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:3.1.3.9 (glucose-6-phosphatase)
3,081 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three preterm infants born at 26-30 weeks' gestation who died between 103 and 266 days after birth were found to have elevated hepatic glycogen levels. Kinetic analysis of the hepatic microsomal glucose-6-phosphatase system demonstrated that one infant had abnormally low levels of activity of the glucose-6-phosphatase enzyme (partial type 1a glycogen storage disease) and two had deficiencies of T2, a microsomal phosphate/pyrophosphate transport protein (type 1c glycogen storage disease). In all three cases glycogen storage disease was not suspected prior to death even though both hypo- and hyperglycaemic episodes were recorded in the first 15 days after birth indicating that they had somewhat disordered blood glucose regulation. In the infant with low glucose-6-phosphatase enzyme activity, abnormal development of the glucose-6-phosphatase enzyme cannot be ruled out. This is the first description of abnormalities in the glucose-6-phosphatase system in preterm infants.
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PMID:Impairment of the activity of the hepatic microsomal glucose-6-phosphatase system in three preterm infants. 132 22

Twenty-four male (12 obese and 12 lean) and 21 female (11 obese and 10 lean) SHR/N-cp rats were fed a diet containing either 54% sucrose or starch for periods of 3-4 months. Rats were killed after a 14-16 h fast and liver enzyme activities were determined in both sex groups. Liver glucose-6-phosphatase (G6Pase), fructose 1,6-bisphosphatase (FBPase), phosphoenolpyruvate carboxykinase (PEPCK), glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), malic enzyme (ME), phosphofructokinase (PFK), glucokinase (GK), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels (per total liver capacity) were significantly affected by phenotype (obese > lean). Arginase and ornithine transcarbamylase levels were analysed only in male rats and were found to be elevated in obese rats as compared to lean littermates. Some of the above changes in enzyme levels were exaggerated by sucrose feeding but not the changes in FBPase, PEPCK, ME and GK (in both sexes) plus AST, arginase and arginine synthase activities in male rats and ALT levels in female rats. Results from SHR/N-cp rats published in this paper were compared to results obtained from LA/N-cp rats published previously. Comparison of the non-diabetic obese LA/N-cp with the diabetic obese SHR/N-cp male shows a greater excess in lipogenic capacity of the liver in the LA/N-cp male rat. The SHR/N-cp obese female also shows a greater liver lipogenic capacity as compared with the obese male SHR/N-cp rat. The results suggest that an adaptation of excessive lipogenesis in the liver of obese rats may be an anti-diabetogenic adaptation resulting in increased glucose conversion to lipids, thus reducing blood glucose levels.
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PMID:Adaptation in enzyme (metabolic) pathways to obesity, carbohydrate diet and to the occurrence of NIDDM in male and female SHR/N-cp rats. 133 Sep 56

Coccinia indica (Family: Cucurbitaceae, locally known as telakucha) leaves were extracted with 95% ethanol. Following evaporation of the solvents, the residue was suspended in distilled water. When this suspension was fed orally to male normal-fed and 48-hr starved rats, the blood glucose was lowered 21% (P less than 0.01) in normal-fed and 24% (P less than 0.001) in 48-hr starved animals respectively. Starvation had induced a 3-fold increase in the activity of glucose-6-phosphatase and this activity was depressed 19% (P less than 0.05) by extract feeding while basal activity of the enzyme in normal-fed rats remained unaffected. Consistent with the depression of glucose-6-phosphatase, urea cycle enzyme arginase was also depressed 21% (P less than 0.001) and 12% (P less than 0.01) in the liver of 48 hr-starved and normal-fed animals respectively. Unlike glucose-6-phosphatase, starvation induced levels of gluconeogenic enzymes alanine aminotransferase and aspartate aminotransferase were not affected by Coccinia extract. These results suggest that the hypoglycemic effect of C. indica is partly due to the repression of the key gluconeogenic enzyme glucose-6-phosphatase.
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PMID:Hypoglycemic effects of Coccinia indica: inhibition of key gluconeogenic enzyme, glucose-6-phosphatase. 133 43

The retinal glucose-6-phosphatase system was studied in rabbits. Following subcellular fractionation of the retina by differential centrifugation, the microsomal fraction was used for spectrophotometrical assay of the phosphate release. Assays were performed with intact and Triton X-100-treated preparations. Intactness of the microsomal preparations was assessed by using 2 mM mannose-6-phosphate as a substrate. Latencies towards glucose-6-phosphate and mannose-6-phosphate were 13.1 +/- 4.1% (n = 5) and 92.5 +/- 2.8% (n = 5) respectively; the difference between them was significant (P < 0.001). Pyridoxal-5'-phosphate specifically inhibited the retinal glucose-6-phosphate translocase activity at concentrations of 5-10 mM. Postnatal development was studied at postnatal days 1, 10, 17, 25, 36, 46, 54 and 70. At the postnatal 17th day, the retinal glucose-6-phosphatase specific activity was 60.1 +/- 3.8 (n = 3) nmol/min/mg protein which was one-third of the adult level [173.6 +/- 26.2 (n = 6) nmol/min/mg protein] (P < 0.001). This finding suggested that, in the rabbit, development of this enzyme system might coincide with development of retinal glucose catabolism.
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PMID:The glucose-6-phosphatase system in the retina. 133 21

Once a child is born its survival depends on the maturation of the blood glucose homeostatic control mechanisms. When this fails or where there is an inborn error of metabolism the infant is susceptible to potentially fatal hypoglycaemic episodes. A variety of environmental stresses, either singly or in combination, such as inappropriate or low caloric intake, acute infections of childhood, endotoxaemia, fever, xenobiotic exposure, oxidative stress or anaphylaxis, can greatly exacerbate the deficiency of the normal homeostatic compensatory mechanism and result in the onset of hypoglycaemia. Various inborn errors have been found in infants who died of SIDS. Our approach to this problem has been to use the six microsomal glucose-6-phosphatase proteins as a model system to study defects in carbohydrate metabolism in cases of SIDS. Initial studies determined the ontogeny of the glucose-6-phosphatase proteins and showed that intact microsomes isolated from unfrozen liver samples can be used to study glucose-6-phosphatase in cases of SIDS that were presumably due to the low concentrations of liver lipid peroxidation. More recently we have used a combination of techniques to demonstrate the abnormalities of glucose-6-phosphatase in cases of SIDS. Classic gross pathology and histology have now clearly defined the various subgroups of sudden and unexpected deaths of infancy. This now enables us to develop new molecular approaches to predict and prevent hypoglycaemia in infants who are at risk of SIDS.
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PMID:Glucose metabolism and hypoglycaemia in SIDS. 133 59

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

The effects of i.p. piroxicam administration on hepatic glycogen levels and enzymatic activities of key enzymes involved into glycogen metabolism in fed female rats were studied. Liver glycogen concentrations in treated rats decreased with increasing time of treatment and doses of piroxicam administered. The fall in glycogen caused by piroxicam persisted for several days after it was discontinued. Neither nadolol nor phenobarbital administration were able to prevent the depleting effect of piroxicam. In the treated rats, glucose-6-phosphatase, glycogen phosphorylase and glycogen synthase activities remained unchanged respect to control. Also, proportion of phosphorylase in the active (a) form was not significantly affected by successive piroxicam daily doses. In contrast, we demonstrated a decrease in the glycogen synthase in the active I form. This reduction was time-dependent on piroxicam treatment. Further, glucose loads were not capable to restore activity in the synthase enzyme and liver glycogen synthesis in animals treated with piroxicam. The impairment into glycogen metabolism produced by piroxicam administration suggests liver becomes unable to maintain glucose homeostasis. Furthermore, glycogen depletion might produce an impairment in the metabolism of drugs administered simultaneously with piroxicam, because biotransformation of xenobiotics is a process depending on glycogen storage in the liver cells.
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PMID:Hepatic glycogen depletion in fed female rats induced by piroxicam. 133 86

Hypoglycemia at the initial stage of the prenatal development decreased the level of glucose in the rat blood, increased glucose-6-phosphatase in the liver. Hyperglycemia increase the glucose content in the blood with relatively minor changes of the glucose-6-phosphatase activity and oxidation of hydrocarbonates.
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PMID:[The effect of prenatal hyper- and hypoglycemia on liver mitochondrial function and carbohydrate metabolism in rat pups]. 133 74

1. Effects of subcutaneous injections of either L-glucose, L-alanine or L-ascorbate into newly-hatched, fasted turkey poults were examined. 2. There were no effects of injections on blood glucose concentrations at 20 hr post-injection. 3. Glucose injections inhibited hepatic glucose-6-phosphatase activity while alanine injections did not. 4. Both glucose and alanine injections enhanced hepatic glycogen reserves at 20 hr post-injection.
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PMID:Effects of injections of L-alanine, L-glucose and L-ascorbic acid in newly-hatched turkey poults on glucose metabolism. 135 59

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


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