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[PMID]:28592437
[Au] Autor:Coady MJ; Wallendorff B; Lapointe JY
[Ad] Endereço:Groupe d'Étude des Protéines Membranaires, Département de Physique, Université de Montréal, Montréal, Québec, Canada.
[Ti] Título:Characterization of the transport activity of SGLT2/MAP17, the renal low-affinity Na -glucose cotransporter.
[So] Source:Am J Physiol Renal Physiol;313(2):F467-F474, 2017 Aug 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cotransporter SGLT2 is responsible for 90% of renal glucose reabsorption, and we recently showed that MAP17 appears to work as a required ß-subunit. We report in the present study a detailed functional characterization of human SGLT2 in coexpression with human MAP17 in oocytes. Addition of external glucose generates a large inward current in the presence of Na, confirming an electrogenic transport mechanism. At a membrane potential of -50 mV, SGLT2 affinity constants for glucose and Na are 3.4 ± 0.4 and 18 ± 6 mM, respectively. The change in the reversal potential of the cotransport current as a function of external glucose concentration clearly confirms a 1:1 Na-to-glucose transport stoichiometry. SGLT2 is selective for glucose and α-methylglucose but also transports, to a lesser extent, galactose and 3- -methylglucose. SGLT2 can be inhibited in a competitive manner by phlorizin ( = 31 ± 4 nM) and by dapagliflozin ( = 0.75 ± 0.3 nM). Similarly to SGLT1, SGLT2 can be activated by Na, Li, and protons. Pre-steady-state currents for SGLT2 do exist but are small in amplitude and relatively fast (a time constant of ~2 ms). The leak current defined as the phlorizin-sensitive current in the absence of substrate was extremely small in the case of SGLT2. In summary, in comparison with SGLT1, SGLT2 has a lower affinity for glucose, a transport stoichiometry of 1:1, very small pre-steady-state and leak currents, a 10-fold higher affinity for phlorizin, and an affinity for dapagliflozin in the subnanomolar range.
[Mh] Termos MeSH primário: Glucose/metabolismo
Rim/metabolismo
Proteínas de Membrana/metabolismo
Reabsorção Renal
Transportador 2 de Glucose-Sódio/metabolismo
Sódio/metabolismo
[Mh] Termos MeSH secundário: 3-O-Metilglucose/metabolismo
Animais
Compostos Benzidrílicos/farmacologia
Transporte Biológico
Relação Dose-Resposta a Droga
Galactose
Glucosídeos/farmacologia
Seres Humanos
Rim/efeitos dos fármacos
Cinética
Potenciais da Membrana
Proteínas de Membrana/genética
Metilglucosídeos/metabolismo
Florizina/farmacologia
Reabsorção Renal/efeitos dos fármacos
Transportador 2 de Glucose-Sódio/antagonistas & inibidores
Transportador 2 de Glucose-Sódio/genética
Xenopus laevis
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(3-(4-ethoxybenzyl)-4-chlorophenyl)-6-hydroxymethyltetrahydro-2H-pyran-3,4,5-triol); 0 (Benzhydryl Compounds); 0 (Glucosides); 0 (Membrane Proteins); 0 (Methylglucosides); 0 (PDZK1IP1 protein, human); 0 (SLC5A2 protein, human); 0 (Sodium-Glucose Transporter 2); 146-72-5 (3-O-Methylglucose); 54L5T38NI8 (methylglucoside); 9NEZ333N27 (Sodium); CU9S17279X (Phlorhizin); IY9XDZ35W2 (Glucose); X2RN3Q8DNE (Galactose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170609
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00628.2016


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[PMID]:28385801
[Au] Autor:Sun EW; de Fontgalland D; Rabbitt P; Hollington P; Sposato L; Due SL; Wattchow DA; Rayner CK; Deane AM; Young RL; Keating DJ
[Ad] Endereço:Discipline of Human Physiology and Centre for Neuroscience, Flinders University, Adelaide, South Australia, Australia.
[Ti] Título:Mechanisms Controlling Glucose-Induced GLP-1 Secretion in Human Small Intestine.
[So] Source:Diabetes;66(8):2144-2149, 2017 Aug.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intestinal glucose stimulates secretion of the incretin hormone glucagon-like peptide 1 (GLP-1). The mechanisms underlying this pathway have not been fully investigated in humans. In this study, we showed that a 30-min intraduodenal glucose infusion activated half of all duodenal L cells in humans. This infusion was sufficient to increase plasma GLP-1 levels. With an ex vivo model using human gut tissue specimens, we showed a dose-responsive GLP-1 secretion in the ileum at ≥200 mmol/L glucose. In ex vivo tissue from the duodenum and ileum, but not the colon, 300 mmol/L glucose potently stimulated GLP-1 release. In the ileum, this response was independent of osmotic influences and required delivery of glucose via GLUT2 and mitochondrial metabolism. The requirement of voltage-gated Na and Ca channel activation indicates that membrane depolarization occurs. K channels do not drive this, as tolbutamide did not trigger release. The sodium-glucose cotransporter 1 (SGLT1) substrate α-MG induced secretion, and the response was blocked by the SGLT1 inhibitor phlorizin or by replacement of extracellular Na with -methyl-d-glucamine. This is the first report of the mechanisms underlying glucose-induced GLP-1 secretion from human small intestine. Our findings demonstrate a dominant role of SGLT1 in controlling glucose-stimulated GLP-1 release in human ileal L cells.
[Mh] Termos MeSH primário: Duodeno/metabolismo
Peptídeo 1 Semelhante ao Glucagon/secreção
Glucose/administração & dosagem
Íleo/metabolismo
Edulcorantes/administração & dosagem
[Mh] Termos MeSH secundário: Canais de Cálcio/fisiologia
Relação Dose-Resposta a Droga
Duodeno/secreção
Glucose/fisiologia
Transportador de Glucose Tipo 2/fisiologia
Glutamatos/metabolismo
Seres Humanos
Íleo/secreção
Infusões Parenterais
Metilglucosídeos/metabolismo
Mitocôndrias/metabolismo
Florizina/metabolismo
Transportador 1 de Glucose-Sódio/antagonistas & inibidores
Transportador 1 de Glucose-Sódio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels); 0 (Glucose Transporter Type 2); 0 (Glutamates); 0 (Methylglucosides); 0 (SLC2A2 protein, human); 0 (SLC5A1 protein, human); 0 (Sodium-Glucose Transporter 1); 0 (Sweetening Agents); 3081-62-7 (gamma-glutamylmethylamide); 54L5T38NI8 (methylglucoside); 89750-14-1 (Glucagon-Like Peptide 1); CU9S17279X (Phlorhizin); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170408
[St] Status:MEDLINE
[do] DOI:10.2337/db17-0058


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[PMID]:28219973
[Au] Autor:Goddard-Borger ED; Williams SJ
[Ad] Endereço:ACRF Chemical Biology Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia.
[Ti] Título:Sulfoquinovose in the biosphere: occurrence, metabolism and functions.
[So] Source:Biochem J;474(5):827-849, 2017 Feb 20.
[Is] ISSN:1470-8728
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The sulfonated carbohydrate sulfoquinovose (SQ) is produced in quantities estimated at some 10 billion tonnes annually and is thus a major participant in the global sulfur biocycle. SQ is produced by most photosynthetic organisms and incorporated into the sulfolipid sulfoquinovosyl diacylglycerol (SQDG), as well as within some archaea for incorporation into glycoprotein N-glycans. SQDG is found mainly within the thylakoid membranes of the chloroplast, where it appears to be important for membrane structure and function and for optimal activity of photosynthetic protein complexes. SQDG metabolism within the sulfur cycle involves complex biosynthetic and catabolic processes. SQDG biosynthesis is largely conserved within plants, algae and bacteria. On the other hand, two major sulfoglycolytic pathways have been discovered for SQDG degradation, the sulfo-Embden-Meyerhof-Parnas (sulfo-EMP) and sulfo-Entner-Doudoroff (sulfo-ED) pathways, which mirror the major steps in the glycolytic EMP and ED pathways. Sulfoglycolysis produces C3-sulfonates, which undergo biomineralization to inorganic sulfur species, completing the sulfur cycle. This review discusses the discovery and structural elucidation of SQDG and archaeal N-glycans, the occurrence, distribution, and speciation of SQDG, and metabolic pathways leading to the biosynthesis of SQDG and its catabolism through sulfoglycolytic and biomineralization pathways to inorganic sulfur.
[Mh] Termos MeSH primário: Glicolipídeos/metabolismo
Metilglucosídeos/metabolismo
Complexo de Proteínas do Centro de Reação Fotossintética/fisiologia
Enxofre/metabolismo
Tilacoides/metabolismo
[Mh] Termos MeSH secundário: Archaea/metabolismo
Cianobactérias/metabolismo
Citocromos/química
Citocromos/metabolismo
Glucosiltransferases/química
Glucosiltransferases/metabolismo
Glicolipídeos/química
Lipídeos/química
Redes e Vias Metabólicas
Metilglucosídeos/química
Modelos Moleculares
Fotossíntese/fisiologia
Complexo de Proteínas do Centro de Reação Fotossintética/química
Plantas/metabolismo
Tilacoides/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytochromes); 0 (Glycolipids); 0 (Lipids); 0 (Methylglucosides); 0 (Photosynthetic Reaction Center Complex Proteins); 0 (sulfolipids); 0 (sulfoquinovosyl diglyceride); 3458-06-8 (sulfoquinovose); 70FD1KFU70 (Sulfur); EC 2.4.1.- (Glucosyltransferases); EC 2.4.1.121 (UDP-sulfoquinovose synthase, Chlamydomonas reinhardtii)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170614
[Lr] Data última revisão:
170614
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170222
[St] Status:MEDLINE
[do] DOI:10.1042/BCJ20160508


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[PMID]:28174043
[Au] Autor:Yamazaki Y; Harada S; Wada T; Hagiwara T; Yoshida S; Tokuyama S
[Ad] Endereço:Department of Clinical Pharmacy, School of Pharmaceutical Sciences, Kobe Gakuin University, 1-1-3 Minatojima, Chuo-ku, Kobe 650-8586, Japan.
[Ti] Título:Sodium influx through cerebral sodium-glucose transporter type 1 exacerbates the development of cerebral ischemic neuronal damage.
[So] Source:Eur J Pharmacol;799:103-110, 2017 Mar 15.
[Is] ISSN:1879-0712
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We recently reported that cerebral sodium-glucose transporter type 1 (SGLT-1) plays a role in exacerbation of cerebral ischemia. However, the mechanism by which cerebral SGLT-1 acts remains unclear. Here we demonstrated that sodium influx through cerebral SGLT-1 exacerbates cerebral ischemic neuronal damage. SGLT-specific sodium ion influx was induced using α-methyl-D-glucopyranoside (α-MG). Intracellular sodium concentrations in primary cortical neurons were estimated using sodium-binding benzofuran isophthalate fluorescence. SGLT-1 knockdown in primary cortical neurons and mice was achieved using SGLT-1 siRNA. The survival rates of primary cultured cortical neurons were assessed using biochemical assays 1 day after treatment. Middle cerebral artery occlusion (MCAO) was used to generate a focal cerebral ischemic model in SGLT-1 knockdown mice. The change in fasting blood glucose levels, infarction development, and behavioral abnormalities were assessed 1 day after MCAO. Treatment with 200mM α-MG induced a continuous increase in the intracellular sodium concentration, and this increase was normalized after α-MG removal. Neuronal SGLT-1 knockdown had no effect on 100µM H O -induced neuronal cell death; however, the knockdown prevented the neuronal cell death induced by 17.5mM glucose and the co-treatment of 100µM H O /8.75mM glucose. Neuronal SGLT-1 knockdown also suppressed the cell death induced by α-MG alone and the co-treatment of 100µM H O /0.01mM α-MG. Our in vivo results showed that the exacerbation of cerebral ischemic neuronal damage induced by the intracerebroventricular administration of 5.0µg α-MG/mouse was ameliorated in cerebral SGLT-1 knockdown mice. Thus, sodium influx through cerebral SGLT-1 may exacerbate cerebral ischemia-induced neuronal damage.
[Mh] Termos MeSH primário: Isquemia Encefálica/metabolismo
Isquemia Encefálica/patologia
Neurônios/patologia
Transportador 1 de Glucose-Sódio/metabolismo
Sódio/metabolismo
[Mh] Termos MeSH secundário: Animais
Transporte Biológico/efeitos dos fármacos
Transporte Biológico/genética
Encéfalo/efeitos dos fármacos
Encéfalo/metabolismo
Encéfalo/patologia
Isquemia Encefálica/genética
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/genética
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/genética
Técnicas de Silenciamento de Genes
Hiperglicemia/complicações
Espaço Intracelular/efeitos dos fármacos
Espaço Intracelular/metabolismo
Masculino
Metilglucosídeos/farmacologia
Camundongos
Neurônios/efeitos dos fármacos
RNA Interferente Pequeno/genética
Proteínas de Transporte de Sódio-Glucose/metabolismo
Transportador 1 de Glucose-Sódio/deficiência
Transportador 1 de Glucose-Sódio/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Methylglucosides); 0 (RNA, Small Interfering); 0 (Slc5a1 protein, mouse); 0 (Slc5a4b protein, mouse); 0 (Sodium-Glucose Transport Proteins); 0 (Sodium-Glucose Transporter 1); 54L5T38NI8 (methylglucoside); 9NEZ333N27 (Sodium)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170428
[Lr] Data última revisão:
170428
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170209
[St] Status:MEDLINE


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[PMID]:27806092
[Au] Autor:Pal A; Rhoads DB; Tavakkoli A
[Ad] Endereço:Department of Surgery, Brigham and Women's Hospital, 75 Francis Street, Boston, MA, 02115, United States of America.
[Ti] Título:Effect of Portal Glucose Sensing on Systemic Glucose Levels in SD and ZDF Rats.
[So] Source:PLoS One;11(11):e0165592, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The global epidemic of Type-2-Diabetes (T2D) highlights the need for novel therapeutic targets and agents. Roux-en-Y-Gastric-Bypass (RYGB) is the most effective treatment. Studies investigating the mechanisms of RYGB suggest a role for post-operative changes in portal glucose levels. We investigate the impact of stimulating portal glucose sensors on systemic glucose levels in health and T2D, and evaluated the role of sodium-glucose-cotransporter-3 (SGLT3) as the possible sensor. METHODS: Systemic glucose and hormone responses to portal stimulation were measured. In Sprague-Dawley (SD) rats, post-prandial state was simulated by infusing glucose into the portal vein. The SGLT3 agonist, alpha-methyl-glucopyranoside (αMG), was then added to further stimulate the portal sensor. To elucidate the neural pathway, vagotomy or portal denervation was followed by αMG+glucose co-infusion. The therapeutic potential of portal glucose sensor stimulation was investigated by αMG-only infusion (vs. saline) in SD and Zucker-Diabetic-Fatty (ZDF) rats. Hepatic mRNA expression was also measured. RESULTS: αMG+glucose co-infusion reduced peak systemic glucose (vs. glucose alone), and lowered hepatic G6Pase expression. Portal denervation, but not vagotomy, abolished this effect. αMG-only infusion lowered systemic glucose levels. This glucose-lowering effect was more pronounced in ZDF rats, where portal αMG infusion increased insulin, C-peptide and GIP levels compared to saline infusions. CONCLUSIONS: The portal vein is capable of sensing its glucose levels, and responds by altering hepatic glucose handling. The enhanced effect in T2D, mediated through increased GIP and insulin, highlights a therapeutic target that could be amenable to pharmacological modulation or minimally-invasive surgery.
[Mh] Termos MeSH primário: Glicemia/metabolismo
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Tipo 2/metabolismo
Metilglucosídeos/administração & dosagem
Obesidade/metabolismo
Veia Porta/metabolismo
Proteínas de Transporte de Sódio-Glucose/metabolismo
[Mh] Termos MeSH secundário: Animais
Diabetes Mellitus Experimental/cirurgia
Diabetes Mellitus Tipo 2/cirurgia
Derivação Gástrica
Masculino
Metilglucosídeos/farmacologia
Ratos
Ratos Sprague-Dawley
Ratos Zucker
Transdução de Sinais
Vagotomia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Methylglucosides); 0 (Sodium-Glucose Transport Proteins); 54L5T38NI8 (methylglucoside)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170626
[Lr] Data última revisão:
170626
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0165592


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[PMID]:27555600
[Au] Autor:Chintalapati C; Keller T; Mueller TD; Gorboulev V; Schäfer N; Zilkowski I; Veyhl-Wichmann M; Geiger D; Groll J; Koepsell H
[Ad] Endereço:Institute of Anatomy and Cell Biology (C.C., V.G., M.V.-W., H.K.), and Department of Molecular Plant Physiology and Biophysics, Julius-von-Sachs-Institute (T.K., T.D.M., N.S., D.G., H.K.), University of Würzburg, Würzburg, Germany; and Department of Functional Materials in Medicine and Dentistry, Un
[Ti] Título:Protein RS1 (RSC1A1) Downregulates the Exocytotic Pathway of Glucose Transporter SGLT1 at Low Intracellular Glucose via Inhibition of Ornithine Decarboxylase.
[So] Source:Mol Pharmacol;90(5):508-521, 2016 Nov.
[Is] ISSN:1521-0111
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Na -d-glucose cotransporter 1 (SGLT1) is rate-limiting for glucose absorption in the small intestine. Shortly after intake of glucose-rich food, SGLT1 abundance in the luminal membrane of the small intestine is increased. This upregulation occurs via glucose-induced acceleration of the release of SGLT1-containing vesicles from the trans-Golgi network (TGN), which is regulated by a domain of protein RS1 (RSC1A1) named RS1-Reg. Dependent on phosphorylation, RS1-Reg blocks release of vesicles containing SGLT1 or concentrative nucleoside transporter 1. The hypothesis has been raised that RS1-Reg binds to different receptor proteins at the TGN, which trigger release of vesicles with different transporters. To identify the presumed receptor proteins, two-hybrid screening was performed. Interaction with ornithine decarboxylase 1 (ODC1), the rate-limiting enzyme of polyamine synthesis, was observed and verified by immunoprecipitation. Binding of RS1-Reg mutants to ODC1 was characterized using surface plasmon resonance. Inhibition of ODC1 activity by RS1-Reg mutants and the ODC1 inhibitor difluoromethylornithine (DFMO) was measured in the absence and presence of glucose. In addition, short-term effects of DFMO, RS1-Reg mutants, the ODC1 product putrescine, and/or glucose on SGLT1 expressed in oocytes of Xenopus laevis were investigated. High-affinity binding of RS1-Reg to ODC1 was demonstrated, and evidence for a glucose binding site in ODC1 was provided. Binding of RS1-Reg to ODC1 inhibits the enzymatic activity at low intracellular glucose, which is blunted at high intracellular glucose. The data suggest that generation of putrescine by ODC1 at the TGN stimulates release of SGLT1-containing vesicles. This indicates a biomedically important role of ODC1 in regulation of glucose homeostasis.
[Mh] Termos MeSH primário: Regulação para Baixo/efeitos dos fármacos
Exocitose/efeitos dos fármacos
Glucose/farmacologia
Proteínas de Transporte de Monossacarídeos/metabolismo
Ornitina Descarboxilase/metabolismo
Transportador 1 de Glucose-Sódio/metabolismo
[Mh] Termos MeSH secundário: Animais
Transporte Biológico/efeitos dos fármacos
Células CACO-2
Membrana Celular/efeitos dos fármacos
Membrana Celular/metabolismo
Eflornitina/farmacologia
Eletroforese em Gel de Poliacrilamida
Células HEK293
Seres Humanos
Imunoprecipitação
Espaço Intracelular/metabolismo
Cinética
Metilglucosídeos/farmacologia
Modelos Biológicos
Proteínas de Transporte de Monossacarídeos/química
Oócitos/efeitos dos fármacos
Oócitos/metabolismo
Florizina/farmacologia
Ligação Proteica/efeitos dos fármacos
Domínios Proteicos
Proteínas Recombinantes/metabolismo
Frações Subcelulares/efeitos dos fármacos
Frações Subcelulares/metabolismo
Ressonância de Plasmônio de Superfície
Xenopus laevis
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Methylglucosides); 0 (Monosaccharide Transport Proteins); 0 (RSC1A1 protein, human); 0 (Recombinant Proteins); 0 (Sodium-Glucose Transporter 1); CU9S17279X (Phlorhizin); EC 4.1.1.17 (Ornithine Decarboxylase); IY9XDZ35W2 (Glucose); ZQN1G5V6SR (Eflornithine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170509
[Lr] Data última revisão:
170509
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160825
[St] Status:MEDLINE


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[PMID]:27297390
[Au] Autor:Xia M; Hesser DC; De P; Sakala IG; Spencer CT; Kirkwood JS; Abate G; Chatterjee D; Dobos KM; Hoft DF
[Ad] Endereço:Division of Infectious Diseases, Allergy & Immunology, Edward A. Doisy Research Center, Saint Louis University School of Medicine, St. Louis, Missouri, USA.
[Ti] Título:A Subset of Protective γ9δ2 T Cells Is Activated by Novel Mycobacterial Glycolipid Components.
[So] Source:Infect Immun;84(9):2449-62, 2016 Sep.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:γ9δ2 T cells provide a natural bridge between innate and adaptive immunity, rapidly and potently respond to pathogen infection in mucosal tissues, and are prominently induced by both tuberculosis (TB) infection and bacillus Calmette Guérin (BCG) vaccination. Mycobacterium-expanded γ9δ2 T cells represent only a subset of the phosphoantigen {isopentenyl pyrophosphate [IPP] and (E)-4-hydroxy-3-methyl-but-2-enylpyrophosphate [HMBPP]}-responsive γ9δ2 T cells, expressing an oligoclonal set of T cell receptor (TCR) sequences which more efficiently recognize and inhibit intracellular Mycobacterium tuberculosis infection. Based on this premise, we have been searching for M. tuberculosis antigens specifically capable of inducing a unique subset of mycobacterium-protective γ9δ2 T cells. Our screening strategy includes the identification of M. tuberculosis fractions that expand γ9δ2 T cells with biological functions capable of inhibiting intracellular mycobacterial replication. Chemical treatments of M. tuberculosis whole-cell lysates (MtbWL) ruled out protein, nucleic acid, and nonpolar lipids as the M. tuberculosis antigens inducing protective γ9δ2 T cells. Mild acid hydrolysis, which transforms complex carbohydrate to monomeric residues, abrogated the specific activity of M. tuberculosis whole-cell lysates, suggesting that a polysaccharide was required for biological activity. Extraction of MtbWL with chloroform-methanol-water (10:10:3) resulted in a polar lipid fraction with highly enriched specific activity; this activity was further enriched by silica gel chromatography. A combination of mass spectrometry and nuclear magnetic resonance analysis of bioactive fractions indicated that 6-O-methylglucose-containing lipopolysaccharides (mGLP) are predominant components present in this active fraction. These results have important implications for the development of new immunotherapeutic approaches for prevention and treatment of TB.
[Mh] Termos MeSH primário: Glicolipídeos/imunologia
Ativação Linfocitária/imunologia
Mycobacterium tuberculosis/imunologia
Receptores de Antígenos de Linfócitos T gama-delta/imunologia
Subpopulações de Linfócitos T/imunologia
Tuberculose/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa/imunologia
Animais
Antígenos de Bactérias/imunologia
Hemiterpenos/imunologia
Metilglucosídeos/imunologia
Compostos Organofosforados/imunologia
Polissacarídeos/imunologia
Subpopulações de Linfócitos T/microbiologia
Tuberculose/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Bacterial); 0 (Glycolipids); 0 (Hemiterpenes); 0 (Methylglucosides); 0 (Organophosphorus Compounds); 0 (Polysaccharides); 0 (Receptors, Antigen, T-Cell, gamma-delta); 144058-44-6 (Mycobacterium tuberculosis antigens); 2461-70-3 (6-O-methylglucose); 358-71-4 (isopentenyl pyrophosphate)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170512
[Lr] Data última revisão:
170512
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160615
[St] Status:MEDLINE
[do] DOI:10.1128/IAI.01322-15


  8 / 2125 MEDLINE  
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[PMID]:27139580
[Au] Autor:Yamazaki Y; Harada S; Wada T; Yoshida S; Tokuyama S
[Ad] Endereço:Department of Clinical Pharmacy, School of Pharmaceutical Sciences, Kobe Gakuin University, Chuo-ku, Kobe, Japan.
[Ti] Título:Sodium transport through the cerebral sodium-glucose transporter exacerbates neuron damage during cerebral ischaemia.
[So] Source:J Pharm Pharmacol;68(7):922-31, 2016 Jul.
[Is] ISSN:2042-7158
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: We recently demonstrated that the cerebral sodium-glucose transporter (SGLT) is involved in postischaemic hyperglycaemia-induced exacerbation of cerebral ischaemia. However, the associated SGLT-mediated mechanisms remain unclear. Thus, we examined the involvement of cerebral SGLT-induced excessive sodium ion influx in the development of cerebral ischaemic neuronal damage. METHODS: [Na+]i was estimated according to sodium-binding benzofuran isophthalate fluorescence. In the in vitro study, primary cortical neurons were prepared from fetuses of ddY mice. Primary cortical neurons were cultured for 5 days before each treatment with reagents, and these survival rates were assessed using biochemical assays. In in vivo study, a mouse model of focal ischaemia was generated using middle cerebral artery occlusion (MCAO). KEY FINDINGS: In these experiments, treatment with high concentrations of glucose induced increment in [Na+]i, and this phenomenon was suppressed by the SGLT-specific inhibitor phlorizin. SGLT-specific sodium ion influx was induced using a-methyl-D-glucopyranoside (a-MG) treatments, which led to significant concentration-dependent declines in neuronal survival rates and exacerbated hydrogen peroxide-induced neuronal cell death. Moreover, phlorizin ameliorated these effects. Finally, intracerebroventricular administration of a-MG exacerbated the development of neuronal damage induced by MCAO, and these effects were ameliorated by the administration of phlorizin. CONCLUSIONS: Hence, excessive influx of sodium ions into neuronal cells through cerebral SGLT may exacerbate the development of cerebral ischaemic neuronal damage.
[Mh] Termos MeSH primário: Córtex Cerebral/metabolismo
Infarto da Artéria Cerebral Média/fisiopatologia
Transportador 1 de Glucose-Sódio/metabolismo
Sódio/metabolismo
[Mh] Termos MeSH secundário: Animais
Glicemia
Isquemia Encefálica/metabolismo
Isquemia Encefálica/patologia
Isquemia Encefálica/fisiopatologia
Morte Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Córtex Cerebral/patologia
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Glucose/antagonistas & inibidores
Glucose/farmacologia
Peróxido de Hidrogênio/efeitos adversos
Peróxido de Hidrogênio/antagonistas & inibidores
Infarto da Artéria Cerebral Média/patologia
Infusões Intraventriculares
Metilglucosídeos/administração & dosagem
Metilglucosídeos/antagonistas & inibidores
Metilglucosídeos/farmacologia
Camundongos
Neurônios/metabolismo
Neurônios/patologia
Florizina/administração & dosagem
Florizina/farmacologia
Cultura Primária de Células
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Methylglucosides); 0 (Sodium-Glucose Transporter 1); 9NEZ333N27 (Sodium); BBX060AN9V (Hydrogen Peroxide); CU9S17279X (Phlorhizin); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170619
[Lr] Data última revisão:
170619
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160504
[St] Status:MEDLINE
[do] DOI:10.1111/jphp.12571


  9 / 2125 MEDLINE  
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[PMID]:27098211
[Au] Autor:Zhang H; Yu M; Zhang H; Bai L; Wu Y; Wang S; Ba X
[Ad] Endereço:a College of Chemistry and Environmental Science, Hebei University , Baoding , P.R. China.
[Ti] Título:Synthesis, characterization and fluorescent properties of water-soluble glycopolymer bearing curcumin pendant residues.
[So] Source:Biosci Biotechnol Biochem;80(8):1451-8, 2016 Aug.
[Is] ISSN:1347-6947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Curcumin is a potential natural anticancer drug with low oral bioavailability because of poor water solubility. The aqueous solubility of curcumin is enhanced by means of modification with the carbohydrate units. Polymerization of the curcumin-containing monomer with carbohydrate-containing monomer gives the water-soluble glycopolymer bearing curcumin pendant residues. The obtained copolymers (P1 and P2) having desirable water solubility were well-characterized by infrared spectroscopy (IR), nuclear magnetic resonance (NMR), gel permeation chromatography (GPC), UV-Vis absorption spectroscopy, and photoluminescence spectroscopy. The copolymer P2 with a molar ratio of 1:6 (curcumin/carbohydrate) calculated from the proton NMR results exhibits a similar anticancer activity compared to original curcumin, which may serve as a potential chemotherapeutic agent in the field of anticancer medicine.
[Mh] Termos MeSH primário: Antineoplásicos/química
Curcumina/análogos & derivados
Lipase/química
Metacrilatos/química
Metilglucosídeos/química
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Sobrevivência Celular/efeitos dos fármacos
Curcumina/farmacologia
Relação Dose-Resposta a Droga
Células HeLa
Seres Humanos
Metilaminas/química
Polimerização
Solubilidade
Soluções
Água/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Methacrylates); 0 (Methylamines); 0 (Methylglucosides); 0 (Solutions); 059QF0KO0R (Water); EC 3.1.1.- (Novozyme 435); EC 3.1.1.3 (Lipase); IT942ZTH98 (Curcumin); L76O6653IO (methacryloyl chloride); LHH7G8O305 (trimethylamine)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170118
[Lr] Data última revisão:
170118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160422
[St] Status:MEDLINE
[do] DOI:10.1080/09168451.2016.1171696


  10 / 2125 MEDLINE  
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[PMID]:27045200
[Au] Autor:Sutrina SL; Griffith MS; Lafeuillee C
[Ad] Endereço:Department of Biological and Chemical Sciences, University of the West Indies, Cave Hill Campus, Barbados.
[Ti] Título:2-Deoxy-d-glucose is a potent inhibitor of biofilm growth in Escherichia coli.
[So] Source:Microbiology;162(6):1037-46, 2016 Jun.
[Is] ISSN:1465-2080
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Escherichia coli strain 15 (ATCC 9723), which forms robust biofilms, was grown under optimal biofilm conditions in NaCl-free Luria-Bertani broth (LB*) or in LB* supplemented with one of the non-metabolizable analogues 2-deoxy-d-glucose (2DG), methyl α-d-mannopyranoside (αMM), or methyl α-d-glucopyranoside (αMG). Biofilm growth was inhibited by mannose analogue 2DG even at very low concentration in unbuffered medium, and the maximal inhibition was enhanced in the presence of either 100 mM KPO4 or 100 mM MOPS, pH 7.5; in buffered medium, concentrations of 0.02 % (1.2 mM) or more inhibited growth nearly completely. In contrast, mannose analogue αMM, which should not be able to enter the cells but has been reported to inhibit biofilm growth by binding to FimH, did not exhibit strong inhibition even at concentrations up to 1.8 % (108 mM). The glucose analogue αMG inhibited biofilm growth, but much less strongly than did 2DG. None of the analogues inhibited planktonic growth or caused a change in pH of the unbuffered medium. Similar inhibitory effects of the analogues were observed in minimal medium. The effects were not strain-specific, as 2DG and αMG also inhibited the weak biofilm growth of E. coli K12.
[Mh] Termos MeSH primário: Antimetabólitos/farmacologia
Biofilmes/crescimento & desenvolvimento
Desoxiglucose/farmacologia
Escherichia coli/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: AMP Cíclico/farmacologia
Escherichia coli/efeitos dos fármacos
Glucose-6-Fosfato/farmacologia
Metilglucosídeos/farmacologia
Metilmanosídeos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites); 0 (Methylglucosides); 0 (Methylmannosides); 51023-63-3 (methylmannoside); 54L5T38NI8 (methylglucoside); 56-73-5 (Glucose-6-Phosphate); 9G2MP84A8W (Deoxyglucose); E0399OZS9N (Cyclic AMP)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160406
[St] Status:MEDLINE
[do] DOI:10.1099/mic.0.000290



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