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:3.1.1.8 (cholinesterase)
12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 20 patients who underwent open-heart surgery, the plasma concentrations of glucose, insulin, glucagon, growth hormone, free hemoglobin, and cholinesterase were measured before, during and after pulsatile and continuous perfusion. Pulsatile flow was achieved by modification of a roller pump to effect rapid acceleration and slowing. The driving motor was interfaced with a control module to enable ECG-triggered perfusion. In addition to the clinical studies, investigations were performed in 9 dogs to assess the effects of pulsatile and continuous perfusion on liver and pancreas flow during total bypass. During pulsatile perfusion there was a significant increase in insulin which, however, was clearly diminished in relation to glucose levels. The response of the beta-cells was markedly more compromised after continuous than pulsatile perfusion. The secondary postoperative increase in insulin can be accounted for by intravenous administration of glucose and, particularly, after pulsatile perfusion, indicates an almost completely normal response of pancreatic beta-cells. As opposed to the effects of continuous perfusion, the low glucose, glucagon, and growth hormone levels, the insulin increase during and after pulsatile perfusion as well as normal cholinesterase values observed in association with pulsatile perfusion appear to be the result of improved pancreatic and hepatic function. This contention is supported by the experimental finding of significantly increased pancreas and liver perfusion during pulsatile perfusion.
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PMID:[Clinical and experimental studies on pulsatile and continuous flow during extracorporeal circulation (author's transl)]. 700 92

Obesity is often associated with coronary heart disease and metabolic disorders. In this study, the relationship between obesity and metabolic disorders and between obesity and fatty liver by ultrasonography was investigated in 307 university students (18-20 years old, men: 196, women; 111). The correlation between Body Mass Index (BMI) and the thickness of subcutaneous fat (ST) was significant between BMI and the ratio between waist and hip circumference (WHR) was more significant in male students (r = 0.838, p < 0.001) than in female students (r = 0.639, p< 0.001). The incidence of fatty liver was significantly higher in male obese students (68.6%) than in female obese students (27.3%). After adjustment for BMI, ST, WHR and sigma glucose, the mean values for serum transaminase, cholinesterase, total cholesterol, uric acid, fasting plasma insulin and sigma insulin were significantly higher in male obese students with fatty liver than in male obese students without fatty liver. The present study suggested that male obese students with fatty liver are more likely to have metabolic disorders than male obese students without fatty liver.
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PMID:[Fatty liver and obesity in university students]. 747 66

Injury and stress are accompanied by a characteristic hormonal response and altered energy utilisation. Hyperglycaemia and negative nitrogen (N) balance are the leading symptoms of the metabolic changes in the post-operative state. In a prospective, randomised study the efficacy and metabolic effects of glucose-xylitol (GX) 35% (1:1) versus glucose (G) 40% were investigated in patients undergoing major surgery. METHOD. Twenty-four patients undergoing abdomino-thoracic oesophageal cancer surgery were treated in a standardised manner. Total parenteral nutrition was administered over 6 days (kg body wt.-1/day): day of surgery 1-1.25 g carbohydrate (CH); 1st postoperative day (POD) 1.5 g CH, 1 g amino acids (AA); 2nd POD 3 g CH, 1.5 g AA, 1.0 g fat; from 3rd POD 3 g CH, 1.5 g AA, 1.5 g fat (CH GX35% (n = 12) or G40% (n = 12), AA Intrafusin 15%, fat Intralipid 20%). Daily and cumulative N balances, blood-G profiles, blood chemistry, and physical parameters were determined. Glucagon and insulin profiles, CH losses, and oxalic acid secretion were measured. RESULTS. Both groups were comparable for age, body mass index, clinical and physical parameters, and blood chemistry. Mean cumulative N balances after 6 days were -12.0 +/- 16.3 g N for GX35% and -5.6 +/- 19.4 g N for G40% (n.s.; Wilcoxon, P < 0.05). Blood G was similar for both groups with values ranging from 130 to 240 mg/dl on the day of surgery and below 150 mg/dl on the consecutive days. In each group 1 patient needed additional insulin therapy. Glucagon and insulin levels did not show a significant difference between the groups. CONCLUSION. No difference in tolerance and efficacy of nutritional support by GX versus G at a dose of 3 g.kg body wt.-1.d in oesophagectomised patients could be observed. Similar blood G profiles were in accordance with comparable glucagon and insulin levels. Because of the high standard deviations of N balances, differences in efficacy could not be proven. A significantly lower level of pseudocholinesterase (PCHE) for G40% on day 7 might indicate enhanced hepatic protein synthesis in the GX group.
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PMID:[Glucose-xylitol 35% (1:1) versus glucose 40%. Effectiveness and metabolic effects after major surgery]. 797 78

1. The activity of serum butyrylcholinesterase ('pseudocholinesterase', EC3.1.1.8) was investigated in 56 patients with type 1 diabetes mellitus, 51 patients with type 2 diabetes mellitus and 101 healthy control subjects. 2. Butyrylcholinesterase activity was significantly elevated in both type 1 (8.10 +/- 3.35 units/ml) and type 2 (7.22 +/- 1.95 units/ml) diabetes compared with the control subjects (4.23 +/- 1.89 units/ml) (P < 0.001). 3. In the patients with type 1 and type 2 diabetes, serum butyrylcholinesterase activity was correlated with log serum fasting triacylglycerol concentration (r = 0.41 and r = 0.43, respectively, P < 0.001). In the type 2 population serum butyrylcholinesterase activity was also correlated with insulin sensitivity (r = -0.51, P < 0.001). 4. Serum butyrylcholinesterase activity was unrelated to age, gender, serum gamma-glutamyltranspeptidase activity, body mass index, or treatment for diabetes in both the diabetic populations. 5. In 37 non-diabetic patients with butyrylcholinesterase deficiency serum triacylglycerol levels were in the normal range. 6. These results are consistent with the view that butyrylcholinesterase may have a role in the altered lipoprotein metabolism in hypertriglyceridaemia associated with insulin insensitivity or insulin deficiency in diabetes mellitus.
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PMID:Relationship between serum butyrylcholinesterase activity, hypertriglyceridaemia and insulin sensitivity in diabetes mellitus. 814 99

The osmotic effect of intravenous glucose was investigated in eight healthy volunteers. Increases in plasma glucose can induce water movement from the intracellular to the extracellular space. Serum choline esterase was used as an endogenous marker of serum dilution. Intravenous tests with 5, 15, 30 and 35 g of glucose showed that the water shift was proportional to the amount infused. The respective dilutions of choline esterase were 1.3 +/- 0.7%, 3.3 +/- 0.9%, 6.3 +/- 0.8% and 7.8 +/- 0.5%. The effect on extracellular water was maintained when plasma glucose remained elevated (inhibition of insulin secretion with a somatostatin analogue). In comparison to glucose, infusion of 10 g of a mixture of amino acids produced a less pronounced effect than expected. The acute water shift after intravenous glucose dilutes serum components including glucose (8% of total extracellular glucose at 35 g). This can be misinterpreted as glucose clearance when calculating metabolic rates. For estimated amounts a proportional correction should be made (3.5% per 5 mmol l-1 increase). A measured plasma glucose of 22.2 mmol l-1 should be corrected to 24.8 mmol l-1, while a plasma glucose value of 5.0 mmol l-1 needs no correction.
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PMID:Glucose-induced water movement from the intracellular to the extracellular space and its influence on calculations of glucose metabolism. 835 32

Accuracy in measurement of plasma free fatty acids (FFA), and therefore prevention of the in vitro lipolysis, is a crucial step to understand the physiologic role of plasma FFA and their relationships in the pathogenesis of important metabolic disorders such as central obesity, insulin resistance, and diabetes mellitus. As lipoprotein triglyceride-fatty acids are elevated in these states, in vitro lipolysis of triglycerides may artifactually increase FFA. Plasma FFA were measured in subjects before and after heparin administration, under different experimental conditions affecting the in vitro activity of lipoprotein lipase (LPL) and hepatic lipase (HL). Paraoxon, a cholinesterase inhibitor neurotoxin known to block plasma lipolytic activity, and preextraction timing and temperature of collection were tested. Paraoxon was required to prevent triglyceride hydrolysis in: a) preheparin plasma allowed to stand at room temperature (21 degrees C) for 2 h, before being frozen at -20 degrees C (FFA = 1817 +/- 291 vs. 698 +/- 66 microEq/l, P < 0.005, mean +/- SEM, without and with paraoxon, respectively); and b) in postheparin plasma immediately stored at -20 degrees C (FFA = 2682 +/- 357 vs. 1299 +/- 150 microEq/l, P < 0.005, without and with paraoxon, respectively). No difference in the FFA level was found in preheparin plasma collected either with or without paraoxon when: a) the samples were placed in ice and immediately assayed; b) the specimens were immediately frozen at -70 degrees C and assayed 60 days later.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analysis of techniques to obtain plasma for measurement of levels of free fatty acids. 835 49

In patients with hyperlipaemia, serum paraoxonase activities were polymodally distributed with 75% individuals in the low activity mode. In the same patients the distribution of serum cholinesterase activities was unimodal, but asymmetrical. Patients with impaired glucose tolerance or non-insulin-dependent diabetes mellitus had slightly higher cholinesterase activities than patients with hyperlipaemia only.
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PMID:Serum paraoxonase and cholinesterase activities in individuals with lipid and glucose metabolism disorders. 839 41

1. Diabetic modifications of nicotinic receptor-operated noncontractile Ca2- mobilization observed in the presence of anticholinesterase were investigated by measuring Ca(2+)-aequorin luminescence in diaphragm muscles of mice with diabetes induced by injections of streptozotocin (150 mg kg-1, bolus i.v.) and alloxan (85 mg kg-1, bolus i.v.). 2. The diabetic state accelerated the decline of noncontractile Ca2+ transients without affecting their peak amplitude. Insulin treatment reversed this alteration. 3. The increase in contractile Ca2+ transients by cholinesterase inhibition was attenuated 0.6 fold and became resistant to changes in [Ca2+]o in the diabetic state. 4. Changes in extracellular pH from 7.6 to 5.6 depressed the peak amplitude of noncontractile Ca2+ transients without affecting their duration, and enhanced the peak amplitude of contractile Ca2+ transients. 5. These results suggest that the inactivation process of noncontractile Ca2+ mobilization is promoted in diabetic muscles, presumably by desensitization of the nicotinic acetylcholine receptor.
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PMID:Diabetic state-induced rapid inactivation of noncontractile Ca2+ mobilization operated by nicotinic acetylcholine receptor in mouse diaphragm muscle. 859 Sep 90

There are data indicating that cholinergic activity is precociously impaired in Down's syndrome (DS). On the other hand, acetylcholine as well as arginine (ARG) play a major stimulatory role in the neural control of growth hormone (GH) secretion in humans, likely acting via the inhibition of hypothalamic somatostatin release. The aim of the present study was to verify the effects of pyridostigmine (PD, 120 mg p.o.), a cholinesterase inhibitor, and ARG (0.5 g/kg i.v.) on the growth hormone-releasing hormone (GHRH) (1 microgram/kg i.v.)-induced GH rise in 15 adult patients with DS (M/F: 8/7; age 26.5 +/- 2.2 years; body mass index, BMI: 25.7 +/- 1.0 kg/m2) in which the potentiating effect of PD on GH secretion has been reported to be reduced. The results in DS were compared to those in 15 normal subjects (NS) (M/F: 8/7; age: 30.0 +/- 1.3 years; BMI: 21.4 +/- 0.4 kg/m2). Basal GH and insulin growth factor I (IGF-1) levels in DS (1.8 +/- 0.7 and 206.5 +/- 21.0 micrograms/l) were similar to those in NS (1.4 +/- 0.3 and 179.4 +/- 11.0 micrograms/l). The GH response to GHRH alone in DS (526.5 +/- 120.1 micrograms/l/h) was lower (p < 0.05) than that recorded in NS (895.4 +/- 153.7 micrograms/l/h). The GHRH-induced GH rise was potentiated by PD both in DS (1,138 +/- 184.2 micrograms/l/h; p < 0.02 vs. GHRH alone) and in NS (2,213.8 +/- 212.8 micrograms/l/h; p < 0.005 vs. GHRH alone); however, as the percent potentiating effect of PD was similar in both groups (215 and 247%, respectively) the GH response to GHRH + PD in DS was lower (p < 0.005) than that in NS. The GHRH-induced GH rise was also potentiated by ARG in both DS (2,243 +/- 362.4 micrograms/h; p < 0.001 vs. GHRH alone) and NS (2,764.3 +/- 325.7 micrograms/l/h; p < 0.005 vs. GHRH alone). As the percent potentiating effect of ARG in DS was more marked than in NS (425 vs. 308%, respectively), the GH response to GHRH + ARG became similar in both groups. No sex-related difference was found in the GH response to various stimuli both in DS and NS. In conclusion, these data demonstrate that the potentiating effect of PD but not that of ARG is impaired in adults with DS in whom a reduced somatotrope responsiveness to GHRH is present. These findings indicate that in DS the pituitary GH releasable pool is fully preserved while an impairment of the tuberoinfundibular cholinergic pathways could lead to somatostatinergic hyperactivity and low somatotrope responsiveness to GHRH.
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PMID:Further evidence of cholinergic impairment of the neuroendocrine control of the GH secretion in Down's syndrome. 952 98

ICA69 is a diabetes autoantigen with no homologue of known function. Given that most diabetes autoantigens are associated with neuroendocrine secretory vesicles, we sought to determine if this is also the case for ICA69 and whether this protein participates in the process of neuroendocrine secretion. Western blot analysis of ICA69 tissue distribution in the mouse revealed a correlation between expression levels and secretory activity, with the highest expression levels in brain, pancreas, and stomach mucosa. Subcellular fractionation of mouse brain revealed that although most of the ICA69 pool is cytosolic and soluble, a subpopulation is membrane-bound and coenriched with synaptic vesicles. We used immunostaining in the HIT insulin-secreting beta-cell line to show that ICA69 localizes in a punctate manner distinct from the insulin granules, suggesting an association with the synaptic-like microvesicles found in these cells. To pursue functional studies on ICA69, we chose to use the model organism Caenorhabditis elegans, for which a homologue of ICA69 exists. We show that the promoter of the C. elegans ICA69 homologue is specifically expressed in all neurons and specialized secretory cells. A deletion mutant was isolated and found to exhibit resistance to the drug aldicarb (an inhibitor of acetylcholinesterase), suggesting defective neurotransmitter secretion in the mutant. On the basis of the aldicarb resistance phenotype, we named the gene ric-19 (resistance to inhibitors of cholinesterase-19). The resistance to aldicarb was rescued by introducing a ric-19 transgene into the ric-19 mutant background. This is the first study aimed at dissecting ICA69 function, and our results are consistent with the interpretation that ICA69/RIC-19 is an evolutionarily conserved cytosolic protein participating in the process of neuroendocrine secretion via association with certain secretory vesicles.
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PMID:The diabetes autoantigen ICA69 and its Caenorhabditis elegans homologue, ric-19, are conserved regulators of neuroendocrine secretion. 1102 35


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