Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clonal nature of atherosclerotic plaques has been examined in diet-induced atherosclerosis of interspecies hybrid hare females (Lepus timidus (female) X Lepus europaeus (male], which exhibit genetic mosaicism with respect to glucose-6-phosphate dehydrogenase (G6P-D). Four diet groups have been used: control pellet diet, hyperlipemic (HL) diet, and HL diet supplemented with two different concentrations of 25-hydroxycholesterol. Lesion and nonlesion tissue samples and primary cultures developed from similar samples were used to determine the G6P-D variant patterns. A close correlation was observed, using regression analysis, between the in vivo and the in vitro phenotype. As has been reported earlier by us, most lesions in this animal model were heterozygous and the few homozygous areas recorded were all in the diet groups supplemented with 25-hydroxycholesterol. However, in tissue culture, homozygosity appeared with greater frequency, still of the T phenotype. In order to rule out maternal dominance as a factor, preliminary experiments involving G6P-D analysis have been carried out using tissue samples and cell cultures derived from a reverse cross. These also show a strong bias toward the T phenotype. The studies presented here highlight the difficulties in interpretation using G6P-D analysis as the sole criterion to determine the clonal nature of the atherosclerotic plaques. It also seems likely that the kind of diet given to induce atherosclerosis might influence the nature of the clonal growth. Studies using transfection are essential to determine whether transforming sequences are present in atherosclerotic lesions.
Exp Mol Pathol 1988 Jun
PMID:Clonal nature of atherosclerotic plaques. 337 61

The possibility was examined that mutational events can be delayed for more than one or two cell divisions following treatment of Chinese hamster cells with the DNA alkylating agent ethyl methane sulfonate. If mutations in mammalian cells are delayed, the proportion of mutant cells in colonies grown from single mutagen-treated cells will reflect the cell division at which the mutation is genetically fixed, i.e., a first division mutation yields a 1/2 mutant colony, a fifth division mutation produces a 1/32 mutant colony, etc. In the present study, replating of cells from single colonies grown for six to seven days after mutagen treatment resulted in the discrete ratios of glucose-6-phosphate dehydrogenase (G6PD)-deficient mutant to wild-type colonies expected for a delayed mutational process which produces mutations over at least 8-10 cell generations. Further, when cells from 7- to 10-day colonies, grown from ethyl methane sulfonate (EMS)-treated cells were replated into selective medium containing 6-thioguanine (6TG), the number of 6TG-resistant colonies obtained per flask was distributed over a very wide range, consistent with a mutational delay process. These results could not be explained by differences in the number of cells per colony or plating efficiency in selective medium. Assuming that the relative number of 6TG-resistant colonies per flask reflects the time of mutation, EMS treatment produced two groups of mutational events: one which occurred within the first five cell generations and another uniformly distributed over at least the next eight to nine divisions. These results support the conclusion that EMS induces mutants for at least 10-14 cell generations after treatment and raise the possibility that current methods to assess the mutagenic potential of an agent might lead to significant underestimation. The role of delayed mutation in the phenomenon of "mutation expression time" is also discussed.
Somat Cell Mol Genet 1987 Jan
PMID:Delayed mutation in Chinese hamster cells. 346 33

Liver glucose 6-phosphate dehydrogenase and phosphogluconate dehydrogenase activities were significantly decreased in both diabetic and fasted rats. Treatment of diabetic rats with insulin resulted in liver glucose 6-phosphate dehydrogenase and phosphogluconate dehydrogenase activities that were significantly greater than controls. Insulin promoted an increase in food consumption that was blocked by adrenaline. Insulin, when administered together with adrenaline, restored hepatic glucose 6-phosphate dehydrogenase and phosphogluconate dehydrogenase activities of diabetic animals to control values, without altering food consumption. Brain glucose 6-phosphate dehydrogenase and phosphogluconate dehydrogenase activities were not significantly altered by either dietary restriction, diabetes or insulin treatment. These results demonstrate a dissociation between the action of insulin on hepatic glucose 6-phosphate dehydrogenase activity and its action to increase food intake.
Mol Cell Biochem 1986 May
PMID:Regulation of liver and brain hexose monophosphate dehydrogenases by insulin and dietary intake in the female rat. 352 10

Fat cells of hypophysectomized and fasted rats metabolize 10 times less glucose than adipocytes of normal rats in the presence of insulin. Glucose transport (3-O-methylglucose influx), transport plus phosphorylation (2-deoxyglucose uptake), hexokinase, pyruvate dehydrogenase and glucose-6-phosphate dehydrogenase activities were determined in an attempt to localize the metabolic defects. Insulin stimulates 3-O-methylglucose influx 5-fold in normal cells and 3-fold in cells of fasted rats. The basal influx in cells of fasted rats is increased and even more so in cells of hypophysectomized rats where the rate of basal influx is the same as that in cells of normal rats under maximal insulin stimulation. It cannot be further stimulated by insulin. In contrast to 3-O-methylglucose influx, basal uptake and phosphorylation of 2-deoxyglucose in cells of fasted and hypophysectomized rats is drastically decreased and stimulation by insulin is abolished. Total hexokinase and pyruvate dehydrogenase activities are drastically reduced in the homogenate of fat cells of hypophysectomized and fasted rats. Phosphorylation by hexokinase appears to become one of the rate-limiting steps of glucose metabolism in cells of hypophysectomized rats.
Mol Cell Endocrinol 1986 Oct
PMID:Glucose uptake and phosphorylation in fat cells of fasted and hypophysectomized rats. 353 Aug 35

The regulation of hepatic glucose-6-phosphate dehydrogenase (G6PDH; EC 1.1.1.49) RNA by thyroid hormone and high carbohydrate (sucrose) diet was studied. Previous studies from several laboratories have demonstrated that thyroid hormone modulates G6PDH activity. However, the point at which thyroid hormone exerts this regulation has not been adequately addressed. In order to assess the role of thyroid hormone in this regulation, levels of G6PDH mRNA were determined in hypothyroid rats maintained on normal or high carbohydrate diets with or without thyroid hormone (triiodothyronine; T3) supplementation. A dot-blot hybridization procedure with nick-translated cDNA probes was used to directly assess the relative concentrations of G6PDH mRNA. Enzyme activity increased when the animals were treated with T3 and/or placed on a high carbohydrate diet. However, there was no effect of T3 and diet, alone or in combination, on G6PDH mRNA levels in hypothyroid rats. The data suggests that thyroid hormone and high carbohydrate diet are acting at a translational level to increase G6PDH enzyme activity in these animals.
Mol Cell Endocrinol 1987 May
PMID:Regulation of glucose-6-phosphate dehydrogenase by diet and thyroid hormone. 359 96

Rates of NADPH generation by the pentose phosphate pathway were evaluated in perfused livers from ethanol-fed or control rats by measuring the production of 14CO2 from 1-14C-glucose. Under basal perfusion conditions, livers from ethanol-fed rats released lactate and pyruvate into the perfusate at rates that were only 19% of the control values. Under these conditions, calculated rates of NADPH generation by the pentose cycle in livers of the ethanol-fed rats were only 50% of rates obtained with livers of control rats. 7-Ethoxycoumarin (7-EC), a substrate for mixed function oxidation, was infused to increase rates of hepatic NADPH utilization. In livers from control rats, 7-EC was oxidized at a rate of 2.6 mumol/g/hr, but rates of NADPH generation by the pentose cycle were increased by 8.8 mumol/g/hr. In livers from ethanol-fed rats, 7-EC was metabolized at rates of 7.2 mumol/g/hr, but the generation of NADPH by the pentose cycle was increased by only 3.9 mumol/g/hr. The infusion of 7-EC was associated with increases in rates of O2 uptake that exceeded rates of mixed function oxidation in both groups of animals. Ethanol feeding decreased the activity of glucose-6-phosphate dehydrogenase by 40% and decreased the concentrations of glycogen by 66%. Thus, the decrease in pentose cycle flux in perfused livers may be due to diminished activity of the rate-controlling enzyme and/or diminished substrate supply from glycogen. However, cytosolic NADP+/NADPH ratios were identical in livers of both groups. Because NADPH was not depleted during the mixed function oxidation of 7-EC in livers from ethanol-fed rats, it is concluded that other hepatic sources of NADPH compensate for the diminished generation by the pentose cycle.
Mol Pharmacol 1987 Jun
PMID:Diminished pentose cycle flux in perfused livers of ethanol-fed rats. 360 Jun 8

Studies were carried out on glucose-6-phosphate dehydrogenase (G6P-DH) during the differentiation of rabbit bone marrow erythroid cells. It was found that G6P-DH, although displaying a 7-fold activity decrease, did not change the relative amounts of its three dimeric forms. Using homogeneous enzyme preparations, we observed that from dividing to non-dividing erythroblasts the following properties remained constant: V max dependence on pH and temperature, Km for G6P dependence on pH, heat stability, 2-deoxy glucose-6-phosphate utilization, molecular weight, while the Km for NADP significantly increased in non-dividing erythroblasts. These results indicate that no shift towards the oxidized form of the enzyme and no substantial modifications of the protein take place during cell differentiation.
Mol Cell Biochem 1987 Jun
PMID:Rabbit bone marrow glucose-6-phosphate dehydrogenase during erythroid cell development. 362 10

Liver regeneration after partial hepatectomy was used as an experimental model for studying mammalian cell division and replication. The rate of cell proliferation in this hyperplastic model was correlated with hepatic de novo synthesis of cholesterol, with the hexose monophosphate shunt pathway of glucose metabolism, and with serum lipoproteins. An increase of hepatic cholesterol esters and of incorporation of tritiated water in cholesterol esters was observed at 24 hr after partial hepatectomy. Partial hepatectomy also resulted in an increase of hepatic glucose-6-phosphate dehydrogenase and in alteration of serum lipoproteins, primarily due to a selective decline in high density lipoprotein fraction.
Exp Mol Pathol 1986 Apr
PMID:Hepatic glucose-6-phosphate dehydrogenase, cholesterogenesis, and serum lipoproteins in liver regeneration after partial hepatectomy. 369 35

Glucose utilization by different metabolic pathways in bovine adrenal medulla has been studied using freshly isolated adrenal chromaffin cells. The rate of net glucose utilization in resting cells was 10.5 mumoles X g-1 X h-1. 50% was transformed into lactate and pyruvate, the lactate to pyruvate ratio ranging from 3 to 7.27% was metabolized through the tricarboxylic acid cycle and 3.1% was oxidized in the pentose phosphate pathway. The ratio of 14CO2 production from [1-14C] glucose and [6-14C] glucose was close to 2 at one hour of incubation. 3.2% of total glucose consumed was used in protein synthesis, and 1% was incorporated into lipids. Oxygen utilization in respiration by isolated adrenal chromaffin cells was 18.2 mumoles X g-1 X h-1, corresponding to 3.1 mumoles glucose X g-1 X h-1 or about 30% of total glucose consumed. The activities of hexokinase, enolase, pyruvate kinase, lactate dehydrogenase, glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase were assayed in extracts of bovine adrenal medulla, being 1.0, 23, 40, 37, 6.0 and 3.0 U/g respectively. Hexokinase activity was identified as belonging mainly to isoenzyme I, with some isoenzyme II. Enolase was predominantly the alpha gamma hybrid. Pyruvate kinase activity corresponded to a mixture of isoenzymes K and M. Lactate dehydrogenase activity corresponded to isoenzymes 1, 2 and 3, with smaller proportions of isoenzymes 4 and 5. Results are discussed mainly with respect to those reported for the brain.
Mol Cell Biochem 1986 Apr
PMID:Enzymes and pathways of glucose utilization in bovine adrenal medulla. 371 7

Endothelial cells which cover the inner wall of blood vessels were extracted for bioluminescence analyses of nucleotides and enzymes. The contaminating blood was removed by heparinization and rinsing with ammonium chloride. The content of the endothelial cells of the rat aorta was reached by time governed laminar elution, using a saponin solution to disrupt the cell membranes. Uniformity of extraction was achieved with a Hamilton programmable pump. All the analyses of the eluted fractions showed a characteristic and reproducible peak. The activities of glucose-6-phosphate dehydrogenase and adenylate kinase were significantly higher in the diabetic animals whereas the amount of nucleotides did not differ between diabetic and control rats. The laminar elution technique combined with bioluminescence assay represents a new approach to studies of biochemical alterations in the endothelial cells. The method is also useful for extraction and analyses of other surface layers.
Mol Cell Biochem 1987 Jan
PMID:A new approach to the biochemical pathology of the vascular system, using time governed laminar elution and bioluminescence analyses. 380 99


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