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:2.7.1.1 (hexokinase)
5,274 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to evaluate the existence of a glucosensor in different regions of the brain and in the Brockmann bodies (BB) of the rainbow trout, Oncorhynchus mykiss. Five groups (n = 12) of trout were injected intraperitoneally with saline alone (control) or saline-containing bovine glucagon (100 mug/kg), bovine insulin (4 mg/kg), 2-deoxy-d-glucose (100 mg/kg), or d-glucose (500 mg/kg) to promote hyperglycemia (glucagon, d-glucose, 2-deoxy-d-glucose) or hypoglycemia (insulin). Six hours after injection, samples from four brain regions (hypothalamus, telencephalon, hindbrain, and midbrain) and the entire BB were taken. Our results demonstrate within the BB and both the hypothalamus and hindbrain a metabolic response different to that observed in other tissues (midbrain, telencephalon) but similar to that described in tissues known to be glucosensors in mammals. The metabolic responses of these areas to changes in plasma glycemia were characterized by parallel changes in GLUT-2 expression, hexokinase-IV, or glucokinase activity and expression, glycolytic potential, and levels of glycogen and glucose. These changes are similar to those reported in mammalian pancreatic beta-cells and glucose-excited (GE) neurons, two cell types containing glucosensors. This study provides evidence for the presence of glucosensors responsive to hyper- and hypoglycemia in rainbow trout BB, hypothalamus, and hindbrain.
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PMID:Evidence for the presence of a glucosensor in hypothalamus, hindbrain, and Brockmann bodies of rainbow trout. 1717 Feb 35

The hypoglycemic and hypocholesterolemic effects of high and low molecular weight chitosan were evaluated in streptozotocin (STZ)-induced diabetic rats. Rats were divided into three groups of normal rats (Experiment I) and three groups of diabetic rats (Experiment II). The first group received a cellulose (control) diet, the second group received a low MW (1.4 x 10(4)Da) chitosan diet and the third group received a high MW (1.0 x 10(6)Da) chitosan diet. All three diets were containing 0.5% cholesterol. Experiment I: rats fed with high MW or low MW chitosan diet had increased high density lipoprotein (HDL) cholesterol. However, chitosan did not affect plasma glucose in normal rats. Experiment II: significantly decreased plasma glucose and total cholesterol and increased HDL cholesterol and fecal cholesterol excretion were observed in diabetic rats fed with high MW chitosan diet than animals fed with cellulose diet. However, no statistical significant difference in plasma glucose and total cholesterol was observed in diabetic rats fed with low MW chitosan. The total content of SCFAs in cecum was significantly increased and the ratio of acetate to propionate was slight but significantly decreased in diabetic rats after consuming high MW chitosan diet. The activities of hepatic hexokinase were significantly increased and the intestinal disaccharidases including sucrase and maltase were significantly decreased in normal and diabetic rats fed with high MW chitosan diet. Results obtained from the present study demonstrated the potential of high MW chitosan in reducing hyperglycemia and hypercholesterolemia in STZ-induced diabetic rats.
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PMID:A comparative study on hypoglycemic and hypocholesterolemic effects of high and low molecular weight chitosan in streptozotocin-induced diabetic rats. 1825 11

A novel preparation of a dialysed aqueous extract of fenugreek seeds (FSE) that stimulates the insulin signalling pathway was reported previously (Vijayakumar et al., 2005). The present study was designed to investigate the long-term effects (multiple dose effect) of this FSE preparation on the blood glucose level and body weight, and a short-term effect (single dose effect) on serum insulin and hepatic enzymes, in experimentally induced diabetic conditions. The multiple dose effect of FSE on the glucose level and body weight was studied in alloxan (AXN)-diabetic mice in comparison with the vehicle treated control diabetic mice. Intraperitoneal (i.p.) administration of FSE (15 mg/kg body weight (BW)) for 5 consecutive days reduced hyperglycemia in AXN-diabetic mice on day 5 and this effect was further sustained for 10 days. The FSE-induced hypoglycemic effect was accompanied without any reduction in the body weight compared with the diabetic mice in which the body weight was reduced significantly. A single dose effect of FSE on hepatic glucokinase (GK) and hexokinase (HK) enzymes was studied in streptozotocin (STZ)-diabetic mice. Intraperitoneal administration of FSE (15 mg/kg BW) by 90 min decreased the blood glucose levels significantly (p < 0.01) in STZ-diabetic mice and the effect was comparable to that achieved by insulin (1.5 U/kg BW) injection. This effect was associated with a significant enhancement in the liver GK and HK activities on a par with that of insulin. In normal glucose loaded mice, FSE improved the intraperitoneal glucose tolerance accompanied by a reduction in serum insulin concentration. These results are indicative of an extra-pancreatic mode of action of FSE. The present study concludes that this novel FSE preparation corrects metabolic alterations associated with diabetes by exhibiting insulin-like properties and has a potential for clinical applications.
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PMID:Hypoglycemic effect of a novel dialysed fenugreek seeds extract is sustainable and is mediated, in part, by the activation of hepatic enzymes. 1833 83

High intake of dietary fructose has been shown to exert a number of adverse metabolic eff ects in humans and experimental animals. The present study was designed to investigate the eff ect of the aqueous extract of Tinospora cordifolia stem (TCAE) on the adverse eff ects of fructose loading toward carbohydrate and lipid metabolism in rats. Adult male Wistar rats of body weight around 200 g were divided into four groups, two of which were fed with starch diet and the other two with high fructose (66 %) diet. Plant extract of TC (400 mg/kg/day) was administered orally to each group of the starch fed rats and the highfructose fed rats. At the end of 60 days of experimental period, biochemical parameters related to carbohydrate and lipid metabolism were assayed. Hyperglycemia, hyperinsulinemia, hypertriglyceridemia, insulin resistance, and elevated levels of hepatic total lipids, cholesterol, triglycerides, and free fatty acids (p < 0.05) observed in fructose-fed rats were completely prevented with TCAE treatment. Alterations in the activities of enzymes of glucose metabolism (hexokinase, phosphofructokinase, pyruvate kinase, glucose-6-phosphatase, fructose-1,6-bisphosphatase, and glucose-6-phosphate dehydrogenase) and lipid metabolism (fatty acid synthetase, lipoprotein lipase, and malic enzyme) as observed in the high fructose-fed rats were prevented with TCAE administration. In conclusion, our fi ndings indicate improvement of glucose and lipid metabolism in high-fructose fed rats by treatment with Tinospora cordifolia, and suggest that the plant can be used as an adjuvant for the prevention and/or management of insulin resistance and disorders related to it.
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PMID:Beneficiary effect of Tinospora cordifolia against high-fructose diet induced abnormalities in carbohydrate and lipid metabolism in Wistar rats. 1976 7

During diabetes mellitus, endogenous hepatic glucose production is increased as a result of impaired activities of the key enzymes of carbohydrate metabolism, which leads to the condition known as hyperglycemia. D-pinitol, a bioactive constituent isolated from soybeans, has been shown to reduce hyperglycemia in experimental diabetes. We therefore designed this study to investigate the effect of oral administration of D-pinitol (50 mg/kg b. w. for 30 days) on the activities of key enzymes in carbohydrate and glycogen metabolism in the liver tissues of streptozotocin-induced diabetic rats. The efficacy was compared with glyclazide, a standard hypoglycemic drug. Oral administration of D-pinitol to diabetic group of rats showed a marked decrease in the levels of blood glucose, glycosylated hemoglobin and an increase in plasma insulin and body weight. The activities of the hepatic enzymes such as hexokinase, pyruvate kinase, glucose-6-phosphate dehydrogenase, glycogen synthase and hepatic glycogen content were significantly (p < 0.05) increased whereas the activities of glucose-6-phosphatase, fructose-1,6-bisphosphatase, lactate dehydrogenase and glycogen phosphorylase were significantly (p < 0.05) decreased in diabetic rats treated with D-pinitol. The results suggest that alterations in the activities of key metabolic enzymes of carbohydrate metabolism could be one of the biochemical rationale by which D-pinitol attenuates the hyperglycemic effect in diabetic rats.
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PMID:D-pinitol attenuates the impaired activities of hepatic key enzymes in carbohydrate metabolism of streptozotocin-induced diabetic rats. 2003 88

The present work describes the effects of metformin on hexokinase (HK) and phosphofructokinase (PFK) activities and localization in different tissues from streptozotocin-induced diabetic mice. Diabetic mice present lower HK and PFK activities (50%) in skeletal muscle, liver and adipose tissue, as compared with control (P<0.05). Treatment with 250 mg/kg metformin reverses this pattern of enzyme inhibition with concomitant reversal of hyperglycemia and hypolactacidemia. Furthermore, the treatment increases the cytoskeleton-associated PFK activity in skeletal muscle; this activity has been described as an important mechanism for the enzyme activation. This effect might be due to the increased phosphorylation of serine residues in the enzyme, a modification which has been described to increase the interaction of PFK with f-actin. The current work supports the hypothesis that metformin hypoglycemic effects involve the activation of glycolysis through its regulatory enzymes, which may be potential targets for the development of new hypoglycemic drugs.
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PMID:Metformin reverses hexokinase and 6-phosphofructo-1-kinase inhibition in skeletal muscle, liver and adipose tissues from streptozotocin-induced diabetic mouse. 2011 72

Decoctions and infusions of Artocarpus communis (Forst.) (family: Moraceae) root-bark are commonly used traditionally among the Yoruba-speaking people of Western Nigeria as folk remedies for the management, control and/or treatment of an array of human diseases, including type 2, adult-onset diabetes mellitus. Although numerous bioactive flavonoids have been isolated from the roots, stem-bark and leaves of A. communis, to the best of our knowledge, the effects of the plant's root-bark extract on animal model of diabetes mellitus and on liver tissues have hitherto, not been reported in the biomedical literature. In view of this, the present study was undertaken to investigate the glycaemic effect of, and hepatic tissue ultrastructural, morphological and metabolic changes induced by A. communis root-bark aqueous extract (ACE) in Wistar rats. The ultrastructural, morphological and metabolic effects of ACE have been compared with those induced by streptozotocin (STZ) in rat experimental paradigms. Four groups (A, B, C and D) of Wistar rats, each group containing 10 rats, were used. Diabetes mellitus was induced in the diabetic groups B and C animals by intraperitoneal injections of STZ (75 mg/kg body weight), while group A rats received A. communis root-bark aqueous extract (ACE, 100 mg/kg body weight, i.p.) alone. Control group D rats received distilled water in quantities equivalent to the volume of ACE administered intraperitoneally. The rats in group C were additionally treated with ACE (100 mg/kg body weight i. p.) daily from day 3 to day 10 after STZ treatment. Hepatic glucokinase, hexokinase, glutamate dehydrogenase, succinate dehydrogenase, beta-hydroxybutyrate dehydrogenase, serum insulin and blood glucose levels of the animals were measured and recorded before and after ACE, STZ and STZ+ACE treatments. Hepatic tissues were also processed for transmission electron microscopy. Electron microscopic examinations showed toxic, deleterious alterations in the ultrastructures of groups A, B and C hepatic cells, the most prominent deleterious effects being on the hepatocytes. Ultrastructural changes observed within the hepatocytes of groups A, B and C rats include disrupted mitochondria with increase in lipid droplets, extensive hepatocellular vacuolation, scanty rough endoplasmic reticulum (RER) and ribosomes. Large glycogen clusters were also noticed displacing the mitochondria and RER in group A rats. Group A rats also developed significant hyperglycemia (p<0.05) immediately after ACE administration, while groups B and C rats developed hyperglycemia 24 hours after STZ treatment. When compared with the control group D rats, the activities of all the three subsystems were disrupted, leading to overall inhibition of oxidative phosphorylation of the liver mitochondria in groups A, B and C rats, but remain normal in the untreated group D control rats. The findings of the present study indicate that A. communis root-bark aqueous extract induces hyperglycaemia in the experimental animal model used, and that the plant's extract disrupts the ultrastructural characteristics and architecture of hepatocytes as well as oxidative energy metabolism.
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PMID:Artocarpus communis Forst. root-bark aqueous extract- and streptozotocin-induced ultrastructural and metabolic changes in hepatic tissues of Wistar rats. 2016 8

The aim of the present study was to evaluate the effects of aqueous seed extract of Tephrosia purpurea (TpASet) on blood glucose and antioxidant status in streptozotocin induced diabetic rats. Hyperglycemia associated with an altered hexokinase and glucose-6-phosphatase activities, elevated lipid peroxidation, disturbed enzymatic [Superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx)] and non enzymatic [Glutathione, vitamin C and vitamin E] antioxidant status were observed in streptozotocin induced diabetic rats. Oral administration of "TpASet" at a dose of 600 mg/kg body weight showed significant improvement in above mentioned parameters. Our results clearly indicate that "TpASet" has potent antihyperglycemic and antioxidant effects in streptozotocin-induced diabetic rats and therefore further studies are warranted to isolate and characterize the bioactive principles from "TpASet".
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PMID:Effects of Tephrosia purpurea aqueous seed extract on blood glucose and antioxidant enzyme activities in streptozotocin induced diabetic rats. 2016 45

Glucokinase Glucokinase (GK GK ; EC 2.7.1.1.) phosphorylates and regulates glucose metabolism in insulin-producing pancreatic beta-cells, hepatocytes, and certain cells of the endocrine and nervous systems allowing it to play a central role in glucose homeostasis glucose homeostasis . Most importantly, it serves as glucose sensor glucose sensor in pancreatic beta-cells mediating glucose-stimulated insulin biosynthesis and release and it governs the capacity of the liver to convert glucose to glycogen. Activating and inactivating mutations of the glucokinase gene cause autosomal dominant hyperinsulinemic hypoglycemia and hypoinsulinemic hyperglycemia in humans, respectively, illustrating the preeminent role of glucokinase in the regulation of blood glucose and also identifying the enzyme as a potential target for developing antidiabetic drugs antidiabetic drugs . Small molecules called glucokinase activators (GKAs) glucokinase activators (GKAs) which bind to an allosteric activator allosteric activator site of the enzyme have indeed been discovered and hold great promise as new antidiabetic agents. GKAs increase the enzyme's affinity for glucose and also its maximal catalytic rate. Consequently, they stimulate insulin biosynthesis and secretion, enhance hepatic glucose uptake, and augment glucose metabolism and related processes in other glucokinase-expressing cells. Manifestations of these effects, most prominently a lowering of blood glucose, are observed in normal laboratory animals and man but also in animal models of diabetes and patients with type 2 diabetes mellitus (T2DM T2DM ) type 2 diabetes mellitus (T2DM) . These compelling concepts and results sustain a strong R&D effort by many pharmaceutical companies to generate GKAs with characteristics allowing for a novel drug treatment of T2DM.
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PMID:Research and development of glucokinase activators for diabetes therapy: theoretical and practical aspects. 2148 79

We previously showed that total sleep deprivation increased antioxidant responses in several rat brain regions. We also reported that chronic hypoxia enhanced antioxidant responses and increased oxidative stress in rat cerebellum and pons, relative to normoxic conditions. In the current study, we examined the interaction between these two parameters (sleep and hypoxia). We exposed rats to total sleep deprivation under sustained hypoxia (SDSH) and compared changes in antioxidant responses and oxidative stress markers in the neocortex, hippocampus, brainstem, and cerebellum to those in control animals left undisturbed under either sustained hypoxia (UCSH) or normoxia (UCN). We measured changes in total nitrite levels as an indicator of nitric oxide (NO) production, superoxide dismutase (SOD) activity and total glutathione (GSHt) levels as markers of antioxidant responses, and levels of thiobarbituric acid-reactive substances (TBARS) and protein carbonyls as signs of lipid and protein oxidation products, respectively. We found that acute (6h) SDSH increased NO production in the hippocampus and increased GSHt levels in the neocortex, brainstem, and cerebellum while decreasing hippocampal lipid oxidation. Additionally, we observed increased hexokinase activity in the neocortex of SDSH rats compared to UCSH rats, suggesting that elevated glucose metabolism may be one potential source of the enhanced free radicals produced in this brain region. We conclude that short-term insomnia under hypoxia may serve as an adaptive response to prevent oxidative stress.
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PMID:Sleep deprivation under sustained hypoxia protects against oxidative stress. 2190 78


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