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)

Time and feeding influences on cholesterol, triglyceride, glucose and insulin levels, and serum cholinesterase activity were assessed in a genetically-hyperlipidemic hyperphagic obese rat model, and compared with its lean litter-mate. Following a 28-day acclimation to a 12-hr light/dark cycle, blood samples were obtained every 2 hr from rats via tail bleed for a 24-hr period. Synchronization with other animal studies was established by endogenous serum cortisol levels [acrophase 18-20 hr after light onset (HALO) in both groups]. Triglycerides cholesterol, insulin and glucose levels were significantly elevated in obese versus lean rats. Obese rats were observed to feed throughout the 24-hr cycle, whereas lean litter-mates ate only during the dark cycle. No circadian rhythmicity was found in glucose levels with either rat group. Insulin levels were not correlated. Although triglyceride levels peaks at 13 HALO in lean rats, no pattern was observed in obese rats. Cholesterol levels were unchanged with time in either group. Cholinesterase activity followed a circadian rhythm in the lean, but not obese, rats with an acrophase estimated at 8 HALO. In contrast to previous reports, enzyme activity was not correlated with triglyceride levels in either rat group. Circadian similarities in insulin levels between rat groups suggest changes in insulin metabolism and/or secretion which are likely to be independent of feeding or activity. Conversely, triglyceride levels remained elevated throughout the 24-hr period in obese rats, whereas significant increases were observed in lean rats during the dark active cycle. These data suggest that triglyceride levels, and not insulin and cholesterol levels, are most likely dependent on feeding patterns.
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PMID:Circadian assessment of lipids in the hyperphagic obese rat compared with lean litter-mates. 268 Jan 23

Many of the drugs used in anesthesia and intensive care may cause blockade of the central cholinergic neurotransmission. Acetylcholine is of significance in modulation of the interaction among most other central transmitters. The clinical picture of the central cholinergic blockade, known as the central anticholinergic syndrome (CAS), is identical with the central symptoms of atropine intoxication. This behaviour consists of agitation including seizures, restlessness, hallucinations, disorientation or signs of depression such as stupor, coma and respiratory depression. Such disturbances may be induced by opiates, benzodiazepines, phenothiazines, butyrophenones, ketamine, etomidate, propofol, nitrous oxide, and halogenated inhalation anesthetics as well as by H2-blocking agents such as cimetidine. There is an individual predisposition for CAS--but unpredictable from laboratory findings or other signs. Reports of postanesthetic occurrence of the CAS requiring treatment are not unanimous, varying between 1 and 40%. Differential diagnosis of the CAS includes disorders of glucose and electrolyte metabolism, severe hormonal imbalance, respiratory disorders (hypoxia, hypercarbia), hypothermia, hyperthermia and neuropsychiatric diseases (cerebral hypoxia, stroke, catatony, acute psychosis). The CAS may considerably impair the postanesthetic period especially when agitation is prevalent, which may endanger the patient or the surgical results. The diagnosis is confirmed ex iuvantibus by the sudden increase in the acetylcholine level in the brain. This is achieved with physostigmine, a cholinesterase inhibitor able to easily cross the blood-brain barrier. Its peripheral muscarinic effects are minimal. Postanesthetic CAS can be prevented by administration of physostigmine during the anesthesia procedure. During intensive care (IC), agitated forms of CAS may occur in patients undergoing mechanical ventilation, particularly during prolonged high-dose sedation. Artificial ventilation of such patients becomes very difficult and muscle relaxation may be necessary. In these cases of IC-CAS, physostigmine is of value and has proven beneficial during weaning from mechanical ventilation. Dealing with the CAS for more than a decade has improved knowledge of the central cholinergic transmission. For example, it can be said that CAS occurs alongside general anesthesia, being no more than a frequent side-effect. Furthermore, acetylcholine is involved in nociception through the endorphinergic and the serotoninergic systems. There is a close relation between the central cholinergic transmission and actions of nitrous oxide. Moreover, cholinergic transmission is involved in withdrawal from (among others) alcohol, opiates, hallucinogens and nitrous oxide. In some intoxications with psychoactive agents, physostigmine is useful for reversal of the central nervous symptoms of the acute intoxication itself. In addition it can be used for prevention of some withdrawal states. In
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PMID:Central anticholinergic syndrome (CAS) in anesthesia and intensive care. 268 49

Groups of 21 male and 21 female Sprague-Dawley (SD) rats were fed diets containing pyriproxyfen at concentrations of 0, 80, 400, 2,000 and 10,000 ppm for 6 months. No death was found in any group. Alopecia in the neck and/or back, and soft feces were noticed in both sexes fed 10,000 ppm. A marked decrease in body weight gain was observed in both sexes fed 10,000 ppm throughout the treatment period, accompanying a decrease in food-consumption and an increase in water-intake during the initial stage of treatment. In terms of urinalysis, proteinuria, increases in K excretion, and, in number, yellowness or browish-yellowness in appearance, were observed in both sexes fed 10,000 ppm. In females fed 10,000 ppm, increases in bilirubin, Na excretion and specific gravity, and a decrease in ketone bodies, were observed. In hematology, decreases in erythrocyte count, hemoglobin concentration and hematocrit value, were observed in both sexes fed 10,000 ppm and in males fed 2,000 ppm. Also, an increase in MCH (in males), decreases in MCHC and platelet count (in females) were observed in 10,000 ppm group. Blood biochemistry revealed increases in total protein, albumin, alpha 2-globulin fraction, blood urea nitrogen, calcium (in both sexes fed 10,000 ppm), A/G ratio (in males fed 2,000 and 10,000 ppm), total cholesterol, phospholipid (in males fed 2,000 and 10,000 ppm, and in females fed 10,000 ppm), sodium (in females fed 2,000 and 10,000 ppm), gamma-glutamyl transpeptidase activity (in males fed 10,000 ppm) and alpha 1-globulin fraction (in females fed 10,000 ppm), and decreases in glucose, GOT (in both sexes fed 10,000 ppm), beta-globulin fraction (in males fed 2,000 and 10,000 ppm, and in females fed 10,000 ppm), GPT (in females fed 2,000 and 10,000 ppm), triglyceride, potassium (in males fed 10,000 ppm), and cholinesterase activity (in female fed 10,000 ppm). In organ weight, increases in liver (in males fed 2,000 ppm and 10,000 ppm, and in females fed 10,000 ppm), kidney (in both sexes fed 10,000 ppm) and thyroid (in females fed 10,000 ppm) and a decrease in pituitary (in females fed 2,000 and 10,000 ppm) were observed. Gross pathology revealed a higher incidence of blackish-brown coloration of the liver, and a lower incidence of accentuated lobular pattern of the liver (in males fed 10,000 ppm). An enlargement of the liver was seen in a few of both sexes fed 10,000 ppm. Histopathological examination showed that the sole effect attributable to treatment of this compound was on slight hypertrophy in the liver of both sexes fed 10,000 ppm, with a higher incidence.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A six-month chronic dietary toxicity study of pyriproxyfen in rats]. 273 65

Chronic effects of a sublethal dose (150 mg/kg body weight) of dimethoate, an organophosphorus insecticide, on blood constituents were investigated in rats after exposure of 15 and 30 days. A significant decrease was observed in haemoglobin concentration, total RBC and WBC counts and in haematocrit values. After 30 days of exposure, the levels of blood glucose, cholesterol, urea, total bilirubin and the activities of glutamic-oxalacetic transaminase, glutamic- pyruvic transaminase and amylase markedly increased, but the activities of acid phosphatase and cholinesterase significantly decreased. There was no effect on total plasma protein content. The rats exposed to dimethoate for 30 days showed more prominent changes in all the blood constituents than those exposed for 15 days.
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PMID:Haematological changes induced by dimethoate in rat. 280 6

The influence of cholinergic agonists on central nervous system (CNS) regulation of blood sugar homeostasis was studied in fasted rats. When carbachol, muscarine, bethanechol, methacholine, or neostigmine was injected into the third cerebral ventricle, it caused a dose-dependent increase in the hepatic venous plasma glucose concentration. However, in the case of 1,1-dimethylphenyl-4-piperazinium iodide (DMPP) or nicotine, the level of hepatic venous glucose did not differ from that of the saline-treated control rats. The increase in glucose level caused by neostigmine was dose-dependently suppressed by coadministration of atropine. These facts suggest that cholinergic activation of muscarinic receptors in the CNS plays a role in increasing hepatic glucose output. Injection of neostigmine (5 X 10(-8) mol), an inhibitor of cholinesterase, into the ventricle resulted in the increase of not only glucose, but also glucagon, epinephrine, and norepinephrine in the hepatic venous plasma. However, constant infusion of somatostatin through a femoral vein completely prevented the increase of glucagon after administration of neostigmine, although the increase of hepatic venous glucose and epinephrine levels were still observed. Neostigmine-induced increments in glucose did not occur in adrenalectomized rats. This suggests that the secreted epinephrine acts directly on the liver to increase hepatic glucose output.
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PMID:Mechanism of central hyperglycemic effect of cholinergic agonists in fasted rats. 287 43

Biochemical and hemodynamic changes were assessed in 13 dogs subjected to sub-coronary valvular aortic stenosis and chronic protein-calorie malnutrition (PCM). Red blood cell, hemoglobin, serum albumin, free fatty acids, blood glucose, cholinesterase and blood amino acid levels were measured. The dynamic geometry of the left ventricle (LV) was assessed with chronically implanted sonomicrometric piezoelectric crystals. Cardiac function was evaluated by mean velocity of circumferential fiber shortening (mean VcF) and the relationship between LV end-systolic pressure (LVESP) or LV wall stress (LVWst) and LV end-systolic diameter (LVESD). The following results were obtained: A decrease in body weight and increases in free fatty acids and 3-Methylhistidine were observed following long-term PCM. Mean VcF was not depressed in dogs subjected to PCM. The relationship between LVESP or LVWst and LVESD shifted downward and to the right after PCM, indicating reduced myocardial contractility. These findings suggest that the left ventricle in hypertrophied dog hearts subjected to PCM retains normal pump function, despite a low state in the myocardium.
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PMID:Biochemical and hemodynamic changes in the hypertrophied dog heart subjected to chronic protein-calorie malnutrition. 295 29

A prospective randomized double blind investigation was made in 24 multiple injured patients. All patients were treated with a combined parenteral-enteral nutrition during 7 days. A group of 11 patients received as a continuous infusion over 16 h 60 mg/kg BW carnitine daily. Beside carnitine and acetylcarnitine levels in plasma and urine the following parameters were determinated to evaluate the effect of carnitine: for the metabolism of fatty acids: triglycerides, free fatty acids (FFA), alpha-hydroxy-butyrate for the metabolism of carbohydrates: glucose, insulin and lactate in plasma. Finally for amino acid metabolism: urea, creatinine, cholinesterase and kolloid osmotic pressure in plasma as well as ureanitrogen and alpha-aminonitrogen excretion in urine. In the patients receiving carnitine especially acetyl-carnitine in plasma and acetyl-carnitine excretion in urine increased, proving that the administered carnitine can pass through the mitochondrial membrane. In these patients the plasma level of FFA was markedly lower than in the group without carnitine. Simultaneously the level of the alpha-hydroxybutyrate was elevated, equivalent to an increased oxydation of fatty acids. There was no difference between the two groups in the metabolism of carbohydrates. Administration of carnitine caused a slight increase of the production of urea (PU), catabolism could not be reduced. The excretion of alpha-aminonitrogen in urine augmented after carnitine infusion. Carnitine is an AA itself and so the amount of excreted alpha-amino nitrogen will increase; additionally the reabsorption of AA in the proximal renal tubulus may be inhibited by carnitine.
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PMID:[Experiences with L-carnitine in the post-stress phase]. 310 Apr 46

The positive influence of L-carnitine administration on postaggression metabolism was investigated. Clinical examinations were executed on three groups of patients K1, K2, K3). Comparable surgical operations like stomach- and intestinal- resections were performed on these groups of patients. During the first three days after operation a nutritional diet (parenteral, standardized hypocaloric) with (K2: 2 g; K3: 4g) and without L-carnitine (K1) was given. The effects of L-carnitine administration were evaluated by the following parameters: free fatty acids (FFS), triglycerides (TG), beta-hydroxybutyric acid (beta-OH-BS), acetacetate (ACAC), blood sugar (BZ), insulin (INS), lactate (LAK), pyruvate (PYR), total protein (GE), cholinesterase (CHE), urea production rate (PU), nitrogen of alpha-aminogroups (alpha-AN), nitrogen balance (NB), catabolic index (KI), BUN-Creatinine-quotient (B/K), total carnitine (GC), free carnitine (FC), acetyl carnitine (AC) and also the ratio between acetyl carnitine and free carnitine (AC/FC) in serum and urine. The results show no statistical significance. But they could lead to the following conclusions: Carnitine obviously reduces the insulin resistance. But it does not influence the post-operative perturbation of glucose-utilization. Carnitine reinforces the utilization of long chain fatty acids and thus improves the energy conversion. Carnitine leads to an earlier positive nitrogen balance. By giving 4 g of carnitine a day, already after three days a repletion of tissue deposits is possible, and a dose dependence for carnitine administration exists for the utilization of long chain fatty acids and the repletion of tissue deposits.
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PMID:[Effect of L-carnitine on post-stress metabolism in surgical patients]. 310 72

Children undergoing ABMT, a procedure which entails massive doses of chemotherapy along with total-body irradiation, are candidate to develop severe gastrointestinal toxicity and prolonged anorexia requiring administration of Parenteral Nutrition (PN) for variable periods. We report a series of 35 consecutive children affected by malignancies who underwent 37 courses of PN after ablative therapy followed by ABMT. Age ranged from 8 months to 17 years; 16 were females, 19 males. There were 23 cases of neuroblastoma, 5 of Wilms' tumor, 3 of acute myelogenous leukemia, 2 of Ewing's sarcoma, 1 case each of rhabdomyosarcoma and acute lymphoblastic leukemia. All patients developed severe neutropenia for 9-42 days (median 18 d). Fever occurred in all patients; sepsis was documented in 10. Duration of PN ranged from 10 to 64 days (23 +/- 9; mean +/- SD). PN solution, containing crystalline L-Aminoacids (8.5%) mixed with 33% glucose, minerals, trace elements and vitamins provided for children a caloric intake of 49.8 +/- 17.3 Kcal/Kg/day with a nitrogen intake of 0.26 +/- 0.27 g/Kg/day. Nutritional assessment, utilizing percent ideal body weight, serum protein electrophoresis, C3, pseudocholinesterase and fibrinogen, was performed at the beginning and at the completion of each course of PN. Mean percent ideal body weight was 95.8 before PN, 98.5 on last day of PN (p less than 0.0005). Other parameters did not change significantly. No metabolic complication nor severe electrolyte imbalance were observed except for 5 patients who developed hypokalemia in coincidence with administration of Amphotericin B.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Autologous bone marrow transplantation in children. Use of parenteral nutrition]. 311 38

Inhibition of central nervous system cholinesterase with a single pulse of physostigmine induces a pronounced increase of blood flow in the neocortex, cingulate gyrus, claustrum, and amygdala. This phenomenon is not accompanied by an increase in energy metabolism and may help explain the effect of this drug on memory in normal humans and patients with Alzheimer's disease, as well as other conditions. In contrast, a parallel increase of blood flow and metabolism was observed in the superior colliculus, a component of the visual pathways. Prolonged administration of physostigmine lead to persistent vasodilatation in the neocortex, a lessening of this effect in cingulate gyrus, claustrum and amygdala, and an increase in primary olfactory cortex and hippocampus when compared with single pulse administration. Effects of physostigmine on glucose utilization remained essentially the same as with pulse administration.
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PMID:Physostigmine enhances blood flow-metabolism ratio in neocortex. 315 Aug 7


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