A, B and D cell functions, which should be taken into account for interpretation of results during in vivo experiments.
 ...
PMID:The nervous control of rat somatostatin, glucagon and insulin secretions. 612 63

We have investigated in normal subjects the possible role of plasma free fatty acids (FFA) and blood ketone bodies (KB) in the regulation of human somatostatin secretion. Heparin injected during the intravenous infusion of a fat emulsion raised FFA levels acutely from 0.4 +/- 0.1 to near 3 mmol/L. Plasma somatostatin-like immunoreactivity (SLI) rose from a mean (+/- SEM) basal value of 9.2 +/- 1.0 ng Eq S14/L to 20.0 +/- 6.0 ng Eq S14/L (P less than 0.05). Plasma immunoreactive insulin (IRI) level was unchanged and glucagon (IRG) concentration decreased from 156 +/- 20 to 107 +/- 2 ng/L (P less than 0.05). During this test, there was a rise not only in FFA but also in plasma triglycerides (TG) and in blood glycerol and KB levels. The infusion of a fat emulsion alone increased triglyceride and glycerol levels to a similar extent but induced also a mild rise of FFA (0.37 +/- 0.05 to 1.13 +/- 0.5 mmol/L, P less than 0.01), KB (78 +/- 12 to 360 +/- 45 mumol/L, P less than 0.01), and SLI (14.8 +/- 4.6 to 23.8 +/- 7.1 ng Eq S14/L, P less than 0.05). The induction by DL-Na-3-hydroxybutyrate infusion of a rise of KB was associated with a decrease of FFA (P less than 0.05) and SLI (P less than 0.05) without modification of IRI or IRG levels. Phentolamine infusion did not modify the SLI or glucagon response to acute elevations of FFA, whereas propranolol suppressed the increase of SLI without preventing the concomitant decrease of IRG.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Regulation of somatostatin secretion in man: study of the role of free fatty acids and ketone bodies. 614 47

It has been reported that insulin secretion decreases during hypoxia both in vitro and in vitro, while an increase in glucagon secretion is found only in vivo. The effect of acute hypoxia on the secretion of glucagon and insulin was studied in the perfused rat pancreas. Phentolamine, an alpha-adrenergic blocker, was perfused during the period of hypoxia to elucidate the role of alpha-adrenergic stimulation. Sodium ATP and dibutyryl cAMP were also administered to study their effects on insulin and glucagon responses during hypoxia. In the present experiments, insulin secretion was suppressed while glucagon secretion was increased during hypoxia. Phentolamine did not cause any change in insulin of glucagon secretion. When dibutyryl cAMP was added, the increased glucagon secretion was reduced to the basal level, whereas the decreases in insulin secretion were not altered. The addition of sodium ATP reversed the hypoxia-induced decrease in insulin and the increase in glucagon secretion. These results suggest that a decrease in ATP production, which leads to impaired cAMP generation, pays a role in, and that alpha-adrenergic stimulation does not participate in the changes in, insulin and glucagon secretion during hypoxia in vitro.
 ...
PMID:The effect of hypoxia on insulin and glucagon secretion in the perfused pancreas of the rat. 628 79


<< Previous 1 2 3 4 Next >>