Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.9 (glucose-6-phosphatase)
 3,081 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of fetal hypoglycemia and hypoinsulinemia on fetal rat hepatic glucose-6-phosphatase activity was studied. Fetal hypoglycemia and hypoinsulinemia were produced by inducing maternal hyperinsulinemia and hypoglycemia secondary to the exogenous administration of insulin via implantation of osmotically driven minipumps on day 15 of gestation into 15 experimental animals. 13 animals served as sham-operated controls. Cesarean sections were performed on day 20 or 21 of gestation under pentobarbital anesthesia. Liver glucose-6-phosphatase activity was increased in the hypoinsulinemic fetuses. In contrast, the hyperinsulinemic mothers had suppressed hepatic glucose-6-phosphatase activity. Hypoinsulinemia would appear to be the primary stimulus for enhanced fetal glucose-6-phosphatase in this model.
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PMID:Induction in utero of hepatic glucose-6-phosphatase by fetal hypoinsulinemia. 298 86

Previous studies have demonstrated that sera from patients with severe liver damage after halothane anesthesia ("halothane hepatitis") contain antibodies reacting with novel antigenic determinants expressed on hepatocytes from rabbits exposed previously to halothane. To determine the structure of the halothane-induced antigen(s), immunoblotting experiments were performed using patient sera and rabbit liver subcellular fractions. Three polypeptide antigens (Mr 100,000, 76,000 and 57,000) expressed in liver fractions from animals sacrificed 16 hr after exposure to 1% halothane in oxygen for 45 min, but not in fractions from unexposed animals, were identified. Analysis of fractions prepared by differential and sucrose density gradient centrifugation, and characterized by enzyme marker analysis, localized all three antigens to a microsomal subfraction relatively enriched in glucose-6-phosphatase activity, therefore, presumably derived from the endoplasmic reticulum. Antibodies to these antigens were detected in 19 of 24 sera from patients with halothane hepatitis, and four distinct patterns of antibody specificity were observed: 100,000 + 76,000 (seven patients), 100,000 alone (seven patients), 76,000 alone (three patients) and 57,000 alone (two patients). Such antibodies were not detectable in sera from 24 normal blood donors or 36 control patients. Thus, halothane induces expression of three distinct polypeptide antigens in liver, and patients with halothane hepatitis differ in patterns of recognition of these antigens by circulating antibodies.
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PMID:Identification by immunoblotting of three halothane-induced liver microsomal polypeptide antigens recognized by antibodies in sera from patients with halothane-associated hepatitis. 330 10

Von Gierke's disease, a form of glycogen storage disturbance, is a rare metabolic disorder with important implications for anesthesiologists. It is caused by the lack of the glucose-6-phosphatase, which is necessary for the liver to convert glycogen to glucose. To avoid severe hypoglycemia, it is crucial to keep oral feeding at intervals 2-3 hr for maintaining a normal blood sugar level. The metabolic derangements of von Gierke's disease may result in serious complications in patients undergoing surgery and anesthesia. We report the anesthetic managements of a patient with von Gierke's disease in two operations with different encounters.
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PMID:Two different anesthetic managements of a patient with von Gierke's disease. 1662 10

In the present work the effect of intramuscular administration of 30.000, 50.000 and 100.000 IU of vitamin A palmitate daily for seven days, respectively, on the liver enzyme activity in 45 white male Wistar rats, aged 12 weeks and weighing 180-200 g, have been studied. The group control was integrated by 15 healthy rats with similar characteristics (strain, gender, age and weight) to treated animals. Food and water consumption and body weights were recorded at the end of the experimental period. Rats were observed for clinical signs of toxicity. At the end of the study, rats were sacrificed under ether anesthesia. Liver samples were taken for the determination of enzyme activity. Administration of excess of vitamin A produced a significant (p < 0.05) increase in the content of liver vitamin A, determined diverse and variable clinical signs (such as, anorexia, loss of body weight, alopecia, conjunctivitis, external and internal hemorrhages, skin abnormalities and death) and increased (p < 0.05) the activity of the following enzymes: alanine aminotransferase, aspartate aminotransferase, acid maltase (acid alpha-1,4-glucosidase), acid proteases, lactate dehydrogenase and alkaline phosphatase while glucose-6-phosphatase, glycogen phosphorylase, alpha-amylase, cholinesterase and arginase decreased (p < 0.05) as compared with untreated controls. These changes depend on the doses given of vitamin A. In conclusion, our results provide evidence that short-term administration of high doses of vitamin A determined diverse and variable clinical signs and produces a marked alteration of activity of liver enzymes.
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PMID:[Clinical and biochemical alterations in rats treated with high doses of vitamin A]. 1827

It is suggested that general anesthetics invade the "hydrogen belts" of neuronal plasma membranes, i.e. the regions of the bilayer containing hydrogen bond acceptors (CO of phospholipids) and donors (OH of cholesterol, sphingosin, ?-hydroxy fatty acids, proteins), and that they restructure the H-bond patterns between membrane lipids and proteins. The evidence is 2-fold. (1) The postulated existence of protein lipid hydrogen bonding has previously been demonstrated for glucose-6-phosphatase and for protein kinase C. (2) The prediction that changes in the H-bonding part of an anesthetic may influence its potency, but changes in the lipophilic part should not, can be verified. For a structurally widely varied group of monohydroxy compounds the range of anesthetic potency (inverse of intramembrane ED(50)(M) for loss of tadpole righting reflex) was smaller than 4-fold, while for n-hexane derivatives with different H-bonding headgroups the range of ED(50)(M) was about 100-fold. Although the results permit contributions by other factors they suggest that a restructuring of hydrogen belt H-bonding patterns is a general step in anesthesia.
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PMID:Mechanism of anesthesia: Anesthetics may restructure the hydrogen belts of membranes. 2050 97

In South-west Nigeria, water decoctions of Hunteria umbellata seeds are highly valued by traditional healers in the local management of diabetes mellitus, obesity and hyperlipidemia. Previous studies hypothesized one of the antihyperglycemic mechanisms of the aqueous seed extract of Hunteria umbellata (HU) to be mediated probably via increased peripheral glucose utilization. The present study, therefore, was designed at evaluating the peripheral glucose utilization and anti-oxidative mechanisms of 50 mg/kg, 100 mg/kg and 200 mg/kg of HU in alloxan-induced diabetic rats in Groups IV-VI rats as well as in the control groups (Groups I-III). Experimental type 1 DM was induced in male Wistar rats through intraperitoneal injection of 150 mg/kg of alloxan monohydrate in cold 0.9% normal saline after which the diabetic rats were orally treated with 50-200 mg/kg of HU for 14 days. Effects of HU on the rat body weight, percentage body weight changes and fasting blood glucose (FBG) were determined on days 1 and 15 of the experiment. Also, on day 15 of the experiment, HU effect on serum insulin, liver enzyme markers, proteins, albumin, triglyceride, total cholesterol and lactate dehydrogenase as well as on hepatic tissue oxidative stress markers, liver glycogen and glucose-6-phosphatase were determined after sacrificing the rats under diethyl ether anesthesia. Results showed that oral treatments with 50-200 mg/kg of HU caused significant (p<0.0001) improvements in the weight loss caused by alloxan-induced diabetes, while causing significant (p<0.05, p<0.001 and p<0.0001) dose-related reductions in the FBG levels despite causing non-significant (p>0.05) alterations in the serum INS levels in the treated rats. Also, repeated oral treatment with HU caused significant (p<0.0001) reversal in the decrease and increase in the hepatic glycogen levels and glucose-6-phosphatase activity, respectively, caused by alloxan-induced diabetes. Similar significant (p<0.0001) and complete reversal effects were recorded in the serum hepatic enzyme markers, total protein, albumin, triglyceride, total cholesterol and lactate dehydrogenase as well as on hepatic tissue oxidative stress markers such as superoxidase dismutase (SOD), catalase (CAT), malonialdehyde (MDA) and reduced glutathione (GSH) of HU-treated rats when compared to that of untreated alloxan-induced diabetic rats. In conclusion, results of this study showed HU treatment to significantly ameliorate the hyperglycemia and oxidative stress in alloxan-induced diabetic rats which was mediated via increased hepatic glycogen deposit, decreased hepatic glucose-6-phosphatase activity and improvement in antioxidant/free radicals scavenging activities.
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PMID:Glucose utilization and anti-oxidative mechanisms of the aqueous hunteria umbellata seed extract in alloxan-induced diabetic rats. 2619 70