3-O-Methylglucose
Glucose
Biological Transport
Brain
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
Escherichia coli O157
A verocytotoxin-producing serogroup belonging to the O subfamily of Escherichia coli which has been shown to cause severe food-borne disease. A strain from this serogroup, serotype H7, which produces SHIGA TOXINS, has been linked to human disease outbreaks resulting from contamination of foods by E. coli O157 from bovine origin.
O(6)-Methylguanine-DNA Methyltransferase
Manufactured Materials
Facility Regulation and Control
United States Food and Drug Administration
Cosmetics
Substances intended to be applied to the human body for cleansing, beautifying, promoting attractiveness, or altering the appearance without affecting the body's structure or functions. Included in this definition are skin creams, lotions, perfumes, lipsticks, fingernail polishes, eye and facial makeup preparations, permanent waves, hair colors, toothpastes, and deodorants, as well as any material intended for use as a component of a cosmetic product. (U.S. Food & Drug Administration Center for Food Safety & Applied Nutrition Office of Cosmetics Fact Sheet (web page) Feb 1995)
Hexokinase
An enzyme that catalyzes the conversion of ATP and a D-hexose to ADP and a D-hexose 6-phosphate. D-Glucose, D-mannose, D-fructose, sorbitol, and D-glucosamine can act as acceptors; ITP and dATP can act as donors. The liver isoenzyme has sometimes been called glucokinase. (From Enzyme Nomenclature, 1992) EC 2.7.1.1.
Sunscreening Agents
Sunburn
Sun Protection Factor
Protective Clothing
DEET
Argasidae
Emollients
Dictionaries as Topic
Television
The transmission and reproduction of transient images of fixed or moving objects. An electronic system of transmitting such images together with sound over a wire or through space by apparatus that converts light and sound into electrical waves and reconverts them into visible light rays and audible sound. (From Webster, 3rd ed)
Melanoma
A malignant neoplasm derived from cells that are capable of forming melanin, which may occur in the skin of any part of the body, in the eye, or, rarely, in the mucous membranes of the genitalia, anus, oral cavity, or other sites. It occurs mostly in adults and may originate de novo or from a pigmented nevus or malignant lentigo. Melanomas frequently metastasize widely, and the regional lymph nodes, liver, lungs, and brain are likely to be involved. The incidence of malignant skin melanomas is rising rapidly in all parts of the world. (Stedman, 25th ed; from Rook et al., Textbook of Dermatology, 4th ed, p2445)
Treatment Outcome
Antineoplastic Combined Chemotherapy Protocols
Disease-Free Survival
Survival Rate
Survival Analysis
A class of statistical procedures for estimating the survival function (function of time, starting with a population 100% well at a given time and providing the percentage of the population still well at later times). The survival analysis is then used for making inferences about the effects of treatments, prognostic factors, exposures, and other covariates on the function.
Streptozocin
Diabetes Mellitus, Experimental
Insulin
A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).
Ketoconazole
Hair Preparations
Dermatitis, Seborrheic
A chronic inflammatory disease of the skin with unknown etiology. It is characterized by moderate ERYTHEMA, dry, moist, or greasy (SEBACEOUS GLAND) scaling and yellow crusted patches on various areas, especially the scalp, that exfoliate as dandruff. Seborrheic dermatitis is common in children and adolescents with HIV INFECTIONS.
Lice Infestations
Pediculus
Macrostomia
Micronesia
Hemophilia B
A deficiency of blood coagulation factor IX inherited as an X-linked disorder. (Also known as Christmas Disease, after the first patient studied in detail, not the holy day.) Historical and clinical features resemble those in classic hemophilia (HEMOPHILIA A), but patients present with fewer symptoms. Severity of bleeding is usually similar in members of a single family. Many patients are asymptomatic until the hemostatic system is stressed by surgery or trauma. Treatment is similar to that for hemophilia A. (From Cecil Textbook of Medicine, 19th ed, p1008)
Oral Hemorrhage
Mannose inhibits Arabidopsis germination via a hexokinase-mediated step. (1/363)
Low concentrations of the glucose (Glc) analog mannose (Man) inhibit germination of Arabidopsis seeds. Man is phosphorylated by hexokinase (HXK), but the absence of germination was not due to ATP or phosphate depletion. The addition of metabolizable sugars reversed the Man-mediated inhibition of germination. Carbohydrate-mediated regulation of gene expression involving a HXK-mediated pathway is known to be activated by Glc, Man, and other monosaccharides. Therefore, we investigated whether Man blocks germination through this system. By testing other Glc analogs, we found that 2-deoxyglucose, which, like Man, is phosphorylated by HXK, also blocked germination; no inhibition was observed with 6-deoxyglucose or 3-O-methylglucose, which are not substrates for HXK. Since these latter two sugars are taken up at a rate similar to that of Man, uptake is unlikely to be involved in the inhibition of germination. Furthermore, we show that mannoheptulose, a specific HXK inhibitor, restores germination of seeds grown in the presence of Man. We conclude that HXK is involved in the Man-mediated repression of germination of Arabidopsis seeds, possibly via energy depletion. (+info)Acute increase, stimulated by prostaglandin E2, in glucose absorption via the sodium dependent glucose transporter-1 in rat intestine. (2/363)
BACKGROUND/AIMS: Acute stimulation by cAMP of the sodium dependent glucose cotransporter SGLT1 has previously been shown. As prostaglandin E2 (PGE2) increases intracellular cAMP concentrations via its receptor subtypes EP2R and EP4R, it was investigated whether PGE2 could enhance intestinal glucose absorption. METHODS: The action of PGE2 on carbohydrate absorption in the ex situ perfused rat small intestine and on 3-O-[14C]methylglucose uptake in isolated villus tip enterocytes was determined. Expression of mRNA for the PGE2 receptor subtypes 1-4 was assayed in enterocytes by reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS: In the perfused small intestine, PGE2 acutely increased absorption of glucose and galactose, but not fructose (which is not a substrate for SGLT1); in isolated enterocytes it stimulated 3-O-[14C]methylglucose uptake. The 3-O-[14C]methylglucose uptake could be inhibited by the cAMP antagonist RpcAMPS and the specific inhibitor of SGLT1, phlorizin. High levels of EP2R mRNA and EP4R mRNA were detected in villus tip enterocytes. CONCLUSION: PGE2 acutely increased glucose and galactose absorption by the small intestine via the SGLT1, with cAMP serving as the second messenger. PGE2 acted directly on the enterocytes, as the stimulation was still observed in isolated enterocytes and RT-PCR detected mRNA for the cAMP-increasing PGE2 receptors EP2R and EP4R. (+info)Muscle fiber type-specific defects in insulin signal transduction to glucose transport in diabetic GK rats. (3/363)
To determine whether defects in the insulin signal transduction pathway to glucose transport occur in a muscle fiber type-specific manner, post-receptor insulin-signaling events were assessed in oxidative (soleus) and glycolytic (extensor digitorum longus [EDL]) skeletal muscle from Wistar or diabetic GK rats. In soleus muscle from GK rats, maximal insulin-stimulated (120 nmol/l) glucose transport was significantly decreased, compared with that of Wistar rats. In EDL muscle from GK rats, maximal insulin-stimulated glucose transport was normal, while the submaximal response was reduced compared with that of Wistar rats. We next treated diabetic GK rats with phlorizin for 4 weeks to determine whether restoration of glycemia would lead to improved insulin signal transduction. Phlorizin treatment of GK rats resulted in full restoration of insulin-stimulated glucose transport in soleus and EDL muscle. In soleus muscle from GK rats, submaximal and maximal insulin-stimulated insulin receptor substrate (IRS)-1 tyrosine phosphorylation and IRS-1-associated phosphatidylinositol (PI) 3-kinase activity were markedly reduced, compared with that of Wistar rats, but only submaximal insulin-stimulated PI 3-kinase was restored after phlorizin treatment. In EDL muscle, insulin-stimulated IRS-1 tyrosine phosphorylation and IRS-1-associated PI-3 kinase were not altered between GK and Wistar rats. Maximal insulin-stimulated Akt (protein kinase B) kinase activity is decreased in soleus muscle from GK rats and restored upon normalization of glycemia (Krook et al., Diabetes 46:2100-2114, 1997). Here, we show that in EDL muscle from GK rats, maximal insulin-stimulated Akt kinase activity is also impaired and restored to Wistar rat levels after phlorizin treatment. In conclusion, functional defects in IRS-1 and PI 3-kinase in skeletal muscle from diabetic GK rats are fiber-type-specific, with alterations observed in oxidative, but not glycolytic, muscle. Furthermore, regardless of muscle fiber type, downstream steps to PI 3-kinase (i.e., Akt and glucose transport) are sensitive to changes in the level of glycemia. (+info)An inhibitor of p38 mitogen-activated protein kinase prevents insulin-stimulated glucose transport but not glucose transporter translocation in 3T3-L1 adipocytes and L6 myotubes. (4/363)
The precise mechanisms underlying insulin-stimulated glucose transport still require investigation. Here we assessed the effect of SB203580, an inhibitor of the p38 MAP kinase family, on insulin-stimulated glucose transport in 3T3-L1 adipocytes and L6 myotubes. We found that SB203580, but not its inactive analogue (SB202474), prevented insulin-stimulated glucose transport in both cell types with an IC50 similar to that for inhibition of p38 MAP kinase (0.6 microM). Basal glucose uptake was not affected. Moreover, SB203580 added only during the transport assay did not inhibit basal or insulin-stimulated transport. SB203580 did not inhibit insulin-stimulated translocation of the glucose transporters GLUT1 or GLUT4 in 3T3-L1 adipocytes as assessed by immunoblotting of subcellular fractions or by immunofluorescence of membrane lawns. L6 muscle cells expressing GLUT4 tagged on an extracellular domain with a Myc epitope (GLUT4myc) were used to assess the functional insertion of GLUT4 into the plasma membrane. SB203580 did not affect the insulin-induced gain in GLUT4myc exposure at the cell surface but largely reduced the stimulation of glucose uptake. SB203580 had no effect on insulin-dependent insulin receptor substrate-1 phosphorylation, association of the p85 subunit of phosphatidylinositol 3-kinase with insulin receptor substrate-1, nor on phosphatidylinositol 3-kinase, Akt1, Akt2, or Akt3 activities in 3T3-L1 adipocytes. In conclusion, in the presence of SB203580, insulin caused normal translocation and cell surface membrane insertion of glucose transporters without stimulating glucose transport. We propose that insulin stimulates two independent signals contributing to stimulation of glucose transport: phosphatidylinositol 3-kinase leads to glucose transporter translocation and a pathway involving p38 MAP kinase leads to activation of the recruited glucose transporter at the membrane. (+info)TGF-beta 1 stimulates glucose uptake by enhancing GLUT1 expression in mesangial cells. (5/363)
BACKGROUND: An increase in the expression of transforming growth factor-beta 1 (TGF-beta 1) has been proposed to play an important role in the excessive production of extracellular matrix (ECM) proteins seen in diabetes. Because the linkage between glucose metabolism and ECM protein production was found in mesangial cells overexpressed with the brain-type glucose transporter (GLUT1), we hypothesized that TGF-beta 1 could affect glucose metabolism. METHODS: To prove this hypothesis, we examined the effect of TGF-beta 1 on glucose uptake, the first step of glucose metabolism, in mesangial cells. 2-Deoxy-D-glucose (2DOG) uptake and the expression of GLUT1 were measured in mesangial cells exposed to various concentrations of TGF-beta 1. The kinetic constants were determined using 2DOG and 3-O-methyl-D-glucose (3OMG). The effect of anti-TGF-beta neutralizing antibody on 2DOG uptake and GLUT1 mRNA was also examined in mesangial cells cultured under high-glucose (22.2 mM) conditions for 72 hours. RESULTS: TGF-beta 1 stimulated 2DOG uptake in mesangial cells by approximately 2.5-fold in a dose- (1.25 ng/ml maximum) and time-dependent manner, with a peak stimulation at nine hours. The increase in 2DOG uptake by TGF-beta 1 was completely abolished by the addition of 1 microgram/ml cycloheximide, and kinetic analysis of 2DOG or 3OMG uptake revealed an increase in Vmax by TGF-beta 1. Furthermore, TGF-beta 1 enhanced the expression of GLUT1 mRNA from one hour, followed by an enhancement of the expression of GLUT1 protein at nine hours. Finally, 2DOG uptake was significantly enhanced in cells cultured under high-glucose (22.2 mM) conditions as compared with that in cells under normal glucose (5.6 mM) conditions, and this increase in 2DOG uptake in cells under high-glucose conditions was inhibited by the addition of anti-TGF-beta neutralizing antibody. CONCLUSIONS: TGF-beta 1 stimulates glucose uptake by enhancing the expression of GLUT1 in mesangial cells, which leads to the acceleration of intracellular metabolic abnormalities in diabetes. (+info)Characterization of cyclosporin A transport in cultured rabbit corneal epithelial cells: P-glycoprotein transport activity and binding to cyclophilin. (6/363)
PURPOSE: The purpose of this study was to characterize cyclosporin A (CsA) uptake and transport in cultured rabbit corneal epithelial cells (RCECs). METHODS: CsA uptake was evaluated by measuring time-dependent 3H-CsA accumulation in confluent RCECs. Bidirectional 3H-CsA fluxes were measured across the RCEC layers grown on Transwell-COL culture plate inserts. The anti-P-gp monoclonal antibody C219 was used in western blot analysis to probe for the presence of P-gp in these cells. RESULTS: The accumulation of 3H-CsA was time and temperature dependent. Steady state was reached by 60 minutes. The initial uptake was saturable and was suppressed as a function of increases in preloading with unlabeled CsA. This uptake process was enhanced by metabolic inhibition with either 3-O-methylglucose, MG, or 10 mM NaN3 and 3-O-MG. The largest increase was obtained with 10 mM NaN3 in combination with 3-O-MG. In their presence, uptake increased by 40%. A multidrug-resistance (MDR)-reversing agent (i.e., 500 microM verapamil, 100 microM vincristine, 100 microM progesterone, 100 microM testosterone, 500 microM quinidine, or 100 microM chlorpromazine) significantly increased 3H-CsA accumulation. The largest increase was obtained with 500 microM quinidine (i.e., 36%). Conversely, verapamil and vincristine produced the largest inhibition of 3H-CsA efflux (i.e., 19% and 28%, respectively). However, in the presence of 10 microM unlabeled CsA, 3H-CsA efflux increased. 3H-CsA flux across RCEC layers showed marked directional asymmetry. The stromal (S) to tear (T) side transcellular 3H-CsA permeability coefficient (Ptrans) was approximately seven times higher than that in the T-to-S direction. The S-to-T Ptrans was reduced by an MDR-reversing agent by up to 40%. Western blot analysis of lysates revealed a 170-kDa membrane protein band. CONCLUSIONS: These results suggest that in RCEC the tear-side-facing membrane has a P-gp-mediated drug efflux pump. In addition, there is suggestive evidence for the presence of the cytosolic protein, cyclophilin. The presence of P-gp in these cells could help protect them from being damaged by the uptake of toxic substances. (+info)In vitro analysis of the glucose-transport system in GLUT4-null skeletal muscle. (7/363)
We have characterized the glucose-transport system in soleus muscle from female GLUT4-null mice to determine whether GLUT1, 3 or 5 account for insulin-stimulated glucose-transport activity. Insulin increased 2-deoxyglucose uptake 2.8- and 2.1-fold in soleus muscle from wild-type and GLUT4-null mice, respectively. Cytochalasin B, an inhibitor of GLUT1- and GLUT4-mediated glucose transport, inhibited insulin-stimulated 2-deoxyglucose uptake by >95% in wild-type and GLUT4-null soleus muscle. Addition of 35 mM fructose to the incubation media was without effect on insulin-stimulated 3-O-methylglucose transport activity in soleus muscle from either genotype, whereas 35 mM glucose inhibited insulin-stimulated (20 nM) 3-O-methylglucose transport by 65% in wild-type and 99% in GLUT4-null mice. We utilized the 2-N-4-1-(1-azi-2,2,2-triflu oroethyl)benzoyl-1, 3-bis(D-mannose-4-yloxy)-2-propylamine (ATB-BMPA) exofacial photolabel to determine if increased cell-surface GLUT1 or GLUT4 content accounted for insulin-stimulated glucose transport in GLUT4-null muscle. In wild-type soleus muscle, cell-surface GLUT4 content was increased by 2.8-fold under insulin-stimulated conditions and this increase corresponded to the increase in 2-deoxyglucose uptake. No detectable cell-surface GLUT4 was observed in soleus muscle from female GLUT4-null mice under either basal or insulin-stimulated conditions. Basal cell-surface GLUT1 content was similar between wild-type and GLUT4-null mice, with no further increase noted in either genotype with insulin exposure. Neither GLUT3 nor GLUT5 appeared to account for insulin-stimulated glucose-transport activity in wild-type or GLUT4-null muscle. In conclusion, insulin-stimulated glucose-transport activity in female GLUT4-null soleus muscle is mediated by a facilitative transport process that is glucose- and cytochalasin B-inhibitable, but which is not labelled strongly by ATB-BMPA. (+info)Adipocyte insulin action following ovulation in polycystic ovarian syndrome. (8/363)
The role of anovulation and insulin resistance in the pathogenesis of polycystic ovarian syndrome (PCOS) remains to be determined. The aim of this study was to investigate whether the metabolic abnormality of insulin resistance in PCOS reflects, rather than causes, the ovarian dysfunction. Eight subjects with classical PCOS were studied on two occasions. Adipocyte insulin sensitivity together with hormonal and metabolic changes were investigated in patients with PCOS following prolonged amenorrhoea and then again in the early follicular phase after ovulation. Insulin receptor binding in amenorrhoeic subjects with PCOS was low at 0.78 +/- 0.08% and this increased to 1.18 +/- 0.19% after an ovulatory cycle (P < 0.05). Maximal insulin stimulated 3-O-methylglucose uptake was 0.70 +/- 0. 14 during amenorrhoea and increased to 1.08 +/- 0.25 pmol/10 cm(2) cell membrane (P < 0.05). Plasma testosterone fell (4.0 +/- 0.4 to 2. 3 +/- 0.2 nmol/l; P < 0.001), luteinizing hormone fell (17.6 +/- 2.3 to 6.7 +/- 0.8 IU/l; P < 0.001) but plasma insulin concentrations remained unchanged following ovulation (14.6 +/- 1.9 and 15.7 +/- 3. 8 pmol/l during amenorrhoea and after ovulation respectively). The results of this study suggest that chronic anovulation per se appears to modify the factors contributing to cellular insulin resistance seen in PCOS. (+info)
3-O-Methylglucose
- 3 O Methylglucose
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The equilibrium exchange rate according to PPP and UIP
STP6 - Sugar transport protein 6 - Arabidopsis thaliana (Mouse-ear cress) - STP6 gene & protein
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Eye Liner Products Containing: POLYGLYCERYL-3 METHYLGLUCOSE DISTEARATE || Skin Deep® Cosmetics Database | EWG
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No data available that match "3 o methylglucose"
Lipopolysaccharide biosynthesis in mycobacteriaUptakeDIMETHICONEPropylene GlycolGalactoseGlucosyl-3-phosphoglycerate synthaseEXTRACTPhosphatidylinositol 3-kinaTransportSmall intestineDeoxyglucoseInsulinKcalBiochemical JournalEnzymePlasmaPhosphorylationStimulationSecretionFibroblastsRats2016Mass spectrometryCrystallographic analysisConcentration
Lipopolysaccharide biosynthesis in mycobacteria1
- This enzyme catalyses the first glucosylation step in methylglucose lipopolysaccharide biosynthesis in mycobacteria [4,5]. (qmul.ac.uk)
Uptake13
- 3-O-Methylglucose is used as a marker to assess glucose transport by evaluating its uptake within various cells and organ systems. (curehunter.com)
- The addition of the glucose transporter inhibitor cytochalasin B caused hypoxic hearts to fail early, and hearts perfused with a glucose analogue, 2-deoxyglucose (2-DG), increased glucose uptake 3-fold under hypoxia. (biologists.org)
- Under the conditions employed in these experiments, it is clear that (1) activation of glucose transport is required to support hypoxic performance, (2) the rate-limiting step for glucose utilization is glucose transport rather than glucose phosphorylation, (3) 2-DG uptake accurately reflects glucose transport activity and (4) glucose uptake in cod hearts does not involve an Na + -dependent mechanism. (biologists.org)
- and 3) inhibition of cellular uptake of 3-O-methylglucose. (aspetjournals.org)
- Uptake of radiolabeled 3-O-methylglucose was reduced by 40 to 50 percent. (cdc.gov)
- METHODS The action of PGE 2 on carbohydrate absorption in the ex situ perfused rat small intestine and on 3- O -[ 14 C]methylglucose uptake in isolated villus tip enterocytes was determined. (bmj.com)
- in isolated enterocytes it stimulated 3- O -[ 14 C]methylglucose uptake. (bmj.com)
- The 3- O -[ 14 C]methylglucose uptake could be inhibited by the cAMP antagonist RpcAMPS and the specific inhibitor of SGLT1, phlorizin. (bmj.com)
- cAMP enhanced sugar accumulation in chicken epithelial cells 3 and augmented glucose uptake into brush border membrane vesicles prepared from rat enterocytes. (bmj.com)
- 12 The mRNA expression of G s linked EP2R and EP4R, 10 the observed activation of adenylate cyclase by PGE 2 , 11 and the reported stimulation of 3- O -methylglucose uptake by dbcAMP 4 in enterocytes suggested that PGE 2 should enhance intestinal glucose absorption. (bmj.com)
- Glutamate caused a twofold to threefold increase in the zero-trans uptake rates of the fluorescent hexoses 2-[ N -(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxyglucose (2-NBDG) and 6-[ N -(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-6-deoxyglucose (6-NBDG). (jneurosci.org)
- The first assay measured the uptake of the slowly transported fluorescent hexoses 2-[ N -(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxyglucose (2-NBDG) and 6-[ N -(7-nitrobenz-2-oxa-1,3-diazol-4-yl)-amino]-6-deoxyglucose (6-NBDG). (jneurosci.org)
- Glucose uptake into Langendorff hearts of insulin-resistant Zucker was measured with the [ 14 C] 3-O-methylglucose washout method. (thisisms.com)
DIMETHICONE1
- Methoxy Peg/Ppg-7/3 Aminopropyl Dimethicone. (crabtree-evelyn.com)
Propylene Glycol1
- 6. The water-in-oil microemulsion composition of claim 3 wherein the oil phase comprises C 9-45 triglycerides, C 7-55 diesters of propylene glycol, and mixtures thereof. (google.com)
Galactose1
- GLP-1 concentrations in the mesenteric venous effluent increased significantly after luminal perfusion with substrates of a sodium/glucose co-transporter (D-glucose, D-galactose, methyl-alpha D-glucoside, and 3-O-methyl-D-glucose). (nih.gov)
Glucosyl-3-phosphoglycerate synthase2
- Glucosyl-3-phosphoglycerate synthase (EC 2.4.1.266, GpgS protein, GPG synthase, glucosylphosphoglycerate synthase) is an enzyme with systematic name NDP-glucose:3-phospho-D-glycerate 2-alpha-D-glucosyltransferase. (wikipedia.org)
- Additionally, folP2 overlapped glucosyl-3-phosphoglycerate synthase. (asm.org)
EXTRACT1
- Sub-chronic Hepatotoxicity of Anacardium occidentale (Anacardiaceae) Inner Stem Bark Extract in Rats," Indian Journal of Pharmaceutical Sciences, 73(3):353-357, 2010. (freepatentsonline.com)
Phosphatidylinositol 3-kina4
- Insulin receptor substrate-1 phosphorylation and phosphatidylinositol 3-kinase activity in skeletal muscle from NIDDM subjects after in vivo insulin stimulation. (semanticscholar.org)
- Furthermore, it has been determined that HGF is able to activate phosphatidylinositol 3-kinase in fetal pancreatic islet cells in vitro ( 24 ). (diabetesjournals.org)
- Abbreviations: IRS=insulin regulatory subunit, ERK=extracellular regulated kinase, MEK=mitogen activated kinase kinases, PI3K=phosphatidylinositol 3-kinase, PD98059=ERK/MEK inhibitor, SB203580=p38 MAPK inhibitor, anisomycin=activator of p38 and jun kinase pathways. (nih.gov)
- Abbreviations: PMA= phorbol 12-myristate 13-acetate, PDK-1=protein-dependent kinase-1, PI3K=phosphatidylinositol-3-kinase, PKB=protein kinase B, mTOR=mammalian target of rapamycin, PKCβII=protein kinase C βII. (nih.gov)
Transport8
- Since methyl-alpha D-glucoside is not a substrate of the basolateral glucose transport mechanism and 3-O-methyl-D-glucose is not metabolized within intestinal cells, it is concluded that intracellular metabolism of carbohydrates and intracellular removal are not essential to induce GLP-1 secretion in rats. (nih.gov)
- Inositol phospho-oligosaccharides from rat fibroblasts and adipocytes stimulate 3-O-methylglucose transport. (springer.com)
- Transport of 3-O-methylglucose and 2-deoxyglucose was stimulated approximately twofold by insulin in muscle from normal nonobese subjects and stimulation occurred in the normal physiological range of insulin concentrations. (jci.org)
- In contrast to insulin stimulation of 3-O-methylglucose and 2-deoxyglucose transport in muscle from normal, nonobese subjects, tissue from morbidly obese subjects, with or without NIDDM, were not responsive to insulin. (jci.org)
- Maximal 3-O-methylglucose transport was lower in muscle of obese than nonobese subjects. (jci.org)
- Based on these observations, we conclude that PHA stimulation increases glucose transport partly by inducing the expression of GLUT-1 instead of GLUT-3 and that GLUT-1 expression is induced by signals generated by IL-2 binding to its high affinity receptors. (jimmunol.org)
- 3-O-Methylglucose transport was determined and plasma membranes and low-density microsomes were prepared for Western blotting. (biochemj.org)
- Phospholipase C from Clostridium perfringens (PLC-Cp), which generates diacylglycerol from membrane phospholipids, and 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA) induced increases in glucose transport activity (assessed using 3-O-methylglucose transport) that were approximately 80 and approximately 20% as great, respectively, as that induced by a maximal insulin stimulus. (osti.gov)
Small intestine2
- containing 3 g of 3-O-methylglucose (3-OMG)) that was infused directly into the small intestine. (curehunter.com)
- Besides gastric emptying, numerous factors may theoretically influence the kinetics of 3-O MG absorption, including mucosal integrity, the number of sodium glucose co-transporters, small intestine peristalsis, blood flow, the volume of distribution of the substance, and alterations in renal clearance [ 4 , 6 ]. (pubmedcentralcanada.ca)
Deoxyglucose2
- Two glucose analogs (3-O-[3H]methylglucose and 2-[14C]deoxyglucose) method, originally presented by A. Gjedde was used for determination of GU. (aspetjournals.org)
- Male-to-female intertegumental transfer of(14)C-labeled glucose,(14)C-labeled 3-O-methylglucose, [(14)C]2-deoxyglucose and 2-fluorodeoxyglucose has been demonstrated in schistosomes. (unboundmedicine.com)
Insulin1
- Prevention of streptozotocin-induced alterations in the rat heart by 3-O-methyl glucose and insulin treatments. (semanticscholar.org)
Kcal2
- in 13 patients with a faeces collector because of loose stools, the caloric value of energy loss was a mean of 301 kcal/day, and 3 patients had a loss of more than 500 kcal/day in the stools [ 7 ]. (pubmedcentralcanada.ca)
- A liquid nutrient (3 kcal/min) was administered intraduodenally for 30 min, followed by a bolus of the glucose analog 3- O -methylglucose (3-OMG). (diabetesjournals.org)
Biochemical Journal1
- Biochemical Journal, 473 (3), 335 - 345. (up.pt)
Enzyme3
- This enzyme catalyses the following chemical reaction NDP-glucose + 3-phospho-D-glycerate ⇌ {\displaystyle \rightleftharpoons } NDP + 2-O-(alpha-D-glucopyranosyl)-3-phospho-D-glycerate The enzyme is involved in biosynthesis of 2-O-(alpha-D-glucopyranosyl)-D-glycerate. (wikipedia.org)
- The enzyme is also strictly specific for 3-phospho- D -glycerate as acceptor [1]. (qmul.ac.uk)
- The enzyme from Methanococcoides burtonii is strictly specific for GDP-glucose and 3-phospho- D -glycerate [2]. (qmul.ac.uk)
Plasma4
- Ketoconazole 2% was not detected in plasma in 39 patients who shampooed 4-10 times per week for 6 months, or in 33 patients who shampooed 2-3 times per week for 3-26 months (mean: 16 months). (drugs.com)
- Plasma 3-OMG concentrations were measured to assess absorption kinetics. (diabetesjournals.org)
- After PHA stimulation, GLUT-1 expression was induced predominantly in the plasma membrane, whereas GLUT-3 expression was simultaneously down-regulated. (jimmunol.org)
- We propose to test, in a double blind placebo controlled study, whether coadministration of 1 or 2 grams of quercetin with glucose will reduce plasma glucose concentrations during a 6 hour oral glucose tolerance test with 3 to 6 grams of 3-O-methyl glucose (3OMG) in non-diabetic obese subjects and in obese type 2 diabetic subjects. (clinicaltrials.gov)
Phosphorylation1
- 2016). Ataxin-3 phosphorylation decreases neuronal defects in spinocerebellar ataxia type 3 models . (up.pt)
Stimulation1
- Equilibrium exchange flux of 3-O-methyl glucose (3-O-MG) was stimulated two- and fourfold at 24 and 48 h after PHA stimulation, respectively. (jimmunol.org)
Secretion1
- Glucagon secretion was also measured from mouse islets exposed to 3- o -methylglucose (dashed line). (diabetesjournals.org)
Fibroblasts1
- Preliminary incubation of fibroblasts with 8-bromo cGMP or phosphodiesterase inhibitors, including 3-isobutyl-1-methylxanthine, Ro 20-1724, and cilostamide, however, prevented the ANF suppression of cAMP. (jci.org)
Rats2
- Sixteen male Sprague-Dawley rats (Harlan Sprague Dawley, Indianapolis, IN) weighing 247 ± 3 g were acclimatized and housed in a temperature- and humidity-controlled facility with a 12:12-h light-dark cycle in individual cages. (physiology.org)
- Rats were anesthetized immediately (0hPEX) or 3 hours (3hPEX) after exercise. (arctichealth.org)
20161
- 2016 Apr;56(3):175-87. (nih.gov)
Mass spectrometry1
- 2015). Examination of ataxin-3 (atx-3) aggregation by structural mass spectrometry techniques: A rationale for expedited aggregation upon polyglutamine (polyQ) expansion . (up.pt)
Crystallographic analysis1
- 2008). Crystallization and preliminary crystallographic analysis of mannosyl-3-phosphoglycerate synthase from Rubrobacter xylanophilus . (up.pt)
Concentration1
- Effects of depolarization by 30 mmol/l K + and increase of the glucose concentration from 0 to 3, 7, and 30 mmol/l on [Ca 2+ ] i of individual mouse α- and β-cells. (diabetesjournals.org)