Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.1.1 (hexokinase)
 5,274 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Streptozotocin treatment (125 mg/kg) in the Chinese hamster induced hyperglycaemia, hypoinsulinaemia, hyperglucagonaemia and changes in body, liver, pancreas, stomach, kidney and adipose tissue weights. The pancreatic reserves of insulin and glucagon in the diabetic animals were low, but stomach glucagon high. These animals showed high levels of phosphoenolpyruvate carboxykinase and low levels of glucokinase, hexokinase, isocitrate dehydrogenase and malic enzyme, but normal levels of pyruvate kinase in the liver. Increases in lactate dehydrogenase subunit B and isozymes 2, 3 and 4 were also observed in the liver, but not in the epididymal fat pad, of the diabetic animals. N-Acetyl-beta-D-glucosaminidase was elevated in plasma, liver and heart, but not in the kidney of the treated animals. Renal alpha-galactosidase and beta-glucosidase were depressed, whereas beta-galactosidase and alpha-glucosidase remained essentially normal. These features indicated that there were considerable differences between the biochemical disorders associated with streptozotocin-diabetes in the Chinese hamster and the published observations in the rat.
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PMID:Streptozotocin-induced diabetes in the Chinese hamster. Biochemical and endocrine disorders. 59 Jun 51

Chronic (6 days) hyperinsulinaemia in young rats produced lower blood glucose concentrations and augmented body- and liver-weight gain. The insulin-treated rats had increased hepatic activities of citrate-cleavage enzyme, 'malic' enzyme and high-substrate (6.6 mM-phosphoenolpyruvate) pyruvate kinase, and decreased glucose 6-phosphatase. There were no changes in activities of phosphoenolpyruvate carboxykinase, phosphofructokinase, low-substrate (1.3 mM-phosphoenolpyruvate) pyruvate kinase, glucokinase and hexokinase.
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PMID:Effects of chronic hyperinsulinaemia on hepatic enzymes involved in lipogenesis and carbohydrate metabolism in the young rat. 66 50

The Glucose-Controlled Insulin Infusion System (Biostator) is a modular, computerized, feedback control system for dynamic control of blood glucose concentrations in diabetics. This on-line glucose analyzer for use with whole blood utilizes a novel enzyme (glucose oxidase)-membrane configuration and an electrochemical cell to measure the H202 generated. The analyzer exhibits both short- and long-range stability, and instrument response and analyte concentration are linearly related over the full range of clinical interest. The response is fast, accurate, and precise, and permits determination of blood glucose within 2 min from the moment the blood leaves the patient. Correlation studies were completed to show the agreement between the Biostator Glucose Analyzer and the FDA's recommended hexokinase/glucose-6-phosphate dehydrogenase procedure on whole blood (e.g., average per cent recovered for 11 concentrations between 250 and 900 mg/liter was: hexokinase, 95.6%, Biostator Analyzer, 95.9%; bias and SDd, respectively, at low, normal, and high glucose values were: 12 and 41 mg/liter at the 500 mg/liter level; 4 and 52 mg/liter at the 1000 mg/liter level, and 4 and 128 mg/liter at the 4000 mg/liter level). No appreciable interference is observed with above-normal concentrations of bilirubin, uric acid, creatinine, sodium salicylate, or dextran. Platelet adhesion, which tends to decrease the useful life of the membrane, has been significantly decreased.
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PMID:Development and evaluation of a glucose analyzer for a glucose controlled insulin infusion system ((Biostator). 67 60

A prolonged glucose load was administered to four patients with hypokalaemic periodic paralysis and four healthy control sujbects. Muscle ATP and CP concentrations as well as lactate dehydrogenase, hexokinase and phosphorylase activities were similar in those two groups, but succinate dehydrogenase was approximately 50% higher in the control muscles. Muscles fibre composition was almost identical in the two groups, whereas patients had a higher degree of capillarization. Complete muscle weakness was produced in all patients, accompanied by hypokalaemia. Glucose loading resulted in elevated insulin levels and a minor rise in blood glucose level was seen in the patients compared to the control subjects. Glucose loading decreased hexokinase activity in controls, but increased this in the patients. At similar times, muscle and blood lactate levels and blood pyruvate values were generally higher in the patients over the course of the experiment. Initial glycogen concentrations were higher in patients, but glucose loading did not result in greatly increased glycogen values. These data suggest that patients with hypokalaemic periodic paralysis have an enhanced metabolism of carbohydrates and that insulin seems to be an important factor leading to the onset of muscle weakness.
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PMID:Skeletal muscle characteristics and carbohydrate metabolism after glucose loading in hypokalaemic periodic paralysis. 70 37

To learn whether a single dialysis can acutely improve the intravenous glucose tolerance (i.v.GTT) of chronically dialyzed patients, a standard i.v.GTT was performed on 10 nonobese uremic subjects on maintenance hemodialysis for 27 +/- 9 (mean +/- SEM) mo, and on a control group of 13 normal subjects. The uremic patients were tested first 0.2-17 (range) hr, and then 65-109 hr, from last dialysis. In the uremic sera, plasma glucose was analyzed by 4 methods; 2 reducing (neocopurine and ferricyanide) and 2 enzymatic (hexokinase and glucose oxidase). The reducing methods markedly overestimated plasma glucose concentration because of the presence of nonglucose reducing substances (notably, creatinine). This inteference was significantly cut down by dialysis. A single dialysis, on the other hand, failed to improve the glucose fractional decay rate (KG) computed from the glucose oxidase data (1.69 +/- 0.2%/min before and 1.35 +/- 0.1 after dialysis, versus 1.47 +/- 0.1 of the normal subjects). The same conclusion was derived from the data measured by the other 3 methods of glucose assay. Fasting plasma insulin concentrations were, on average, above normal (5.5 +/- 0.6 muU/ml) both before (12.3 +/- 2.7, p less than 0.05) and after (17.2 +/- 3.5, p less than 0.01) a single dialysis. Likewise, the area under the glucose-induced plasma insulin curve was significantly greater than normal (1.46 +/- 0.21 mU/ml . min) both before (2.26 +/- 0.34, p less than 0.05), and after (2.86 +/- 0.43, p less than 0.01) dialysis. A single dialysis had little effect on either basal or glucose-stimulated insulin release, and no significant difference in the insulinogenic index (insulin area/glucose area) was found between the control and the uremic group in either test. Insulin response was not correlated with KG, whereas it was significantly associated with higher triglyceride levels. Creatinine, urea or methylguanidine did not appear to have any influence on KG, but lower serum potassium levels were significantly associated with poorer i.v.GTT's. Plasma calcium bore a reciprocal relation to the insulinogenic index. Chronically dialyzed subjects show some degree of tissue insulin resistance, which a single dialysis fails to correct. Electrolyte disturbances may play a role in this metabolic derangement.
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PMID:The response to intravenous glucose of patients on maintenance hemodialysis: effects of dialysis. 76 47

An immediate effect of hormones (insulin, oxytocin, glucocorticoids and sex hormones) on the conformation and activity of enzymatically active proteins (hexokinase, glutamate dehydrogenase) was studied. Hormone-enzyme complex of insulin-hexokinase was shown to be formed. This process was accompanied by dissociation of the enzyme into two dimers without a loss of the catalytic activity but with disappearance of the property to be inhibited by glucocorticoids. The effect of insulin on the hexokinase activity was postulated to occur due to reaction of thiol-disulphide exchange between disulphide group of insulin and free sulfhydryl group of hexokinase. The inhibitory effect of sex hormones on the glutamate dehydrogenase activity was shown to be determined by their association with the enzymatically active protein. This phenomenon did not occur under conditions of stabilization of the quaternary structure of the enzyme. If the guanidine groups of glutamate dehydrogenase were blocked the inhibitory effect of sex hormones was found to decrease. These data demonstrate the importance of the guanidine groups in binding of sex hormones.
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PMID:[Effect of insulin and steroid hormones on the conformation and activity of enzyme proteins]. 85 7

Decrease in the activity of hexokinase was found in soluble fraction of stomach smooth muscles of rabbits with alloxane diabetes. Administration of insulin into intact rabbits led to distinct decrease in the activity of lactate and malate dehydrogenases in cells of the stomach fundal part. In smooth muscles of rabbits with alloxane diabetes pyruvate was formed from lactate at a higher rate (increase in content of LDH1 and LDH2) and after administration of insulin into the animals--lactate was formed from pyruvate at an increased rate.
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PMID:[Effect of insulin and insulin deficiency on the activity of hexokinase, malate dehydrogenase, lactate dehydrogenase and its isoenzyme composition in the smooth muscle of the rabbit stomach]. 91 76

The authors investigated the in vitro functional differentiation of fetal mouse liver cultured in Rose's circumfusion system with the use of two biochemical markers: The analysis of the inductive response of key enzymes in carbohydrate metabolism to insulin, and the analysis of the liver-specific isozyme of pyruvate kinase [EC 2.7.1.40]. The glucokinase [EC 2.7.1.2] activity, which is only found in mammalian adult liver, emerged on cultivation of 2-3 days and reached a maximum level equivalent to one-half of the adult level. Two- or 3-fold increases in the glucokinase, pyruvate kinase, and glucose-6-phosphate dehydrogenase [EC 1.1.1.49] were induced by a single dose of insulin in fetal liver after 12 days of cultivaton. Hexokinase [EC 2.7.1.1] activity was barely influenced by insulin. These results suggested that fetal mouse liver cultured in this system for 2 weeks maintained the same response to insulin as in vivo adult mouse liver. The pyruvate kinase isozyme patterns of mouse livers in various developmental stages and of cultured fetal mouse liver in the present system were investigated by isoelectric fractionation. The pyruvate kinase isozymes having the highest relative activity were the pI-5.5 isozyme for the adult liver and the pI-6.5 isozyme for 13- to 14-day-old fetal liver. As development in vivo proceeded, a gradual change in isozyme pattern occurred; this consisted of a progressive decrease of the pI-6.5 pyruvate kinase isozyme, "fetal type," in favor of the pI-5.5 isozyme, "adult type." The pyruvate kinase isozyme pattern in 13- to 14-day fetal liver cultured in the system for 2 weeks was similar to that found in adult liver. Thus, it was shown that "fetal type" pyruvate kinase was also replaced by "adult type" pyruvate kinase in vitro. It can be concluded from these findings that fetal mouseliver cultured in the circumfusion system for 2 weeks maintains its functional and morphological identitites as it differentiates toward the adult liver.
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PMID:Functional differentiation of mouse fetal liver in circumfusion system cultures. 93 74

The marked stimulatory effect of insulin on the conversion of 20 mM D-[6-14C]glucose to CO2, glyceride-glycerol, and fatty acid observed in small rat adipocytes was greatly diminished in large cells from older rats. Similarly, total glucose utilization as estimated by summing the total metabolites accumulated intracellularly plus the release of labeled CO2 and lactate was substantially lower in large cells in the presence of insulin and 5 mM labeled glucose. However, under conditions of 0.2 mM medium glucose where transport of the hexose into adipocytes is relatively more rate-limiting for subsequent metabolism, large cells actually utilized slightly greater total amounts of glucose than small cells in the presence of insulin. Increments of total glucose utilization due to both submaximal and maximal doses of insulin were similar in large and small cells incubated with a low glucose concentration. Under these conditions, conversion of labeled glucose to CO2 and fatty acid in response to insulin was somewhat diminished in large cells, while conversion to glyceride-glycerol was enhanced. The activity of the D-glucose transport system in large and small cells was estimated by monitoring initial rates and small cells was estimated by monitoring initial rates of 3-O-[3H]methylglucose uptake by a rapid filtration method. Transport system activity on a per cell basis was actually severalfold higher in large adipocytes in the basal state as well as in the presence of submaximal and maximal concentrations of insulin compared to small cells. However, the percent stimulation by insulin was less in the large cells. Uptake of 2-deoxyglucose under basal conditions and in response to insulin was also higher in large cells compared to small cells. Analysis of the accumulated label in extracts from fat cells incubated with D-[14C]deoxyglucose revealed the presence of free deoxyglucose, deoxyglucose-6-phosphate, and 6-phosphodeoxygluconate. The levels of these metabolites were significantly higher in large cells compared to small cells indicating hexokinase activity appears not to account for the defective glucose utilization in large cells at high glucose concentrations. It is concluded that (a) possible defects in insulin receptor components, the D-glucose transport system, and the coupling mechanism which links these entities do not significantly contribute to the apparent insulin-insensitivity of large fat cells and (b) the principal cellular defect which confers this blunted insulin response to large rat adipocytes involves one or more intracellular enzymes involved in glucose metabolism.
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PMID:Cellular basis of insulin insensitivity in large rat adipocytes. 93 92

Prolonged, for a period of 5 cycles, immunization of rabbits with tick-borne encephalitis virus, reproduced in the brain of albino mice, caused diabetogenic reaction of the carbohydrate metabolism. It was expressed in hyperglycemia, reduction of hexokinase activity and of glycolysis of hepatic tissue and activation of phosphorylase, glycogenolysis and pentous way of carbohydrate transformation. Metabolic changes were accompanied by a reduction of insulin activity of the immunized rabbit serum. An analogous administration of a more pathogenic virus (of western equine encephalomyelitis) led to changes (equal in value) in the functional condition of the pancreas with much lesser shifts in the biochemical idices of the carbohydrate metabolism.
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PMID:[Peculiarities of carbohydrate metabolism in rabbits following prolonged immunization with viral antigens]. 100 47


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