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)

Catheterization of the portal vein and stereotaxic implantation of electrodes in the lateral hypothalamic area (LHA) were performed in normal rats after thiopental anesthesia. Immunoreactive glucagon (IRG) and insulin (IRI), glucose, catecholamines, and beta-endorphin were monitored in portal and peripheral plasma, before and during electrical stimulation of the LHA. The influences on glucose and hormone concentrations of propranolol, phentolamine, atropine, and naloxone infusions were also investigated in similar rats. A basal portoperipheral concentration gradient was found for IRG, IRI, and catecholamines, but not for beta-endorphin. The LHA stimulation induced a significant rise in portal catecholamine, IRG, and glucose concentrations; IRI remained unchanged; the portoperipheral catecholamine gradient was augmented. These alterations were not observed after bilateral splanchnicectomy. Propranolol infusion abolished the LHA-dependent IRG and glucose rises. Naloxone reduced the IRG rise significantly. Phentolamine and atropine did not modify the LHA-induced reactions. These results suggest that the glucagon release which follows LHA electrical stimulation depends mainly on beta-adrenergic transmission by the splanchnic nerves. Opioid peptide receptors may modulate this effect.
 ...
PMID:Glucagon release after stimulation of the lateral hypothalamic area in rats: predominant beta-adrenergic transmission and involvement of endorphin pathways. 630 29

The effects of alpha- and beta-adrenergic stimulation on ketogenesis were examined in freshly isolated rat hepatocytes in order to determine which alpha- or beta-adrenergic stimulation is involved in the enhancement of ketogenesis. In the presence of 0.3 mmol/L (U-14C)-palmitate, epinephrine, norepinephrine, and phenylephrine at 500 ng/mL increased ketogenesis by 25% (16.0 +/- 0.17 v 12.8 +/- 0.13 nmol/mg protein per hour), 20% (15.3 +/- 0.28) and 20% (15.4 +/- 0.36), respectively. However, isoproterenol even at 1 microgram/mL did not stimulate ketogenesis. Phentolamine (5 micrograms/mL) almost completely abolished the effect of epinephrine on ketogenesis (13.7 +/- 0.30 v 16.0 +/- 0.17) but propranolol did not inhibit the stimulation by epinephrine (15.6 +/- 0.38 v 16.0 +/- 0.17). Trifluoperazine (10 mumol/L), presumably an inhibitor of calcium-dependent protein kinase, abolished the effect of epinephrine (13.6 +/- 0.22 v 16.0 +/- 0.17). These results indicate that catecholamines increase ketogenesis predominantly through the alpha-adrenergic system independent of cyclic AMP, and calcium-dependent protein kinase is thought to be involved in the activation of ketogenesis. On the other hand, glucagon stimulated ketogenesis with an increase of cyclic AMP, which was not inhibited by alpha- and beta-adrenergic antagonists. Alpha-adrenergic stimulation increased hepatic glycogenolysis much more at much lower concentrations when compared with ketogenesis. Stimulation of ketogenesis by catecholamines seemed to be less sensitive and responsive compared with hepatic glycogenolysis.
 ...
PMID:Mechanism of adrenergic stimulation of hepatic ketogenesis. 635 38

Islet-activating protein (IAP) is a substance purified from the culture medium of Bordetella pertussis, and its main action is characterized by the enhancement of secretory response to glucose and other stimuli in pancreatic islet. In this experiment, the effect of IAP on epinephrine-induced secretion of immunoreactive insulin (IRI) and glucagon (IRG) was investigated in normal dogs. Epinephrine suppressed IRI secretion and it had a little increment to IRG secretion in control group, while IRI and IRG secretions were significantly increased by epinephrine in IAP pretreated group. Using beta-blocker (Propranolol) with epinephrine, these increments of IRI and IRG secretions in IAP pretreated group were abolished. However, using alpha-blocker (Phentolamine) with epinephrine, these secretions of IRI and IRG in IAP pretreated group were much more increased than epinephrine alone induced secretions. Blood glucose levels were lower in IAP pretreated group than in control group throughout the loading tests in all of the experiments. These findings suggest that (1) IAP decreases blood glucose level and (2) IAP enhances epinephrine-induced secretion of insulin and glucagon by acceleration of beta-adrenergic effect and by reduction of alpha-adrenergic suppression in dogs.
 ...
PMID:Islet-activating protein (IAP)-induced adrenergic modulation of pancreatic A and B cell in dogs. 637 Aug 19

The effects of adrenergic blockers on the glucagon response to insulin hypoglycemia were investigated in diabetic (10-15 days poststreptozocin [STZ] injection) and age-matched control rats. alpha-(Phentolamine nonspecific but predominantly alpha 1), alpha 2-(yohimbine), or beta-(propranolol) adrenergic blockers alone or in combination did not affect plasma glucose levels or plasma glucagon concentrations, in the basal state, in either control or diabetic rats. None of these adrenergic blockers, alone or in combination, inhibited the glucagon response to insulin hypoglycemia in control or diabetic rats. On the contrary, in control rats, the beta-adrenergic blocker alone or in combination with an alpha-adrenergic blocker and in diabetic rats, the alpha-adrenergic blocker alone significantly stimulated the glucagon response to insulin hypoglycemia. Second, the effects of yohimbine on the glucagon response to epinephrine infusion were studied in both young and old rats. Recently, Cherksey et al. (Proc. Soc. Exp. Biol. Med. 1982; 171:196-200) have reported that the adrenergic receptors on rat pancreatic islet cells are of the alpha 2-subtype. Yohimbine (alpha 2-adrenergic blocker) completely blocked the glucagon response to epinephrine infusion in both young and old rats, but had no inhibitory effect on the glucagon response to insulin hypoglycemia in control and short-term diabetic rats. From these observations, it could be inferred that the lack of glucagon response to insulin hypoglycemia in long-term diabetic rats is unlikely to be explained by an impairment of an adrenergic function.
 ...
PMID:Role of sympathetic nervous system in glucagon response to insulin hypoglycemia in normal and diabetic rats. 638 31

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.
 ...
PMID:Glucagon and insulin secretion and their biological activities in hypothermic rats. 643 6

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.
 ...
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.
 ...
PMID:Effects of cold exposure on insulin and glucagon secretion in sheep. 675 53

The in vitro effect of corticosterone in insulin and glucagon secretion has been examined in the isolated perfused rat pancreas preparation. COrticosterone at physiological concentrations was found to inhibit acutely and strongly the secretion of insulin induced by both glucose and arginine and to potentiate the output of glucagon in a glucose-free medium or when induced by arginine. Phentolamine, an alpha-adrenergic blocking agent, diminished the strong inhibitory effect of corticosterone on insulin secretion. The present results demonstrate that corticosterone has direct effects on pancreatic islet cells, and they suggest that the inhibition of insulin secretion is to some extent related to the alpha-adrenergic receptors.
 ...
PMID:Effect of corticosterone on insulin and glucagon secretion by the isolated perfused rat pancreas. 698 56

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.
 ...
PMID:Adrenergic regulation of glucagon and insulin secretion during immobilization stress in normal and spontaneously diabetic BB rats. 701 96

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.
 ...
PMID:Glucose, glucagon, and insulin during adrenergic blockade in exercising sheep. 703 12


<< Previous 1 2 3 4 Next >>