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)

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

Insulin resistance has been measured in man by nonsteady state tracer methodology. Increase in overall glucose utilization and suppression of glucose production was measured when hyperglycemia was achieved either by infusing glucagon or glucose. With the first method, insulin resistance was assessed in obese man and in lean hypertriglyceridemic patients. With the second method, insulin resistance was assessed in lean mild type II diabetics. These methodologies can only assess deficiences in overall glucose utilization and glucose production, but cannot delineate the defect in glucose uptake by the liver. However, if a given metabolic event is essentially characteristic of only one organ, metabolic abnormalities specific to that organ can be detected in vivo provided there is a probe specific to that metabolic pathway. Therefore, in lean mild type II diabetics the liver glucose futile cycle was assessed by a double tracer method. Previously it was shown that liver glucose futile cycling is increased in diabetic dogs. In healthy control subjects in basal state and during glucose infusion, the futile cycle could not be detected, but it represented a major part of glucose metabolism in liver of type II diabetics. It appears, therefore, that most of the glucose taken up by the liver during the glucose challenge in diabetics reenters the blood stream without being oxidized or polymerized. On the basis of these studies, it was concluded that excessive hyperglycemia in the diabetics during glucose infusion is due to a decrease in irreversible glucose uptake (impaired phosphorylation and futile cycling) and to a decrease in suppression of glucose production. The relative contribution of the liver and periphery to hyperglycemia seems to be almost equivalent. The mechanism behind the increased glucose cycle activity is not clear. It may be due to a relative decrease of glycogen synthase or increase in glucose-6-phosphatase or both. These observations in mild lean type II diabetics may have implications also in some other types of diabetes, since we have observed that futile cycling is even more marked in obese type II diabetics and that it could account in part for the diabetogenic effect of growth hormone in acromegalics.
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PMID:New probes to study insulin resistance in men; futile cycle and glucose turnover. 389 64

Genetically obese normotensive rats, LA/N-corpulent (cp), were fed ad libitum diets containing either 54% sucrose or cooked corn starch for 12 weeks. Twenty-four rats were used for the study; half were corpulent (cp/cp) and half were lean (cp/+ or +/+). Fasting levels of plasma insulin, glucose, corticosterone, glucagon and growth hormone, and activities of liver and epididymal fat pad glucose-6-phosphate dehydrogenase (G6PD), malic enzyme (ME), and liver and kidney glucose-6-phosphatase (G6Pase), fructose 1,6-diphosphatase (FDPase), and phosphoenolpyruvate carboxykinase (PEPCK) were measured. A significant phenotype effect was observed in insulin, corticosterone, growth hormone, and liver G6PD, ME, FDPase, and kidney PEPCK, G6Pase, FDPase, and epididymal fat pad G6PD and ME (corpulent greater than lean), and glucagon (lean greater than corpulent). Diet effect (sucrose greater than starch) was significant for plasma glucose, liver ME, and kidney G6Pase. Although not significant at the P less than 0.05 level, insulin, corticosterone, liver G6PD and FDPase and kidney FDPase tended to be higher in sucrose-fed rats. This study suggests that the corpulent rat is more lipogenic and gluconeogenic than the lean, and that the hormones responsible are effective in keeping both the lipogenic and gluconeogenic enzyme activity elevated.
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PMID:Hormonal and lipogenic and gluconeogenic enzymatic responses in LA/N-corpulent rats. 399 2

Glucagon (0.04-0.09 mg/kg/min) was given intravenously for either 2 or 3 min to eight patients with fasting-induced hypoglycemia. One child had hepatic phosphorylase deficiency, two children had glucose-6-phosphatase deficiency, two children had debrancher enzyme (amylo-1,6-glucosidase) deficiency, and two children and one adult had decreased hepatic fructose-1,6-diphosphatase (FDPase) activity. Liver biopsy specimens were obtained before and immediately after the glucagon infusion. The glucagon caused a significant increase in the activity of FDPase (from 50+/-10.0 to 72+/-11.7 nmol/mg protein/min) and a significant decrease in the activities of phosphofructokinase (PFK) (from 92+/-6.1 to 41+/-8.1 nmol/mg protein/min) and pyruvate kinase (PK) (from 309+/-39.4 to 165+/-23.9 nmol/mg protein/min). The glucagon infusion also caused a significant increase in hepatic cyclic AMP concentrations (from 41+/-2.6 to 233+/-35.6 pmol/mg protein). Two patients with debrancher enzyme deficiency who had biopsy specimens taken 5 min after the glucagon infusion had persistence of enzyme and cyclic AMP changes for at least 5 min. One child with glucose-6-phosphatase deficiency was given intravenous glucose (150 mg/kg/min) for a period of 5 min after the glucagon infusion and biopsy. The plasma insulin concentration increased from 8 to 152 muU/ml and blood glucose increased from 72 to 204 mg/100 ml. A third liver biopsy specimen was obtained immediately after the glucose infusion and showed that the glucagon-induced effects on PFK and FDPase were completely reversed. The glucagon infusion caused an increase in hepatic cyclic AMP concentration from 38 to 431 pmol/mg protein but the glucose infusion caused only a slight decrease in hepatic cyclic AMP concentration (from 431 to 384 pmol/mg protein), which did not appear to be sufficient to account for the changes in enzyme activities. Hepatic glucose-6-phosphatase and fructose-1,6-diphosphate aldolase activities were not altered by either the glucagon or the glucose infusion in any patients. Cyclic AMP (0.05 mmol/kg) was injected into the portal vein of adult rats and caused enzyme changes similar to those seen with glucagon administration in humans. Our findings suggest that rapid changes in the activities of PFK, PK, and FDPase are important in the regulation of hepatic glycolysis and gluconeogenesis, respectively, in humans and that cyclic AMP may mediate the glucagon- but probably not the glucose-insulin-induced changes in enzyme activities.
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PMID:The rapid changes of hepatic glycolytic enzymes and fructose-1,6-diphosphatase activities after intravenous glucagon in humans. 435 16

The metabolic response to the first fast experienced by all mammals has been studied in the newborn rat. Levels of fuels and hormones have been compared in the fetal and maternal circulations at term. Then, after cesarean section just before the normal time of birth, sequential changes in the same parameters were quantified during the first 16 h of the neonatal period. No caloric intake was permitted, and the newborns were maintained at 37 degrees C. Activities of three key hepatic enzymes involved in glucose production were estimated. Marked differences in maternal and fetal hormones and fuels were observed. Lower levels of glucose, free fatty acids, and glycerol but higher levels of lactate, alpha-amino nitrogen, alanine, and glutamine were present in the fetus. Pyruvate, glutamate, and ketone bodies were not significantly different. The combination of a strikingly higher fetal immunoreactive insulin and a slightly lower immunoreactive glucagon (pancreatic) resulted in a profound elevation in the insulin-to-glucagon ratio, a finding consistent with an organism in an anabolic state. The rat at birth presents a body composition with respect to fuels available for mobilization and conversion which is dominated by carbohydrate and protein, since little fat is present. However, at birth a transient period of hypoglycemia occurred, associated with a rapid fall in insulin and rise in glucagon, causing reversal of the insulin-to-glucagon relationship toward ratios such as were observed in the mother. After a lag period, hepatic activities of phosphorylase, glucose-6-phosphatase, and phosphoenolpyruvate carboxykinase increased. Concurrent with these enzyme changes, the blood glucose returned to levels at or above those of the fetus. Interestingly, the fall observed in levels of the gluconeogenic precursors, lactate and amino acids, preceded the rise in enzyme activities and restoration of blood glucose. After 4 h, however, hypoglycemia recurred, during a period of decreasing hepatic glycogen content and blood lactate, pyruvate, and glycerol levels but of stable or increasing amino acid concentrations. Hepatic gluconeogenesis in this phase of depleted glycogen stores was insufficient to maintain euglycemia. Substrates derived from fat showed early changes of smaller magnitude. The rise in free fatty acids which occurred was less than twofold the value at birth, though this rise persisted up to 6 h. Whereas glycerol rose transiently, acetoacetate did not change and beta-hydroxybutyrate concentration fell. Both ketone bodies showed a marked rise at 16 h. at a time of diminished free fatty acid levels. Plasma growth hormone, though higher in the fetal than the maternal circulation, showed no consistent change during the period of observation. The changes in levels of the endocrine pancreatic hormones at birth were appropriate in time, magnitude, and direction to be implicated as prime regulators of the metabolic response during the neonatal period in the rat.
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PMID:Fuels, hormones, and liver metabolism at term and during the early postnatal period in the rat. 475 Apr 49

A substance capable of stimulating pyruvate dehydrogenase (PDH) and suppressing glucose-6-phosphatase (G-6-Pase) in a cell-free system was prepared from insulin-treated human placental plasma membranes and peripheral blood mononuclear cells by formic acid extraction. This material was partially purified by molecular-exclusion chromatography, ion-exchange chromatography, and hydroxylapatite chromatography. This was found to stimulate pyruvate dehydrogenase and inhibit glucose-6-phosphatase in a dose-dependent manner. The amount or ability of this substance to stimulate pyruvate dehydrogenase was increased in the proportion to the concentration of insulin. The stimulation of pyruvate dehydrogenase by the factor was eliminated when sodium fluoride was presented in the assay of the activation. This result implied that the activation of pyruvate dehydrogenase was mediated by the stimulation of the phosphatase of pyruvate dehydrogenase complex. Each material isolated from insulin-treated human placental plasma membranes and mononuclear cells shared a number of important characteristics of putative second messengers of insulin action as follows: (i) heat and acid stability; (ii) a similar molecular weight; (iii) increased activity of pyruvate dehydrogenase in a insulin-dependent manner; and (iv) stimulated pyruvate dehydrogenase by the sodium fluoride-sensitive mechanism. This human putative second messenger of insulin action was eluted from the anion-exchange resin AG1-X8 at an ionic strength of 0.3-0.4 M, as well as from the hydroxylapatite column at a phosphate concentration of 0.2-0.3 M.
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PMID:Partial purification from human mononuclear cells and placental plasma membranes of an insulin mediator which stimulates pyruvate dehydrogenase and suppresses glucose-6-phosphatase. 609 86

Primary cultures of liver cells isolated from adult rats by trypsin and collagenase perfusion techniques were carried out to compare cytologic and biochemical properties between the differently prepared cells. Trypsin-dispersed cells consisted of comparatively smaller cells, whereas collagenase-dispersed cells consisted of larger cells. The cell attachment efficiency on culture day 1 was about twice as high in the liver cells prepared with collagenase than those prepared with trypsin. Mature hepatocytes isolated by collagenase perfusion could be maintained in the primary culture for a longer period than those isolated by trypsin perfusion. Epithelial-like clear cells started to grow much earlier in the primary culture of the trypsin-dispersed liver cells than in that of the collagenase-dispersed liver cells. Earlier proliferation of epithelial-like clear cells could not be induced by in vitro trypsinization of the collagenase-dispersed liver cells. Both kinds of enzymatically prepared liver cells showed albumin production and exhibited glucose 6-phosphatase (D-glucose-6-phosphate phosphohydrolase, EC 3.1.3.9, G6Pase) and tyrosine aminotransferase (L-tyrosine: 2-oxoglutarate amino-transferase, EC 2.6.1.5, TAT) activities for 1 week in the primary culture. Albumin production was higher in the liver cells prepared with collagenase than those prepared with trypsin, whereas G6Pase activity was almost the same between them. TAT activity up to culture day 2 was about 3-fold higher in the liver cells prepared with collagenase than in those prepared with trypsin. Combined supplementation of dexamethasone (1 X 10(-5)M) and insulin (10 micrograms/ml) consistently improved the cell attachment efficiency and was very effective in the maintenance of mature hepatocytes in both types. Furthermore, these hormones enhanced the albumin production and TAT activity in both types.
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PMID:Comparison of cytologic and biochemical properties between liver cells isolated from adult rats by trypsin perfusion and those isolated by collagenase perfusion. 614 85

This study examines the early hepatic biochemical and ultrastructural responses to insulin replacement in streptozotocin-diabetic rats and insulin withdrawal from insulin-maintained diabetic rats. Insulin administration rapidly lowered plasma glucose and the elevated glucose-6-phosphatase (G-6-Pase) specific activity of the diabetic rats. However, hepatic glycogen did not increase until after 3 hr of insulin treatment. Hepatic ultrastructure responded to insulin replacement after the decline in glucose and G-6-Pase. This was seen in periportal hepatocytes as a reduction in the close association between smooth endoplasmic reticulum (SER) and glycogen particles in the diabetic animals. The treated rats showed hepatic SER restricted to the periphery of glycogen masses, as is characteristic of these cells from normal rats, in many cells by 6 hr and all cells by 18 hr. Insulin withdrawal from insulin-treated diabetic rats elicited nearly a total reversal of the above events. Plasma insulin declined to a value half that of the normal rats by 6 hr after withdrawal; concurrently, plasma glucose rose sharply to hyperglycemic values as hepatic glycogen content dropped. Following the rise in plasma glucose and fall in glycogen content, G-6-Pase specific activity increased and by 16 hr reached the high values characteristic of the diabetic animal. Hepatic ultrastructure was also changed as evidenced by an intrusion of elements of the SER into the dense glycogen masses; the result was dispersed glycogen closely associated with SER as seen in the diabetic animal. It is concluded that the hepatic response to insulin replacement in diabetic animals and diabetic onset in insulin-withdrawn animals is rapid and occurs through defined stages.
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PMID:The effects of insulin replacement and withdrawal on hepatic ultrastructure and biochemistry. 623 42

The effects of medroxyprogesterone acetate (MPA) and phenobarbital (PB) on hepatic glucose and drug metabolism were investigated in male rats after liver injury, induced with dimethylnitrosamine (DMN). MPA normalized fasting blood glucose (BG) and serum immunoreactive insulin (IRI) levels and enhanced hepatic glucose-6-phosphatase (G6Pase) and NADPH cytochrome P450 reductase activities and glycogen and cytochrome P450 (cytP450) contents after liver injury. PB improved hepatic glycogen and cytP450 contents and NADPH cytP450 reductase activity in DMN pretreated rats. The increase in drug metabolism was more pronounced after PB than MPA therapy whereas MPA had more effect on glucose metabolism than had PB. This suggests that the inducing properties of these compounds diverge from each other.
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PMID:A comparison of the effects of phenobarbital and medroxyprogesterone acetate on drug and glucose metabolism in rats with chemical liver injury. 623 40

The work presented herein describes many of the physiological properties of the phosphofructokinase regulatory factors. Factor activity can be separated into two discrete fractions, which were designated factor A and factor B, based on their respective charges. A preparation containing both factor A and factor B did not protect the following key carbohydrate-metabolizing enzymes from thermal inactivation: glucokinase, glucose-6-phosphatase (solubilized or nonsolubilized forms), pyruvate kinase, glucose-6-P dehydrogenase, muscle-type phosphofructokinase, or the minor liver phosphofructokinase isozyme. Factor activity in this sample was found to be Pronase sensitive, irreversibly precipitated by trichloroacetic acid, reversibly precipitated by adjusting the sample to a pH of 3.0, and stable to heating at 98 degrees C for 20 min. Distribution studies indicated that factor activity was found only in the soluble cell fraction and not in the mitochondrial or nuclear fractions. Factor activity was retained by 12,000-14,000 molecular weight cut-off (MWCO) dialysis tubing, and not retained by 50,000 MWCO dialysis tubing. These studies indicate that fructose-2,6-P2, calmodulin, or insulin-generated mediator are not associated with factor activity. Although fructose-2,6-P2 did not, both factor preparations protect the major liver phosphofructokinase isozyme (liver PFK) from inactivation by lysosomal extracts. In the diabetic rat, the activities of both factors are greatly reduced but return to near normal levels after 48 h of insulin administration. These data suggest that factor B had little or no effect on the kinetic properties of liver PFK. However, factor A was a K-type activator with respect to fructose-6-P, increasing both the Km and Ki for ATP, and slightly increasing the Vm.
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PMID:Properties of the phosphofructokinase regulatory factors. 624 Feb 27


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