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)

The effects of 5-hydroxytryptamine (5-HT) on plasma cyclic AMP (cAMP) and glucose concentrations were studied in rats in vivo. 5-HT injected i.p. increased plasma cAMP and glucose. Injections of propranolol, hexamethonium, and cyproheptadine inhibited the 5-HT-induced increase in glucose but not in cAMP. Atropine did not inhibit the action of 5-HT. These effects of 5-HT were not seen in adrenomedullectomized rats, and 5-HT did not elevate the concentration of plasma cAMP in anti-glucagon antiserum-injected rats. These results confirm the previously reported finding that 5-HT-induced increase in blood glucose is mediated via adrenaline released from adrenal medulla by 5-HT and suggest that the increase in plasma cAMP, induced by 5-HT, is due to glucagon released by an unknown factor, or factors other than adrenaline released from the adrenal medulla by 5-HT.
 ...
PMID:Effect of 5-hydroxytryptamine on blood glucose and cyclic AMP in the rat. 4 Oct 61

To elucidate the importance of cholinergic innervation for pancreatic beta-cells in vivo, atropine sulphate (0.2 mg/kg body weight) was subcutaneously injected into mice 4 times a day for 10 days. Control animals received 0.9% NaCl. Paraffin sections of the pancreas were stained for beta-cells with aldehyde fuchsin and for alpha-cells (glucagon cells) with silver according to Grimelius. Endocrine and exocrine cell nuclei were measured with an ocular screw micrometer. The light absorbance at 550 nm wave-length of aldehyde-fuchsin-stained islet sections was measured with a microscope photometer. Atropine caused no loss of body weight or apparent food consumption. The nuclei of beta-cells shrank significantly in response to atropine; A550 of islet surfaces showed a significant negative correlation to beta-cell nuclear size. Acinar cell nuclei near islets also became smaller after atropine treatment but to a lesser extent. No such change was observed in the alpha-cells. A trophic influence of the vagal nerve may be important for the long-term control of beta-cell function.
 ...
PMID:Are pancreatic beta-cells under vagal control? 8 61

Toxin from the scorpion Leiurus quinquestriatus was used to release norepinephrine from sympathetic nerve endings in the perfused rat pancrease. Addition of toxin, 10 mug./ml., to perfusate containing 0.3 mg./ml. glucose caused a large increase in release of norepinephrine and glucagon. Glucagon secretion was suppressed by perfusate containing 3.0 mg./ml. glucose but still responded to stimulation with scorpion toxin. Atropine, 10 muM, had no effect on either norepinephrine or glucagon release in response to scorpion toxin. The release of glucagon was blocked by 100 muM propranolol, 10 muM phentolamine, or 30 muM phenoxybenzamine. Somatostatin, 55nM, did not affect the release of norepinephrine by scorpion toxin but totally inhibited the glucagon response. These results suggest that pharmacologic stimulation of the adrenergic nerve endings in the rat pancreas can elicit a rapid release of glucagon. This response can be prevented by appropriate concentrations of either alpha or beta adrenergic blocking agents or somatostatin.
 ...
PMID:Stimulation of glucagon secretion by scorpion toxin in the perfused rat pancreas. 78 80

The vasoactive effects of cholecystokinin-octapeptide (CCK-OP), pentagastrin, synthetic secretin, glucagon, and acetylcholine were assessed in the intestinal circulation of the dog. In pharmacologic doses of glucagon, CCK-OP, and, to a lesser degree, pentagastrin significantly increased blood flow and oxygen consumption. Atropine blocked the vasodilator effects of CCK-OP, pentagastrin, and acetylcholine but did not block those of glucagon. Neither the alpha-adrenergic blocker, phenoxybenzamine, nor the beta-adrenergic blocker, propranolol, blocked the vasodilator response to pentagastrin. Synthetic secretin had no significant effect on either blood flow or oxygen consumption in the intestinal segment. The vasodilator response to CCK-OP and pentagastrin appears to be mediated specifically through cholinergic receptors.
 ...
PMID:Pharmacologic effects of gastrointestinal hormones on intestinal oxygen consumption and blood flow. 116 16

Studies on the mechanism of the hypoglycemia caused by the i.t. administration of morphine (40 micrograms) to nonfasted, unanesthetized mice included assessment of effects of i.t. morphine on circulating levels of immunoreactive insulin and glucagon, on body temperature, as well as testing the effects of i.p. pretreatment with antagonists of cholinergic, beta adrenergic, alpha-1 adrenergic, alpha-2 adrenergic, serotonergic and opioid receptors. Serum levels of insulin were not significantly affected at 30 and 60 min after i.t. morphine, but plasma glucagon levels were significantly increased at both time points. Rectal temperature decreased significantly in mice given either saline or morphine i.t., but there was no significant difference between the two groups over time. Atropine (2 mg/kg), propranolol (10 mg/kg), prazosin (2 mg/kg) and methysergide (2 mg/kg) did not affect morphine-induced hypoglycemia. Naloxone (20 mg/kg) antagonized i.t. morphine. Mecamylamine (2 mg/kg) produced a moderate hypoglycemia in control mice, which appeared to be additive to that caused by i.t. morphine. Yohimbine (1-4 mg/kg i.p.) also produced a moderate hypoglycemia in control mice, but caused a dose-related antagonism of i.t. morphine. The centrally active alpha-2 antagonist, L-657,743 (2S-trans)-1,3,4,5',6,6',7,12b-octahydro-1',3'-dimethylspiro -(2H-benzofuro- (2,3-a)quinolizine-2,4'(1'H)pyrimidin)-2-(3'H)-one hydrochloride) (4-20 mg/kg i.p.), but not the peripherally selective alpha-2 antagonist, L-659,066 (2R-trans)-N-(2-(1,3,4,6,7,12b-he xahydro-2'- oxospiro(2H-benzofuro(2,3-a) quinolizine-2,4-imidazolidin)-3'-yl)ethyl)methanesulfonamide hydrochloride) (4-20 mg/kg i.p.), caused a dose-related antagonism of i.t. morphine. The i.t. coadministration of yohimbine (2 or 10 micrograms) or L-659,066 (10 micrograms) with morphine exhibited no antagonism.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:An insulin-independent mechanism of intrathecal morphine-induced hypoglycemia in mice: mediation through a central alpha-2 adrenergic pathway. 167 29

To determine whether hyperinsulinaemia of human obesity is dependent on the activity of the parasympathetic nervous system, and whether activation of the parasympathetic nervous system plays a role in glucose-induced thermogenesis, the metabolic effect of a continuous intravenous glucose infusion [44.4 mumol kg-1 body weight (bw) min-1] with or without atropine infusion was assessed in 11 obese patients and 10 lean controls. Compared with lean controls, obese patients had increased basal and glucose-stimulated plasma insulin and C-peptide concentrations and increased plasma glucose concentrations during glucose infusion. Glucose oxidation during i.v. glucose was lower in obese patients than in lean controls. Glucose-induced thermogenesis was similar in obese patients and in lean controls. Atropine infusion did not affect basal plasma glucose, insulin or free fatty acid concentrations nor glucose-stimulated plasma glucose, insulin, C-peptide, glucagon or free fatty acid concentrations in both groups of subjects. Glucose and lipid oxidation rates and glucose-induced thermogenesis were also unaffected by atropine administration. It is concluded that (1) glucose-stimulated hyperinsulinaemia in human obesity is not dependent on a hyperactivity of the parasympathetic nervous system, which indicates that human obesity is different from most animal models of obesity; (2) glucose-induced thermogenesis is similar in obese and lean subjects when a similar load of glucose is administered; (3) inhibition of the parasympathetic nervous system does not affect the thermic effect of i.v. glucose.
 ...
PMID:Effects of muscarinic blockade on insulin secretion and on glucose-induced thermogenesis in lean and obese human subjects. 177 22

We previously reported that neostigmine injected into the third cerebral ventricle stimulated adrenal secretion of epinephrine, secretion of glucagon from the pancreas, and direct neural innervation of the liver, resulting in hepatic venous plasma hyperglycemia in anesthetized fed rats. However, receptor type of these 3 mechanisms is not known. Therefore, we examined the effects of intraventricularly injected cholinergic or adrenergic antagonists on neostigmine-induced catecholamines in intact rats, glucagon secretion which is mediated by direct neural innervation of pancreas in bilateral adrenalectomized (ADX) rats, and hepatic venous hyperglycemia which is mediated by direct neural innervation of liver in ADX rats receiving constant infusion of somatostatin from femoral vein. Atropine injected into the third cerebral ventricle suppressed epinephrine secretion and dose-dependently inhibited hepatic venous hyperglycemia induced by neostigmine in intact rats. The neostigmine-induced glucagon secretion which occurs in ADX rats was suppressed by atropine. Atropine also prevented the neostigmine-induced hyperglycemia in ADX rats receiving constant somatostatin infusion through femoral vein (ADX-Somato rats). On the other hand, phentolamine, propranolol and hexamethonium showed no significant inhibitory effect on neostigmine-induced hyperglycemia, epinephrine and glucagon secretion in intact rats, glucagon secretion in ADX rats, or hyperglycemia in ADX-Somato rats. These results suggest that neostigmine-induced epinephrine and glucagon secretion and increased hepatic glucose output stimulated by direct neural innervation to liver is mediated by central muscarinic receptor in fed rats.
 ...
PMID:Neostigmine-induced hyperglycemia is mediated by central muscarinic receptor in fed rats. 233 69

Pancreatic hormone release is generally thought to be regulated through adrenergic as well as muscarinic receptors. We have previously observed possible nicotinic involvement in insulin release. In the present study, we incubated isolated rat islets for 60 min with various concentrations of atropine (a muscarinic receptor blocker), alpha-bungarotoxin (alpha-Btx, a nicotinic receptor blocker), and anti-acetylcholine receptor antibody (IgG) (anti-Ach.R.Ab) obtained from a patient with myasthenia gravis. Atropine suppressed insulin release, and alpha-Btx and anti-Ach.R.Ab potentiated it; atropine did not suppress glucagon release, while alpha-Btx and anti-Ach.R.Ab raised it. None of these agents influenced somatostatin release. These observations suggest that muscarinic as well as nicotinic receptors influence insulin release, as nicotinic receptors do glucagon release. Neither nicotinic nor muscarinic receptors seem to regulate somatostatin release.
 ...
PMID:Participation of nicotinic receptor in hormone release from isolated rat islets of Langerhans. 256 21

Neonatal mice, under fasting conditions, are susceptible to the development of lesions in the arcuate nucleus (AN) of the hypothalamus, with high doses of monosodium L-glutamate (MSG). Feeding of nutrients (e.g., sugars and L-amino acids) has been shown to have a protective effect against the development of these lesions. The purpose of these studies was to elucidate the mechanism of this protective effect. Histopathologic examination of lesions of the AN demonstrated that feeding of weaning mice before subcutaneous administration of toxic doses of MSG suppressed the development of these lesions, as compared to fasted controls. Similarly, the number of necrotic cells in the AN of neonates administered toxic doses of MSG subcutaneously was reduced when D-glucose and L-arginine were administered orally. Atropine obliterated the protective effect of D-glucose. Pretreatments consisting of gastric inhibitory polypeptide (GIP) + oral D-glucose had a protective effect of higher potency than GIP alone. Pretreatments with insulin, anorexigenic peptide (pyroGlu-His-Gly), cholecystokinin, glucagon, bombesin, and substance P (in decreasing order of effectiveness) demonstrated a protective effect against the AN lesion in neonates, whereas somatostatin and beta-endorphin had no effect. Results suggest that the protective effect of nutrients may in part be due to the stimulation of peptide hormone release during the postabsorptive phase. It is postulated that the effect of entero-pancreatic hormone, especially insulin, is to enhance the tolerance of AN neurons of neonatal mice to the toxic dose of L-glutamate.
 ...
PMID:Mealing and related hormone release suppress hypothalamic lesions of neonatal mice by L-glutamate. 288 96

In an attempt to assess pancreatic glucagon's efficacy at repeatedly reducing food ingestion during differing circadian periods, three groups of 8 rats each were randomly assigned to 4-hr food deprivations beginning at 0800, 1200 or 1600 with light off at 2000. Subjects were then refed following injections of pancreatic glucagon (400 micrograms/kg b.wt. dissolved in DMSO) or vehicle alone every third day (no injection on intervening day). Food intake was measured at 1 and 20 hr following each injection. Following 3 cycles of the above procedure, each animal was again food deprived at the appropriate time, stunned and sacrificed by decapitation. The liver was sampled and glycogen determinations were made. Glucagon suppressed food intake when injected at 1200 (49.6%) and at 1600 (43.1%) but not when given at 2000 (-2.2%). Glycogen content measured after similar deprivation ending at these times was 5.6, 3.9 and 2.0%, respectively. With repeated glucagon injections, the hormone lost its ability to reduce food intake. In a second study, designed to evaluate the role of insulin in glucagon's action, three groups of 6 rats each were given atropine plus glucagon or glucagon or atropine injections alone; food ingestion was then measured one hr later. Atropine alone somewhat decreased eating, however, in combination with glucagon (given 10 min following atropine), no significant decrements in ingestion were achieved. Glucagon injected after saline produced a significant reduction in food intake (62.5%). Since glucagon stimulates insulin release and hyperglycemia; perhaps insulin release is necessary for glucagon's satiety effect.
 ...
PMID:Glucagon, satiety from feeding and liver/pancreatic interactions. 377 54


1 2 3 4 Next >>