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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 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

Adult rat hepatocytes were kept in primary culture for 48 h under different hormonal conditions to induce an enzyme pattern which with respect to carbohydrate metabolism approximated that of periportal and perivenous hepatocytes in vivo. 1. Glucagon-treated cells compared with control cells possessed a lower activity of glucokinase, a 4.5-fold higher activity of phosphoenolpyruvate carboxykinase and unchanged levels of glucose-6-phosphatase, phosphofructokinase, fructose-bisphosphatase and pyruvate kinase; they resembled in a first approximation the periportal cell type and are called for simplicity 'periportal'. Inversely, insulin-treated cells compared with control cells contained a 2.2-fold higher activity of glucokinase, a slightly decreased activity of phosphoenolpyruvate carboxykinase, increased activities of phosphofructokinase and pyruvate kinase and unaltered levels of glucose-6-phosphatase and fructose-bisphosphatase; they resembled perivenous cells and are called simply 'perivenous'. Gluconeogenesis and glycolysis were studied under various substrate and hormone concentrations. 2. Physiological concentrations of glucose (5 mM) and lactate (2 mM) gave about 80% saturation of gluconeogenesis from lactate and less than 15% saturation of glycolysis at a simultaneous 40% inhibition of the glycolytic rate by lactate. 3. Comparison of the two cell types showed that under identical assay conditions (5 mM glucose, 2 mM lactate, 0.5 nM insulin, 0.1 muM dexamethasone) gluconeogenesis was 1.5-fold faster in the 'periportal' cells and glycolysis was 2.4-fold faster in the 'perivenous' cells. 4. Metabolic rates were under short-term hormonal control. Insulin increased glycolysis three fold in both cell types with a half-maximal effect at about 0.4 nM, but did not influence the gluconeogenic rate. Glucagon inhibited glycolysis by 70% with a half-maximal effect at about 0.1 nM. Gluconeogenesis was stimulated by glucagon (half-maximal dose: 0.5 nM) 1.8-fold only in 'periportal' cells containing high phosphoenolpyruvate carboxykinase activity, not in the 'perivenous' cells with a low level of this enzyme. 5. A comparison of the two cell types showed that with maximally stimulating hormone concentrations gluconeogenesis was threefold faster in 'periportal' cells and glycolysis was eightfold faster in 'perivenous' cells. The results support the view that periportal and perivenous hepatocytes in vivo catalyse gluconeogenesis and glycolysis at inverse rates.
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PMID:Induction in primary culture of 'gluconeogenic' and 'glycolytic' hepatocytes resembling periportal and perivenous cells. 675 22

The plasma levels of corticosterone, insulin and glucagon, and the concomitant changes in the levels of several liver enzymes and metabolites were measured in intact rats in the basal state during 24 hours and under conditions of food deprivation and hypoxia. The levels of the following enzymes and metabolites were examined: phosphoenolpyruvate carboxykinase, glucose-6-phosphatase, pyruvate kinase, phosphofructokinase, glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, glucose, glucose-6-phosphate, glycogen, fructose-6-phosphate, hexokinase, tyrosine amino-transferase and tryptophan oxygenase. During food deprivation, the increased gluconeogenesis is possibly a result of glucagon activity. In contrast, however, during hypoxia the increase in gluconeogenesis seems to be a result of the higher plasma level of corticosterone. During starvation, the insulin concentration dropped steadily and came close to zero.
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PMID:Plasma concentrations of glucose, corticosterone, glucagon and insulin and liver content of metabolic substrates and enzymes during starvation and additional hypoxia in the rat. 703 Aug 99

Earlier, we have reported that cadmium (Cd) induced gluconeogenesis in male rats. Since females are as much exposed to cadmium as are males, this study was conducted to determine Cd effects on gluconeogenesis in female rats. Adult female rats were injected intraperitoneally (i.p.) with Cd at dose levels of 0.25, 0.75 and 1.25 mg/kg body weight per day for 4 weeks. The controls received saline for the same length of time. Daily food consumption and body weight gain were recorded. At the end of 2 and 4 weeks, 4 rats from each group were killed. Extension of treatment with 1.25 mg Cd for 4 weeks resulted in extreme Cd toxicity killing all animals before the completion of full treatment period. There were no significant changes in total body weight gain and weights of liver and kidney due to Cd. Serum protein increased significantly in animals receiving 0.75 and 1.25 mg Cd for 4 and 2 weeks, whereas serum glucose increased only in animals injected with 1.25 mg Cd for 2 weeks. SGOT and SGPT were elevated (P less than 0.01) in dose- and time-dependent fashion. Activities of three key gluconeogenic enzymes glucose-6-phosphatase (G-6-Pase), fructose-1,6-diphosphatase (FD-Pase), and phosphoenolpyruvate carboxykinase (PEPCK) in liver and kidney were induced significantly (P less than 0.01) in animals injected with 0.75 mg for 2 and 4 weeks and 1.25 mg for 2 weeks, and these increases were dose- and time-related. These results suggest that Cd alters hepatic and renal gluconeogenesis in female rats also.
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PMID:Effect of cadmium on hepatic and renal gluconeogenic enzymes in female rats. 711 99


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