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)

Effects of 3,4,3',4'-tetrachlorobiphenyl (TCB) on glucose-6-phosphatase (G6Pase)-altered hepatic foci of N-nitrosomorpholine (NNM)-treated B6C3F1 mice were investigated. TCB was chosen as a selective 3-methylcholanthrene-type inducer and tumor promoter. To initiate hepatocarcinogenesis, mice were treated with NNM (160 mg/l, in drinking water for 7 weeks), as in previous studies with the rat model. After a treatment-free interval of 22 weeks, TCB was administered (5 x 50 mg/kg, every 3 days), and liver foci were analysed 10 weeks after the start of TCB treatment. Unexpectedly, the number of G6Pase-negative and -positive foci per liver was markedly diminished following TCB treatment (to 32% and 57%, respectively). On the other hand, the mean volume of the remaining G6Pase-altered foci was enhanced, owing to an increase in the percentage of foci of large size (greater than 0.5 mm2). Throughout the experimental period of 39 weeks prolonged liver injury due to NNM and TCB treatment was demonstrated by histology and by elevated serum levels of glutamate-oxaloacetate transaminase. The results suggest that (in contrast to the rat system) TCB exhibited opposing effects on liver foci in the mouse model: (a) moderate tumor-promoting effects and (b) cytotoxic effects in NNM-injured liver, leading to decreased numbers of liver foci.
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PMID:Tumor-promoting activity and cytotoxicity of 3,4,3',4'-tetrachlorobiphenyl on N-nitrosomorpholine-induced murine liver foci. 254 56

The effects of oral fructose on hepatocarcinogenesis were investigated with cytomorphological, cytochemical and stereological methods. Carcinogenesis was induced in male Sprague-Dawley rats by application of N-nitrosomorpholine (NNM) for 7 weeks. Afterwards, the animals received fructose in the drinking water (120 g/l) and food ad libitum (group I) or tap water and food ad libitum (group II). The incidence of hepatocellular carcinoma in rats treated with NNM plus fructose was 46% as compared to 24% in animals receiving NNM alone (P less than 0.05). There was no difference in the incidences of other malignancies between the groups (group I: 32.1%, group II: 32.0%). Morphometric evaluation of preneoplastic liver lesions indicated the enhancing effect of the fructose treatment several months before malignant tumors appeared. As early as 6 weeks after treatment the hepatic parenchyma occupied by focal lesions was increased from 6.7% in the animals which had received NNM alone to 8.5% (P less than 0.05) in animals having received NNM plus fructose. This increase was predominantly caused by an increase in glycogen storing foci (P less than 0.0005). In addition, the fructose treatment caused a histochemically detectable increase in the activity of glucose-6-phosphatase and glucose-6-phosphate dehydrogenase in both the hepatocytes of the focal lesions and the surrounding parenchyma. In the NNM plus fructose group the activity of the glucose-6-phosphatase in the foci was frequently approximately equal to the activity in the parenchyma of untreated controls. The striking increase in the activity of this enzyme in the surrounding hepatocytes, however, still sharply demarcated the lesions. The potential mechanisms by which fructose enhances hepatocarcinogenesis are discussed.
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PMID:Enhancement of hepatocarcinogenesis in rats by dietary fructose. 256 39

The antihistamine methapyrilene was examined for its ability to initiate hepatocarcinogenesis in rats. Rats were first subjected to partial hepatectomy and then were intubated with one of four doses (30, 100, 200 or 300 mg/kg) of methapyrilene hydrochloride (or an equivalent amount of water for controls, or 10 mg diethylnitrosamine/kg for positive controls). Rats were then fed 0.05% phenobarbital in the diet for 3, 6 or 9 months. The number and volume of altered hepatic foci were quantified with the histochemical markers gamma-glutamyl transpeptidase, glucose-6-phosphatase, and ATPase. The number of foci induced was increased 2- to 4-fold by the highest dose of methapyrilene at all 3 time points, but the only statistically significant increase was produced by the 200 mg/kg dose after 3 months of promotion. This study shows that methapyrilene may act as a weak initiator.
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PMID:Effect of the antihistamine, methapyrilene, as an initiator of hepatocarcinogenesis in female rats. 256 26

Eight-week-old, female Wistar fatty rats and their lean littermates were given a 30% sucrose solution in addition to a laboratory chow diet and water for 7 weeks. The fatty rats were hyperinsulinemic and hyperlipidemic, but normoglycemic when they drank only water. The hepatic activities of insulin-inducible glucokinase (GK), pyruvate kinase (PK), and malic enzyme (ME) were higher in the fatty rats than in the lean rats, whereas the insulin-suppressible glucose-6-phosphatase (G6Pase) activity was similar in both types of rats, indicating the normal response of hepatic enzymes to hyperinsulinemia in the fatty rats. When they drank the sucrose solution, the fatty rats, but not the lean rats, developed hyperglycemia over 200 mg/dl. Plasma insulin and triglyceride concentrations increased in both types of rats. Although the hepatic activities of GK, PK, and ME in the lean rats, and PK and ME in the fatty rats increased in response to the increase in plasma insulin, GK activity decreased in the fatty rats. On the other hand, G6Pase activity increased in both types of rats. As a result, the G6Pase/GK ratio, which may reflect net glucose handling in the liver, increased twofold in the fatty rats, but did not alter in the lean rats. From these findings, we conclude that sucrose ingestion induces an increase in hepatic glucose production through derangement of the hepatic enzyme profile and that the resultant decrease in hepatic glucose handling may be one of the pathogenic factors participating in the development of hyperglycemia in Wistar fatty rats.
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PMID:Derangement in hepatic enzymes caused by sucrose-drinking and its implication for the development of hyperglycemia in female Wistar fatty rats. 267 49

It is shown that the ascorbic acid (AA) administration to Wistar male rats (50 mg per animal intraperitoneally 3 times a week) accelerates hepatocarcinogenesis induced by N-nitrosodiethylamine (2.5 mg/kg 6 times a week in drinking water). In this case the activity of glucose-6-phosphate dehydrogenase in liver increases, while that of glucose-6-phosphatase decreases.
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PMID:[Effect of ascorbic acid on the hepatocarcinogenic action of N-nitrosodiethylamine in rats]. 285 47

The in vitro activities of glucose-6-phosphatase (G6P), UDP-glucuronyl transferase (GT) and P-450 were measured in liver homogenate and/or microsomal suspensions from puppies, 0-42 days of age (n = 26), and adult dogs (n = 3). For each of these enzymes, an age-related increase in the in vitro activity was observed, with the lowest value detected at birth. By the 28th-42nd day of postnatal life, P-450-specific activity was 350 and 85%, G6P 225 and 188%, p-nitrophenol GT 430 and 105% and bilirubin GT 317 and 123% of that seen in 0-hour-old puppies and adults dogs, respectively. The age-related changes in G6P and GT were observed when native enzymes or enzymes activated by deoxycholate or UDP-N-acetylglucosamine (GT) were used. However, the ratio between activated and native p-nitrophenol GT activity decreased as a function of age, and UDP-N-acetylglucosamine failed to activate bilirubin GT in puppies of 0-42 days of age. Total liver protein also increased with age, and hepatic water content was significantly higher in 0- to 42-day-old puppies (76.3%) than in adult dogs (71.4%). Thus, differences between puppies and adult animals were not the same when protein content or enzyme activities were expressed per unit of wet or dried liver weight. Phenobarbital, injected intraperitoneally at 15 mg/kg/day for 6 consecutive days to 8- to 13-day-old puppies (n = 3), produced induction of P-450 (235% of age-matched controls) and bilirubin GT activity (160%), diminished G6P activity (81%), and failed to modify p-nitrophenol GT activity (102%). These studies indicate that, in the puppy, (1) the in vitro activities of P-450, G6P and GT are immature at birth and develop during postnatal life; (2) as in other species, bilirubin and p-nitrophenol may be conjugated in the dog liver by two functionally distinct GT.
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PMID:Postnatal changes in hepatic microsomal enzyme activities in the puppy. 298 54

The studies on the effects of phenol (P), 2,4-dinitrophenol (DNP), pentachlorophenol (PCP) individually and in three combinations, viz., (PCP + DNP)/P (highly antagonistic), (DNP + P)/PCP (additive), and (P + DNP)/PCP (highly synergistic), at three sublethal levels (1/10, 1/15, and 1/20 of the 96-hr LC50) on the activity of hydrolytic enzymes (acid, alkaline, and glucose-6-phosphatases and 5-nucleotidase) in the brain and kidney of a fresh-water teleost, Notopterus notopterus revealed inhibition of enzyme activity after 15 and 30 days of exposure. Maximum inhibition (-89.32%) was observed in acid phosphatase activity in brain at 1/10 concentration of (P + DNP)/PCP combination after 30 days, but minimum (-3.64%) in activity of glucose-6-phosphatase in kidney at 1/20 of (PCP + DNP)/P combination after 15 days of exposure. However, biphasic effects of P, DNP, and (PCP + DNP)/P combination were observed in kidney, i.e., inhibition of enzymes activity at higher concentrations and stimulation at lower concentrations after both time intervals.
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PMID:Physiological stress induced by sublethal concentrations of phenolic compounds in Notopterus notopterus: measurement of hydrolytic enzymes. 303

To elucidate the mechanism by which TRH and its metabolite, histidyl-proline diketopiperazine (cyclo(His-Pro], act on the maturation of homoiothermy, the chronic effects of intrathecal administration of the peptides on body temperature, serum thyroid hormone levels, and mitochondrial energy-producing enzyme activities were examined in neonatal rats. The two peptides or an equimolar mixture of both were injected intrathecally at a dose of 3, 6 and 9 nmol for 7 consecutive days during the 1st, 2nd or 3rd week of life, respectively. Control rats were treated with saline and they were sacrificed at 6 weeks of age. Although food and water intake were not decreased, body weight gain was slightly reduced in the rats treated with TRH or cyclo(His-Pro) during the 1st and 2nd week of life, whereas the mixture-treated rats showed normal weight gain. Body temperature at 25 degrees C was not different in the TRH- and cyclo(His-Pro)-treated groups, whereas after cold exposure (5 degrees C for 3 h), the groups treated with TRH during the 1st and 2nd week of life had an impaired thermoregulation at 5 weeks of age. Serum T4 and T3 concentrations were similar in all groups, except in the rats treated with TRH during the 2nd week of life; their thyroid hormone levels were slightly reduced. The TRH treatment suppressed mitochondrial cytochrome c reductase and glucose-6-phosphatase activities, whereas cyclo(His-Pro) reduced cytochrome c reductase and malic enzyme activities. In contrast, alpha-glycerophosphate dehydrogenase was enhanced by both treatments.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term effects of thyrotropin-releasing hormone and histidyl-proline diketopiperazine on the maturation of homeothermia and mitochondrial enzyme activities in neonatal rats. 314 9

Carbohydrates with digestion characteristics between those of lente uncooked starches and rapidly digestible oligosaccharides were administered in a dose of 1.5 g/kg body weight to five patients with glycogenosis from glucose-6-phosphatase deficiency. Postprandial duration of normoglycemia and concentrations of blood insulin and lactate were determined. Uncooked barley groats in water, or incorporated in a meal turned out to behave as lente carbohydrates. Uncooked couscous in water, couscous incorporated in a meal, and partially cooked macaroni given as a meal behaved as semilente carbohydrates as compared with uncooked cornstarch and glucose. The in vitro determination of the digestibility index along with the in vivo tolerance test enables us to choose and incorporate semilente carbohydrates in the day-time treatment of patients.
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PMID:Complex carbohydrates in the dietary management of patients with glycogenosis caused by glucose-6-phosphatase deficiency. 329

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


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