Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.7 (acetylcholinesterase)
28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin release is influenced by the autonomic nervous system. Regarding parasympathetic control, previous reports have shown that regulation of insulin release is executed exclusively through muscarinic receptors in the pancreatic islets. In the present study, however, we examined the effect on insulin release at the islet level of various agents affecting the parasympathetic nervous system, especially nicotinic receptor blockers. Pancreatic islets isolated from adult Wistar male rats were incubated with these agents and insulin release in the media was measured. Acetylcholine chloride (10(-5) M), as well as distigmine bromide (10(-6), 10(-5) M), both of which are cholinesterase inhibitors, stimulated insulin release, whereas atropine (5 x 10(-6), 5 x 10(-5) M) suppressed it. On the other hand, serum and IgG from myasthenia gravis patients, containing anti-acetylcholine receptor antibodies, affected insulin release, and alpha-bungarotoxin (10(-9)-10(-7) M), a nicotinic receptor blocker, stimulated insulin release dose-dependently. The present observations suggest that insulin release is influenced by the parasympathetic nervous system, mediated via not only muscarinic but also nicotinic receptors.
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PMID:Possible involvement of cholinergic nicotinic receptor in insulin release from isolated rat islets. 197 Dec 10

Diagnostic electrocardiostimulation (ECS) of the right atrium with evaluation of the functional state of the heart conduction system and coronary reserve was carried out in 177 patients. The level of blood catecholamines, activity of cholinesterase and content of destroyed acetylcholine, cortisol, free fatty acids, glucose, insulin, thyroxine, triiodothyronine, renin, testosterone, calcium was determined before and at the height of diagnostic ECS. In cases with a tendency to bradycardia one could note compensatory tension of the sympathetic-adrenal system and mechanisms of general adaptation. In organic weakness of the sinus node with stable bradysystole there were signs of exhaustion of the adrenal reserves of catecholamines and cortisol manifested in paradoxic reduction of them in the blood in response to frequent ECS and corresponding changes of energy provision.
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PMID:[The neurohumoral regulation and energy support of the myocardium in patients with heart rhythm disorders]. 197 44

Despite the fact that the significance of red cell membrane acetylcholinesterase (AChE) is unknown, this enzyme of red cell assumes importance since many of its properties have been found to be similar to purified enzyme form of brain tissues. Our investigations on the effect of insulin-dependent diabetes mellitus on red cell AChE revealed that the activity of this enzyme is significantly decreased in diabetes. Insulin treatment restored the activity to the normal level. Solubilization of normal, diabetic and insulin treated diabetic red cell membranes with Triton X-100 (0.2% v/v) caused a general decline in AChE activity, however the per cent decline in activity of diabetic enzyme was lower as compared to normal and insulin treated conditions. From our results it is inferred that the decreased red cell AChE activity in diabetes is due to lesser number of active enzyme molecules and also due to altered membrane microenvironment.
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PMID:Regulation of red cell acetylcholinesterase activity in diabetes mellitus. 219 39

RT6 is an unusual cell membrane protein that is expressed exclusively by postthymic T cells. The inherent defect in its expression has been correlated to lymphopenia and genetically determined susceptibility for insulin-dependent diabetes mellitus in the rat. We report here the primary structure of the RT6.2 alloantigen as deduced from the cDNA sequence. The predicted amino acid sequence of RT6.2 begins with a conventional leader of 20 amino acids and ends in a hydrophobic C-terminal extension peptide of 29 amino acids as is common for phosphatidylinositol-anchored proteins. Native RT6.2 is predicted to comprise 226 amino acids, with a calculated Mr of 26,036. Four cysteine residues account for two intrachain disulfide bonds. The sequence lacks potential N-glycosylation sites and contains an excess of positively charged residues. Homology searches in protein sequence data banks suggest that RT6.2 is not encoded by a member of the immunoglobulin supergene family. Moreover, these analyses did not reveal any close homologies of RT6.2 to known proteins: the highest homology found was 21.2% identity in a 52-amino acid overlap to the torpedo acetylcholinesterase precursor. Southern blot analyses indicate that RT6.2 is the product of a single-copy gene and provide evidence for closely related genes in the mouse and other species. The corresponding gene products remain to be identified.
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PMID:Primary structure of rat RT6.2, a nonglycosylated phosphatidylinositol-linked surface marker of postthymic T cells. 230 May 88

Primary cultures of hippocampal neurons are important for the study of trace elements in epileptogenesis. We developed a model system for culturing hippocampal neurons on poly-L-lysine in Iscove's modification of Dulbecco's MEM (IMDM) supplemented with K+, D-glucose, glutamine, insulin, p-amino benzoic acid, transferrin, BSA, beta-estradiol, gentamycin, and fungizone. Neurons were identified by histochemical staining for cholinesterase. Zinc at concentrations of 10(-9) to 10(-6) M induced metallothionein in hippocampal neuronal cultures. Maximum metallothionein induction occurred after 48 hrs incubation with zinc.
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PMID:Metallothionein induction in rat hippocampal neurons in primary culture. 251 54

This study investigated the relationship between central cholinergic neurons and insulin secretion in bilateral adrenalectomized fed rats. Neostigmine (a cholinesterase inhibitor, 5 x 10(-8) mol) administered into the third cerebral ventricle produced significant increases in hepatic venous plasma insulin and glucose concentrations, whereas i.v. injection of the same dose of neostigmine did not. Prior acute subdiaphragmatic vagotomy or i.p. pre-injection with methylatropine (10(-8) mol) completely prevented the neostigmine-induced rise in plasma insulin concentration. Intraperitoneal pretreatment with hexamethonium (5 x 10(-8) mol) also significantly reduced the plasma insulin response. These peripheral pretreatments did not change the plasma glucose response to neostigmine. Intraventricular co-administration of 10(-9) mol methylatropine, a dose that was ineffective when pre-injected i.p., eliminated the plasma insulin and glucose responses to neostigmine, whereas hexamethonium (5 x 10(-8) mol) had no influence on either response to neostigmine. These observations suggest that stimulation of central cholinergic-muscarinic neurons with third cerebral ventricular injection of neostigmine results in vagally mediated insulin secretion in bilateral adrenalectomized fed rats.
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PMID:Vagally mediated insulin secretion by stimulation of brain cholinergic neurons with neostigmine in bilateral adrenalectomized rats. 257 Jun 20

Right atria from rats rendered diabetic by injection of streptozocin (STZ-D) for 8-10 wk are supersensitive to the negative chronotropic effects of muscarinic agonists but have decreased levels of muscarinic receptors and acetylcholinesterase activity. Insulin treatment completely prevents the development of these changes. The proportion of atrial muscarinic receptors displaying high-affinity agonist binding is lower in STZ-D rats; however, the sensitivity of high-affinity agonist binding to regulation by a guanine nucleotide (5'-guanylylimidodiphosphate) is greater in atria from diabetic rats. Again, insulin treatment eliminates these differences. These findings indicate that alterations in atrial muscarinic systems in STZ-D rats are a consequence of the elaboration of the diabetic state and suggest that an alteration of functional muscarinic receptor-G protein coupling contributes to the altered physiological responsiveness of the heart in diabetes.
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PMID:Insulin prevention of altered muscarinic receptor-G protein coupling in diabetic rat atria. 257 55

The concentrations of acetylcholine (ACh) as a parasympathetic marker and norepinephrine (NE) as a sympathetic marker were investigated in the hearts of rats 2, 4, and 8 wk after the induction of diabetes by an injection of streptozocin (STZ; 65 mg/kg i.v.). ACh and NE were measured by high-performance liquid chromatography with electrochemical detection. Diabetic rats showed low body weight and heart weight at 2, 4, and 8 wk and higher heart-to-body weight ratio and bradycardia at 8 wk, almost all of which were normalized after insulin treatment. Myocardial ACh and NE concentrations in the diabetic rats at 2 and 4 wk were not significantly different from those in age-matched control rats. However, ACh and NE concentrations in the diabetic rats at 8 wk significantly increased compared with the control rats. Diabetic rats at 8 wk also had increased myocardial choline concentration and choline acetyltransferase activity and decreased acetylcholinesterase activity. Insulin treatment normalized all of these changes in the diabetic rats. Thus, in STZ-induced diabetes (STZ-D), the concentrations of both cholinergic and noradrenergic neurotransmitters in the myocardium increased. The results of this study confirm a previously reported increase in sympathetic activity to the heart and also indicate that there is an increase in the synthesis and a decrease in the metabolism of ACh in STZ-D and that adequate insulin treatment normalizes these changes.
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PMID:Altered acetylcholine and norepinephrine concentrations in diabetic rat hearts. Role of parasympathetic nervous system in diabetic cardiomyopathy. 264 43

Examinations of different patients with duodenal ulcer performed during one year revealed seasonal changes in the function of the regulatory systems. Secretion of histamine, serotonin, insulin, and hydrocortisone was increased in spring and reduced in autumn. Secretion of adrenalin, noradrenalin and acetylcholinesterase activity were high in summer and low in autumn. The acid-producing function of the stomach did not depend on the season. It is suggested that deviations in the activity of the regulatory systems in spring and autumn may cause seasonal exacerbations of duodenal ulcer.
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PMID:[Seasonal changes in the regulatory systems in duodenal ulcer]. 265 93

1. The erythrocyte membrane acetylcholinesterase activity is significantly (P less than 0.001) decreased in insulin-dependent diabetes mellitus. 2. The activity is negatively correlated (r = -0.97) with the fasting blood glucose level. 3. Insulin treatment restores the activity to normal. 4. The Km of the enzyme for acetylthiocholine iodide was unchanged; however, the Vmax. was decreased, suggesting a decrease in the number of active enzyme molecules in diabetes.
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PMID:Erythrocyte membrane acetylcholinesterase in type 1 (insulin-dependent) diabetes mellitus. 265 81


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