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)

1. Alterations in carbohydrate metabolism in terms of tissue glycogen contents, phosphorylase (EC 2.4.1.1) activity, hepatic glucose-6-phosphatase (6-6-Pase: EC 3.1.3.9) activity and blood glucose have been evaluated in 30-d-old White Leghorn chicks under induced chronic hypocorticalism (by dexamethasone: DXM) and hypercorticalism (by corticosterone: CORT). 2. DXM treatment showed increased tissue glycogen contents and hypoglycaemia with decreased phosphorylase activity while CORT treatment produced a reverse set of changes. 3. Both steroid treatments increased hepatic G-6-Pase activity. These observations have been taken to indicate a definite role for glucocorticoids in regulating carbohydrate metabolism in neonatal chicks. 4. It is suggested that hypo- or hyper-corticalism could influence carbohydrate metabolism by affecting the secretory/activity ratio of pancreatic hormones.
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PMID:Alterations in carbohydrate metabolism by exogenous dexamethasone and corticosterone in post-hatched White Leghorn chicks. 133 4

Normoglycemic ob/ob mice were treated for 24 or 48 h with either 25 micrograms/day of dexamethasone or saline. After an overnight fast, the animals were killed and pancreatic islets were incubated with 3H2O or [U-14C]glucose or [5-3H]glucose at 5.5 and 16.7 mM glucose. Incorporation of 3H from 3H2O into carbon 2 of medium glucose and the yield of 14CO2 from [U-14C]glucose and 3H2O from [5-3H]glucose were measured. Dexamethasone treatment for 48 h significantly increased the rate of dephosphorylation of glucose in islets both at 5.5 mM (24 vs. 16%) and 16.7 mM (56 vs. 36%) glucose, whereas glucose oxidation and utilization were unaffected. Dexamethasone treatment also inhibited insulin release by approximately 60% at 5.5 and 16.7 mM glucose, either in the presence or absence of 10 mM arginine, but had no effect when insulin release was stimulated by 1 mM 3-isobutyl-1-methylxanthine. Moreover, 24-h treatment with dexamethasone significantly increased glucose cycling at low and high glucose concentrations in the medium and inhibited insulin responsiveness to glucose and arginine. In conclusion, short-term dexamethasone treatment increases glucose flux through glucose-6-phosphatase in islets from ob/ob mice. This effect may contribute to the decreased insulin response to glucose and arginine found in animals treated with dexamethasone.
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PMID:Glucocorticoid increases glucose cycling and inhibits insulin release in pancreatic islets of ob/ob mice. 138 56

Rat liver glucose-6-phosphatase activity was determined in both fully activated and intact microsomal preparations during perinatal development. Activities increased rapidly in both preparations following birth, then gradually fell to adult values. The latency of the glucose-6-phosphatase system also increased neonatally whereas hepatic glycogen concentrations decreased postnatally. The effect of dexamethasone pretreatment on the hepatic glucose-6-phosphatase system was also investigated. Dexamethasone pretreatment failed to decrease the latency of glucose-6-phosphatase in microsomes from neonatal rats but decreased the latency of the enzyme in adult female rat liver from 44 to 12% of total activity.
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PMID:Development of the rat hepatic microsomal glucose-6-phosphatase system and its glucocorticoid inducibility. 284 11

We have cloned and sequenced the first 1.2 kb of the 5' region of the human glucose-6-phosphatase gene. Transfection of H4IIE hepatoma cells with the 1.2 kb fragment fused to a luciferase reporter gene demonstrated both basal and hormone responsive luciferase activity. Dexamethasone increased and insulin decreased luciferase activity. Insulin and dibutyryl cyclic AMP both significantly decreased activity in the presence of dexamethasone.
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PMID:Cloning and sequencing of the 5' region of the human glucose-6-phosphatase gene: transcriptional regulation by cAMP, insulin and glucocorticoids in H4IIE hepatoma cells. 861 93

Fetal glucocorticoids have an important role in the pre-partum maturation of physiological systems essential for neonatal survival such as glucogenesis. Consequently, in clinical practice, synthetic glucocorticoids, like dexamethasone, are given routinely to pregnant women threatened with pre-term delivery to improve the viability of their infants. However, little is known about the effects of maternal dexamethasone treatment on the glucogenic capacity of either the fetus or mother. This study investigated the effects of dexamethasone treatment using a clinically relevant dose and regime on glycogen deposition and the activities of glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK) in the liver and kidney of pregnant ewes and their fetuses, and of non-pregnant ewes. Dexamethasone administration increased the glycogen content of both the fetal and adult liver within 36 h of beginning treatment. It also increased G6Pase activity in the liver and kidney of the fetuses but not of their mothers or the non-pregnant ewes. Neither hepatic nor renal PEPCK activity was affected by dexamethasone in any group of animals. These changes in glycogen content and G6Pase activity were accompanied by rises in the plasma glucose and insulin concentrations and by a fall in the plasma cortisol level in the fetus and both groups of adult animals. In addition, dexamethasone treatment raised fetal plasma tri-iodothyronine (T(3)) concentrations and reduced maternal levels of plasma T(3) and thyroxine, but had no effect on thyroid hormone concentrations in the non-pregnant ewes. These findings show that maternal dexamethasone treatment increases the glucogenic capacity of both the mother and fetus and has major implications for glucose availability both before and after birth.
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PMID:Effects of dexamethasone on the glucogenic capacity of fetal, pregnant, and non-pregnant adult sheep. 1721 Jul 43