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)

Key enzymes of gluconeogenesis in the liver, phosphoenolpyruvate carboxykinase [EC 4.1.1.32] and glucose-6-phosphatase [EC 3.1.3.9], were studied in patients with primary or metastatic hepatic cancer. Liver specimens for enzyme assay were obtained by necropsy performed within four hours after death. It was confirmed that both enzyme activities in rat liver preserved at 4 degrees C remained unchanged within nine hours after the removal of the tissue. Activities of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase decreased to below ten per cent of the control in neoplastic liver tissue of patients with hepatocellular carcinoma accompanied with liver cirrhosis. These two enzyme activities in cirrhotic tissue of patients with hepatocellular carcinoma were lower than those in patients merely with cirrhosis. In patients with metastatic hepatic cancer both two enzyme activities further decreased and were scarcely detected not only in neoplastic tissue but also in non-neoplastic tissue. These results show that hepatic gluconeogenesis markedly decreases in patients with primary or metastatic hepatic cancer. The biochemical analysis of the blood in hepatic cancer, decreased in blood glucose and release in immunoreactive glucagon, also suggested the suppression of gluconeogenesis.
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PMID:Hepatic gluconeogenic key enzymes in patients with hepatic cancer. 625 51

The effects of diabetes on hepatic carbohydrate metabolism were investigated in spontaneously diabetic Bio-Breeding Worcester (BB/W) rats. The juvenile-onset-type syndrome displayed by these animals is characterized by beta-cell destruction with subsequent ketosis-prone insulinopenia. Livers from diabetic animals demonstrated increased adenosine 3',5'-cyclic monophosphate levels but subnormal total protein and glycogen content. Isolated perfused livers of diabetic BB/W rats demonstrated an increased rate of glucose production from [14C]lactate and an impaired rate of glycogen synthesis. These data were consonant with hepatic enzyme studies demonstrating markedly increased activities of component gluconeogenic (glucose-6-phosphatase, fructose-1,6-diphosphatase, phosphoenolpyruvate carboxykinase) and glycogenolytic (glycogen phosphorylase) enzymes with decreased activities of glycolytic (hexokinase, pyruvate kinase) and glycogenic (glycogen synthase) enzymes. These findings agree with previous studies using alloxan- and streptozotocin-induced diabetic animals and suggest that accelerated hepatic gluconeogenesis and impaired glucose utilization are pathognomonic of all insulin-deficient diabetic syndromes.
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PMID:Hepatic carbohydrate metabolism in the spontaneously diabetic Bio-Breeding Worcester rat. 625 45

The variations in enzyme activities involved in the main pathways of liver energetic metabolism--glycolysis, Krebs cycle, gluconeogenesis and lipogenesis--have been studied in rats ranging between the age of 4 days and 21 months. The major changes observed are the following: (1) enzymes involved in glycolysis (pyruvate kinase) and lipogenesis (NADP-malic enzyme, ATP-citrate lyase) decrease in activity during ageing, and (2) gluconeogenic enzymes (phosphoenolpyruvate carboxykinase, glucose-6-phosphatase) are maintained or slightly increased over the same period. The results suggest that an increase in the capacity for gluconeogenesis with respect to that for lipogenesis takes place in the aged rat liver.
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PMID:Metabolic implications of ageing: changes in activities of key lipogenic and gluconeogenic enzymes in the aged rat liver. 626 5

Three experiments were conducted to assess the effects of magnesium deficiency on the activities of hepatic glucose-6-phosphatase (G6Pase), fructose 1,6-bisphosphatase (FDPase) and phosphoenolpyruvate carboxykinase (PEPCK). Experiment 1 was designed to determine if magnesium deficiency interfered with the gluconeogenic response to fasting. Rats were fed either a control (C) or magnesium-deficient (MD) diet for 12 days. One-half of each group of rats was fasted for 24 hours prior to death. Hepatic enzyme activities, plasma and liver magnesium, and whole blood glucose were measured. Activities of G6Pase and PEPCK were higher in fasted group C rats compared to fed group C rats. Activity of FDPase was lower. The response was similar in the MD groups. Comparison of C and MD groups indicated that magnesium deficiency was accompanied by an increase in PEPCK activity. To verify this result and to investigate the role of anorexia in producing increased PEPCK activity, experiment 2 included a pair-fed group (PF). The results indicated that anorexia was not responsible for increased PEPCK activity in MD rats. The relation of circulating insulin and glucagon concentrations to effects of magnesium deficiency was explored in experiment 3. A decreased insulin:glucagon ratio was observed in MD rats. The results of these experiments suggest that magnesium deficiency alters PEPCK activity by affecting secretion of pancreatic hormones.
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PMID:Hepatic gluconeogenic enzymes, plasma insulin and glucagon response to magnesium deficiency and fasting. 627 7

Renal gluconeogenic capacity was enhanced to 150% 24 h after partial hepatectomy, remained increased at 48 h (144%) and returned to normal values at 72 h. Glucose production by renal cortical slices from hepatectomized rats was also enhanced 48 h after surgery when pyruvate, alpha-ketoglutarate and fructose were used as gluconeogenic precursors. The stimulation of renal gluconeogenic capacity seems to be due to the increase of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase activities which behaved similarly to glucose production after hepatectomy. The renal metabolic response may be partially due to starvation in the first 24 h. Afterwards food intake became normalized and the acceleration of glucose production should be attributed to hepatectomy. Since there was no metabolic acidosis in our experimental conditions the involvement of glucocorticoids in the stimulation of renal phosphoenolpyruvate carboxykinase and glucose-6-phosphatase activities is suggested.
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PMID:[Stimulation of gluconeogenic capacity in partially hepatectomized rats (author's transl)]. 628 29

Administration of low levels of lead (0.001, 0.005 and 0.025 micrograms/g/day p.o.) to neonate rats from age three days to eight weeks failed to alter the activities of hepatic glucose-6-phosphatase, fructose-1,6-diphosphatase, pyruvate carboxylase and phosphoenolpyruvate carboxykinase, the four key gluconeogenic enzymes. Administration of lead at a higher dose (0.1 micrograms/g/day p.o.) was also observed to produce no alterations in enzyme activity at eight weeks. However, the higher dose did enhance the activities of fructose-1,6-diphosphatase and phosphoenolpyruvate carboxykinase at age six weeks. Plasma insulin and glucagon were not significantly altered by up to 0.025 micrograms/g exposure to lead until eight weeks of age, although levels of these hormones appear to be slightly dose-responsive tending towards elevated glucagon and decreased insulin levels with increasing lead dosage. At 0.1 micrograms/g/day glucagon was significantly increased at eight weeks. Blood glucose and hepatic glycogen remained unaltered. Blood, hepatic and pancreatic lead levels were unchanged by treatment with lead up to 0.025 micrograms/g/day to eight weeks of age, but there was evidence of lead accumulation in pancreatic tissue whereas levels of the metal in the liver paralleled those in the blood. Significant increases were observed with 0.1 micrograms/g/day lead at six and eight weeks in blood and pancreas. Data are presented which suggest that six week old animals are more influenced by subacute lead exposure than are the eight week old animals, as reflected in some alteration of gluconeogenic enzyme activity in younger rats.
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PMID:Effects of subacute low level lead exposure on glucose homeostasis. 630 42

Parenchymal activities (mumol . min-1 . g liver-1) and distributions of mitochondrial succinate dehydrogenase, cytosolic phosphoenolpyruvate carboxykinase and microsomal glucose-6-phosphatase were studied in regenerating rat liver after two thirds partial hepatectomy. Succinate dehydrogenase activity remained constant with a slight and transient increase for a few hours after operation. The typical periportal localization was changed to an almost even distribution from 8 h to 7 days; it was fully restored after 14 days. Phosphoenolpyruvate carboxykinase activity was increased by 1.8 fold 24 h after surgery; it remained enhanced until about 72 h. The normal periportal to perivenous enzyme gradient was diminished or replaced by a homogeneous distribution between 8 h and 7 days; the zonal heterogeneity was regained after 14 days. Glucose-6-phosphatase activity remained constant after partial hepatectomy. The normal periportal maximum was lost between 4 h and 36 h; the activity became more equally distributed and was even shifted towards the perivenous zone. After 48 h the zonal distribution was reestablished. The results indicate that after partial hepatectomy the gluconeogenic capacity of the liver remnant is increased and that this increase is accompanied by a loss of the normal heterogeneity which is typical for the glucostat function of the organ. They reveal in addition that the three enzymes, representing three different subcellular compartments, change their zonal heterogeneity individually rather than synchronously.
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PMID:Alteration in zonation of succinate dehydrogenase, phosphoenolpyruvate carboxykinase and glucose-6-phosphatase in regenerating rat liver. 632 5

Recently there has been an increased interest in the toxic effects from long term exposure of low levels of cadmium (Cd) in diet. Male, Sprague-Dawley rats were treated with 0, 25, 50, 75 ppm Cd mixed in diet continuously for 180 days. A significant decrease in body weight gain was observed in all Cd treated animals. Serum glucose, serum glutamic oxaloacetic transaminase (SGOT) and serum glutamate pyruvic transaminase (SGPT) were increased parallel to Cd concentration and treatment time. Measured hepatic and renal gluconeogenic enzymes, viz. glucose-6-phosphatase, fructose-1, 6-bisphosphatase and phosphoenolpyruvate carboxykinase were increased with higher Cd dose and time. Low concentration of Cd (25 ppm) had minimal effect with shorter treatment length. Fructose-1, 6-bisphosphatase was found to be very sensitive for assessing Cd-induced nephrotoxicity. Increased serum glucose level and gluconeogenic enzyme activities suggest that Cd might interfere in protein metabolism.
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PMID:Chronic hepatic and renal toxicity by cadmium in rats. 632 37

Chronic fetal hyperinsulinemia, similar to that found in human infants of diabetic mothers, was produced in fetal rhesus monkeys during the latter third of gestation. Fetal plasma glucose and amino acid concentrations were found to be inversely logarithmically correlated with plasma insulin concentration. Fetal plasma glucagon concentrations were suppressed by hyperinsulinemia. Fetal plasma erythropoietin concentrations were increased by hyperinsulinemia in a dose/response manner. The activity of the hepatic gluconeogenic enzymes glucose-6-phosphatase and total phosphoenolpyruvate carboxykinase were reduced by hyperinsulinemia. Fatty acid synthase complex activity was, in contrast, increased by hyperinsulinemia while citrate cleavage enzyme and glucose-6-phosphate dehydrogenase were only increased when supraphysiologic hyperinsulinemia was produced. This model provides an opportunity to study the metabolic effects of hyperinsulinemia separate from those of hyperglycemia on the primate fetus, making it a useful model for the study of fetal pathologic conditions in diabetic pregnancies.
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PMID:Chronic hyperinsulinemia in the fetal rhesus monkey: effects of physiologic hyperinsulinemia on fetal substrates, hormones, and hepatic enzymes. 638 23

Ethanol-induced birth defects may be metabolic or structural. The aim of this study was to examine the effects of prenatal ethanol exposure on the ontogeny of gluconeogenic enzymes. Female rats were fed either liquid diets containing 35% ethanol-derived calories or control diets with isocaloric substitution of corn oil for ethanol. Control diets were pair-fed or given ad libitum. Animals were acclimated to the liquid diets for 7 weeks prior to breeding and the diets were continued through gestation. On day 21, at 4 hr post-caesarean section, ethanol-exposed pups exhibited reduced activities of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase when compared to pair-fed and ad libitum controls. It is concluded that prenatal ethanol exposure delays or impairs the development of gluconeogenic enzymes.
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PMID:Effects of maternal ethanol consumption on the ontogeny of gluconeogenesis in the perinatal period. 667 58


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