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)

Urinary lactate was analyzed in 53 normal children, 7 children with glucose-6-phosphatase-deficient glycogenosis, 1 child with fructose-1,6-diphosphatase deficiency and 1 child with pyruvate dehydrogenase deficiency. Lactate in 24-h urine was expressed as concentration, total excretion, excretion per kg body weight and per 1.73 m2 body surface, and as lactate/creatinine quotient. Of these parameters, the lactate concentration in 24-h urine showed the smallest variation in normal children (0.155 +/- 0.053 mM), whereas in patients with one of the above mentioned enzymopathies 10-300-fold elevations were found. The lactate/creatinine quotient, normal range 0.010 to 0.058 (mM/mM) was also used to correct for unnoticed losses of urine. Both parameters, used in conjunction with blood lactate analysis, are suitable for a first screening of patients with enzymopathies of carbohydrate metabolism, and for the follow-up study of the steady or unsteady state of the patient with an enzyme defect of carbohydrate metabolism.
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PMID:Urinary lactate excretion in normal children and in children with enzyme defects of carbohydrate metabolism. 17 40

To evaluate some of the early effects of methymercury chloride (MMC) male rats were given 10, 20 or 30 mg MMC/kg intraperitoneally. Urine was analysed for vanilmandelic acid (VMA), leucine aminopeptidase (LAP), alkaline phosphatase (AP), and creatinine, blood for glucose-6-phosphatase (G-6-P) and glucose, serum for glutamate-oxalate-transaminase (GOT) and urea. Except for LAP and AP excretion there is no effect of MMC on the parameters investigated. However, the effects on these 2 renal enzymes are to variable to permit their use as a test for MMC toxicity.
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PMID:Effect of methylmercury on some constituents of serum and urine. 71 3

Renal microsomes isolated on day 3 from cisplatin (CDDP, single i.p. injection, 4 or 6 mg/kg)-treated rats were monitored for their susceptibility to lipid peroxidation as compared with microsomes from rats treated with carboplatin (CBDCA, 30 mg/kg), transplatin (TDDP, 6 mg/kg) or CDDP hydrolysis products (4 or 6 mg/kg) or from control animals. Cephaloridine (1 g/kg daily for 4 days, i.p. injection) was used as a positive control. The effect of CDDP on renal microsomal glucose-6-phosphatase activity was investigated in vivo and in vitro. Following treatment with CDDP and CDDP hydrolysis products vs CBDCA and TDDP treatment, microsomes revealed an enhanced susceptibility to lipid peroxidation in a Fe2+ and/or ascorbic acid stimulation system. Increased lipid peroxidation, expressed as an increase in malondialdehyde (MDA) generation, paralleled the alterations in body and kidney weight and the elevations of plasma creatinine and blood urea nitrogen concentrations. Injection of the antioxidant N,N'-diphenyl-p-phenylenediamine (DPPD, 0.5 g/kg, i.p.) at 24 h prior to CDDP treatment abolished the increased vulnerability of renal microsomes to lipid peroxidation. In vivo, only CDDP hydrolysis products exhibited a significant inhibitory effect on renal glucose-6-phosphatase activity. In vitro, rat renal and hepatic microsomal glucose-6-phosphatase activity was decreased by CDDP both time- and concentration-dependently. Nephrotoxicity induced by CDDP and CDDP hydrolysis products might be attributable to iron-dependent lipid peroxidation and microsomes might represent target organelles on a subcellular level.
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PMID:Iron- and ascorbic acid-induced lipid peroxidation in renal microsomes isolated from rats treated with platinum compounds. 193 47

Type I glycogen storage disease (GSD-I) is due to the deficiency of glucose-6-phosphatase activity in the liver, kidney and intestine. Although kidney enlargement occurs in GSD-I, renal disease has not been considered a major problem until recently. In older patients (more than 20 years of age) whose GSD-I disease has been ineffectively treated, virtually all have disturbed renal function, manifested by persistent proteinuria; many also have hypertension, renal stones, altered creatinine clearance or a progressive renal insufficiency. Glomerular hyperfiltration is seen in the early stage of the renal dysfunction and can occur before proteinuria. In younger GSD-I patients, the hyperfiltration is usually the only renal abnormality found; and, in some patients, microalbuminuria develops before clinical proteinuria. The predominant underlying renal pathology is focal segmental glomerulosclerosis. Renal stones and/or nephrocalcinosis are also common findings. Amyloidosis and Fanconi-like syndrome can occur, but rarely. The risk factors for developing the glomerulosclerosis in GSD-I include hyperfiltration, hypertension, hyperlipidemia and hyperuricemia. Dietary therapy with cornstarch and/or nasogastric infusion of glucose, aimed at maintaining normoglycemia, corrects metabolic abnormalities and improves the proximal renal tubular function. Long-term trial will be needed to assess whether the dietary therapy may prevent the evolution or the progression of the renal disease.
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PMID:Type I glycogen storage disease: kidney involvement, pathogenesis and its treatment. 202 44

Growth retardation and lactic aciduria are well-known abnormalities in patients with a deficiency of either glucose-6-phosphatase or glucose-6-phosphate translocase. In 19 patients with glucose-6-phosphatase and two patients with glucose-6-phosphate translocase, growth retardation was quantified by calculating the height standard deviation score. The urinary excretion of lactate and some other metabolites was quantified by calculating the lactate/creatinine, 2-oxoglutarate/creatinine, citrate/creatinine, and glycerol/creatinine ratios in urine. Significant correlations were found between the lactate/creatinine ratio, the 2-oxoglutarate/creatinine ratio, and height SD score. Urinary lactate appeared to respond promptly to changes of the diet, while urinary 2-oxoglutarate responded only slowly, as did growth itself. The citrate/creatinine ratio and the glycerol/creatinine ratio were within the normal range and varied little. It was concluded that the urinary 2-oxoglutarate excretion primarily reflects the severity of the disease as expressed in stunted growth. Thus, while urinary lactate levels are more suitable for monitoring the diet, urinary 2-oxoglutarate levels can be used as an indication for intensive treatment with hyperalimentation.
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PMID:Urinary excretion of lactate, 2-oxoglutarate, citrate, and glycerol in patients with glycogenosis type I. 347 Jul 5

Twenty four hour urine samples of male control and streptozotocin-diabetic Wistar rats were analysed for a series of commonly known kidney-specific enzymes, for electrolytes, creatinine, glucose, total protein and urine volume. The examination was done during two periods of 5 days between the 25th and 30th and the 32nd and 36th day after streptozotocin application. In the first period the animals had free access to food and water, whereas in the second period on days 32, 34 and 36 food was withdrawn. In the first observation period the diabetic rats showed increased excretion rates of 15 measured urinary parameters, while alanine aminopeptidase (EC 3.4.1.2) and gamma-glutamyltransferase (EC 2.3.2.2) activities were lowered and inorganic phosphate was unchanged. The removal of food resulted in decreased excretion values for alanine aminopeptidase, gamma-glutamyltransferase and total protein as compared with fasted nondiabetic animals. The activities of N-acetyl-beta-D-glucosaminidase (EC 3.2.1.30), acid phosphatase (EC 3.1.3.2), lactate dehydrogenase (EC 1.1.1.27), pyruvate kinase (EC 2.7.1.40), C1-fructose 1.6-diphosphatase (EC 3.1.3.11) and the excretion values for sodium, calcium, magnesium, chloride and glucose were higher than in fasted nondiabetic rats. beta-Glucosidase (EC 3.2.1.21), potassium, inorganic phosphate, creatinine, and urine volume showed no differences between fasted diabetic and fasted control animals. The enzymes in the renal cortex at the end of the experiment showed only decreased activity of alanine aminopeptidase in diabetic rats. Lactate dehydrogenase, pyruvate kinase, beta-glucosidase, C1-fructose 1.6-diphosphatase and glucose 6-phosphatase (EC 3.1.3.9) were increased and gamma-glutamyltransferase, N-acetyl-beta-D-glucosaminidase, acid phosphatase and glucose 6-phosphate dehydrogenase (EC 1.1.1.49) showed no change.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enzymuria in streptozotocin-diabetic rats. 353 86

The effects of high-dose indomethacin (three daily dose, 8.5 mg/kg ip) on pathology and histology, on serum and urine biochemistry, and on various hepatic enzyme activities were studied in rats. Hepatic cytochrome P-450 and aminopyrine N-demethylase were decreased by 52-62%, but glucuronyl transferase fell by only 22%. Hepatic glucose-6-phosphatase, aryl esterase, 6-phosphogluconate dehydrogenase and sulphotransferase remained unchanged, while glucose-6-phosphate dehydrogenase increased by 29%. There were no widespread changes in hepatic and renal pathology or histology, but noteworthy was a mild, focal, centrilobular hepatic response. By contrast, there were severe intestinal lesions: the effects on hepatic enzymes might have been partly a consequence of the intestinal damage. There was a reversible uraemia and significant decreases (20-40% below normal) in both serum albumin and protein, while serum levels of creatinine and aspartate-amino-transferase activity remained constant. A reversible N-acetyl-beta-D-glucoseaminidase (NAG) enzymuria occurred (300% above normal), but no significant proteinuria (less than 300 mg/l). Administration of 16, 16-dimethylprostaglandin F2 alpha(0.5 mg/kg iv) concomitantly with the indomethacin greatly ameliorated the intestinal lesions and prevented the decreases in hepatic drug-metabolizing enzymes. Concomitant 16,16-dimethylprostaglandin F2 alpha did not, however, influence the indomethacin-induced decreases in serum protein, albumin or NAG-enzymuria. It was concluded that indomethacin had a highly selective effect causing a decrease in hepatic cytochrome P-450, which was not accompanied by severe damage to hepatocyte structure.
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PMID:Comparative effects of indomethacin on hepatic enzymes and histology and on serum indices of liver and kidney function in the rat. 393 37

Aavirai Kudineer (AK) is an herbal decoction of seven botanical drugs, cited in the Gunapadam; a Tamil Siddha medical text. The anti-diabetic efficacy of this formulation was evaluated using alloxan-induced diabetic and normal rats. Glucose tolerance was observed within 1 hr in AK-treated rats (10 ml/kg body ) as compared to control. A significant decrease in the severe hyperglycemia characteristic of alloxan diabetes was noted after 15 days of AK treatment. Further AK treatment reversed the elevated urea, creatinine, cholesterol and decreased protein values to near normal levels. Assay of glycogen content and chief carbohydrate-metabolizing enzymes, viz. hexokinase, glucose-6-phosphatase and fructose 1,6 diphosphatase in the liver of diabetic and AK-treated diabetic rats clearly ascertains the hypoglycemic efficacy of this formulation. The mode of action of this herbal formulation remains to be elucidated.
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PMID:Biochemical studies on hypoglycemic effect of Aavirai kudineer: a herbal formulation in alloxan diabetic rats. 1183 78

Effect of vanadyl acetylacetonate (VAc) and metformin on gluconeogenesis has been studied in isolated hepatocytes and kidney-cortex tubules of rabbit. Glucose formation from alanine+glycerol+octanoate, pyruvate or dihydroxyacetone was inhibited by 50-80% by 100 microM VAc or 500 microM metformin in renal tubules of control and alloxan-diabetic animals, while the inhibitory action of these compounds in hepatocytes was less pronounced (by about 20-30%). In contrast to VAc, metformin increased the rate of lactate formation by about 2-fold in renal tubules incubated with alanine+glycerol+octanoate. In view of VAc-induced changes in intracellular gluconeogenic intermediates and gluconeogenic enzyme activities, it is likely that this compound may decrease fluxes through pyruvate carboxylase, phosphoenolpyruvate carboxykinase, fructose-1,6-bisphosphatase and glucose-6-phosphatase. In contrast to VAc, metformin-induced decrease in renal gluconeogenesis may result from a decline of cytosolic oxaloacetate level and consequently PEPCK activity. Following 6 days of VAc administration (1.275 mg Vkg(-1) body weight daily) the blood glucose level in alloxan-diabetic rabbits was normalised while blood glucose changes in control animals were not observed. On the contrary, in diabetic animals treated for 6 days with metformin (200 mg kg(-1) body weight day(-1)) a high blood glucose level was maintained. Unfortunately, VAc-treated control and diabetic rabbits exhibited elevated serum urea and creatinine levels. In VAc-treated animals vanadium was accumulated in kidney-cortex up to 7.6+/-0.6 microg Vg(-1) dry weight. In view of a potential vanadium nephrotoxicity a therapeutic application of vanadium compounds needs a critical re-evaluation.
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PMID:Inhibition of gluconeogenesis by vanadium and metformin in kidney-cortex tubules isolated from control and diabetic rabbits. 1196 Jun 14

Effect of vanadyl acetylacetonate (VAc), tungstate and molybdate on gluconeogenesis has been studied in isolated hepatocytes and kidney-cortex tubules. In renal tubules of control and alloxan-diabetic animals, the rank order of the metal-compounds-induced (i) inhibition of glucose formation from alanine+glycerol+octanoate or aspartate+glycerol+octanoate, (ii) decrease in the mitochondrial membrane potential (delta psim), (iii) increase in the hydroxyl free radicals (HFR) generation and (iv) decline in glucose-6-phosphatase activity was the following: VAc > tungstate > molybdate. Moreover, in contrast to VAc, both tungstate and molybdate at 100 microM concentration did not practically decrease glucose production in hepatocytes isolated from diabetic rabbits, and significantly increased the rate of lactate formation in renal tubules. N-acetylcysteine at 2 mM concentration partially attenuated vanadium-induced alterations in glucose formation, delta psim and the cellular glutathione redox state, whereas 0.1 mM melatonin did not abolish vanadium-induced changes in gluconeogenesis despite attenuation of vanadium effects on HFR formation and delta psim decline. However, similarly to control rabbits, following 6 days of intraperitoneal administration of both VAc (1.275 mg V/kg body weight daily) and melatonin (1 mg/kg body weight daily) to alloxan-diabetic animals, vanadium-induced elevated serum creatinine and urea levels were decreased, indicating the beneficial effect of melatonin on diabetes- and vanadium-induced nephrotoxicity in rabbits. As serum glucose levels were also significantly diminished by vanadium+melatonin treatment of diabetic animals, the combination therapy of vanadium compounds and melatonin needs a careful evaluation.
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PMID:Differential effects of vanadium, tungsten and molybdenum on inhibition of glucose formation in renal tubules and hepatocytes of control and diabetic rabbits: beneficial action of melatonin and N-acetylcysteine. 1536 81


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