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  1 / 1509 MEDLINE  
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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


  2 / 1509 MEDLINE  
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[PMID]:28506962
[Au] Autor:Ishida E; Kim-Muller JY; Accili D
[Ad] Endereço:Department of Medicine and Naomi Berrie Diabetes Center, Columbia University, New York, New York.
[Ti] Título:Pair Feeding, but Not Insulin, Phloridzin, or Rosiglitazone Treatment, Curtails Markers of ß-Cell Dedifferentiation in Mice.
[So] Source:Diabetes;66(8):2092-2101, 2017 Aug.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ß-Cell failure is a hallmark of type 2 diabetes. Among several cellular biological mechanisms of cellular dysfunction, we and others have recently proposed that dedifferentiation of ß-cells can explain the slowly progressive onset and partial reversibility of ß-cell failure. Accordingly, we provided evidence of such processes in humans and experimental animal models of insulin-resistant diabetes. In this study, we asked whether ß-cell dedifferentiation can be prevented with diet or pharmacological treatment of diabetes. mice, a widely used model of insulin-resistant diabetes and obesity, were either pair fed or treated with the Sglt inhibitor phloridzin, the insulin-sensitizer rosiglitazone, or insulin. All treatments were equally efficacious in reducing plasma glucose levels. Pair feeding and phloridzin also resulted in significant weight loss. However, pair feeding among the four treatments resulted in a reduction of ß-cell dedifferentiation, as assessed by Foxo1 and Aldh1a3 immunohistochemistry. The effect of diet to partly restore ß-cell function is consistent with data in human diabetes and provides another potential mechanism by which lifestyle changes act as an effective intervention against diabetes progression.
[Mh] Termos MeSH primário: Desdiferenciação Celular/fisiologia
Diabetes Mellitus Tipo 2/fisiopatologia
Ingestão de Alimentos/fisiologia
Hipoglicemiantes/farmacologia
Células Secretoras de Insulina/fisiologia
[Mh] Termos MeSH secundário: Animais
Biomarcadores/sangue
Glicemia/análise
Desdiferenciação Celular/efeitos dos fármacos
Diabetes Mellitus Tipo 2/sangue
Diabetes Mellitus Tipo 2/tratamento farmacológico
Modelos Animais de Doenças
Seres Humanos
Insulina/farmacologia
Células Secretoras de Insulina/efeitos dos fármacos
Camundongos
Florizina/farmacologia
Tiazolidinedionas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Blood Glucose); 0 (Hypoglycemic Agents); 0 (Insulin); 0 (Thiazolidinediones); 05V02F2KDG (rosiglitazone); CU9S17279X (Phlorhizin)
[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:170517
[St] Status:MEDLINE
[do] DOI:10.2337/db16-1213


  3 / 1509 MEDLINE  
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[PMID]:28407923
[Au] Autor:Sun L; Liu D; Sun J; Yang X; Fu M; Guo Y
[Ad] Endereço:Centre of Food Engineering and Nutritional Science, Shaanxi Normal University, Xi'an 710062, PR China; Centre for Nutrition and Food Science, Queensland Alliance for Agriculture and Food Innovation, The University of Queensland, Brisbane 4072, Australia.
[Ti] Título:Simultaneous separation and purification of chlorogenic acid, epicatechin, hyperoside and phlorizin from thinned young Qinguan apples by successive use of polyethylene and polyamide resins.
[So] Source:Food Chem;230:362-371, 2017 Sep 01.
[Is] ISSN:0308-8146
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The method for separating and purifying chlorogenic acid (CA), epicatechin (EC), hyperoside (HY) and phlorizin (PH) simutaneously from young Qinguan apples by successive use of X-5 and polyamide resins has been developed in this study. The order of adsorption capacities of X-5 for the four phenolics was PH>HY>EC>CA, and the adsorption equilibriums of the four phenolics onto X-5 resin conformed to Langmuir isotherms preferentially. The adsorption kinetics of EC and CA onto X-5 conformed to the pseudo-first-order model, while that of HY and PH accorded with the pseudo-second-order model. Interestingly, the values of equilibrium adsorption capacities (Q ) calculated in the preferential kinetics models were closer to that of theoretical maximum adsorption capacities (Q ) calculated by Langmuir isotherms. Through dynamic adsorption and desorption using X-5 and polyamide resins with ethanol solution as strippant, CA, EC, HY and PH were obtained with purities of 96.21%, 95.34%, 95.36% and 97.36%, respectively.
[Mh] Termos MeSH primário: Catequina/química
Ácido Clorogênico/química
Malus/química
Florizina/química
Extratos Vegetais/química
Polietileno/química
Quercetina/análogos & derivados
Resinas Vegetais/química
[Mh] Termos MeSH secundário: Quercetina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Plant Extracts); 0 (Resins, Plant); 318ADP12RI (Chlorogenic Acid); 8O1CR18L82 (hyperoside); 8R1V1STN48 (Catechin); 9002-88-4 (Polyethylene); 9IKM0I5T1E (Quercetin); CU9S17279X (Phlorhizin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE


  4 / 1509 MEDLINE  
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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


  5 / 1509 MEDLINE  
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[PMID]:28365326
[Au] Autor:Lopes LAA; Dos Santos Rodrigues JB; Magnani M; de Souza EL; de Siqueira-Júnior JP
[Ad] Endereço:Laboratório de Genética de Microrganismos, Departamento de Biologia Molecular, Universidade Federal da Paraíba, João Pessoa, Paraíba, Brazil.
[Ti] Título:Inhibitory effects of flavonoids on biofilm formation by Staphylococcus aureus that overexpresses efflux protein genes.
[So] Source:Microb Pathog;107:193-197, 2017 Jun.
[Is] ISSN:1096-1208
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:This study evaluated the efficacy of glycone (myricitrin, hesperidin and phloridzin) and aglycone flavonoids (myricetin, hesperetin and phloretin) in inhibiting biofilm formation by Staphylococcus aureus RN4220 and S. aureus SA1199B that overexpress the msrA and norA efflux protein genes, respectively. The minimum inhibitory concentration (MIC) and minimum biofilm inhibitory concentration (MBIC - defined as the lowest concentration that resulted in ≥50% inhibition of biofilm formation) of flavonoids were determined using microdilution in broth procedures. The flavonoids showed MIC >1024 µg/mL against S. aureus RN4220 and S. aureus SA1199B; however, these compounds at lower concentrations (1-256 µg/mL) showed inhibitory effects on biofilm formation by these strains. Aglycone flavonoids showed lower MBIC values than their respective glycone forms. The lowest MBIC values (1 and 4 µg/mL) were observed against S. aureus RN4220. Myricetin, hesperetin and phloretin exhibited biofilm formation inhibition >70% for S. aureus RN4220, and lower biofilm formation inhibition against S. aureus SA1199B. These results indicate that sub-MICs of the tested flavonoids inhibit biofilm formation by S. aureus strains that overexpress efflux protein genes. These effects are more strongly established by aglycone flavonoids.
[Mh] Termos MeSH primário: Proteínas de Bactérias/genética
Biofilmes/efeitos dos fármacos
Flavonoides/antagonistas & inibidores
Regulação Bacteriana da Expressão Gênica/genética
Staphylococcus aureus/efeitos dos fármacos
Staphylococcus aureus/genética
[Mh] Termos MeSH secundário: Antibacterianos/farmacologia
Biofilmes/crescimento & desenvolvimento
Flavonoides/administração & dosagem
Flavonoides/química
Glicosilação/efeitos dos fármacos
Hesperidina/administração & dosagem
Hesperidina/antagonistas & inibidores
Hesperidina/química
Proteínas de Membrana Transportadoras/genética
Testes de Sensibilidade Microbiana
Proteínas Associadas à Resistência a Múltiplos Medicamentos/genética
Floretina/administração & dosagem
Floretina/antagonistas & inibidores
Floretina/química
Florizina/administração & dosagem
Florizina/antagonistas & inibidores
Florizina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Bacterial Proteins); 0 (Flavonoids); 0 (Membrane Transport Proteins); 0 (Multidrug Resistance-Associated Proteins); 133135-40-7 (NorA protein, Staphylococcus); 5Z0ZO61WPJ (myricitrin); 76XC01FTOJ (myricetin); CU9S17279X (Phlorhizin); E750O06Y6O (Hesperidin); Q9Q3D557F1 (hesperetin); S5J5OE47MK (Phloretin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170403
[St] Status:MEDLINE


  6 / 1509 MEDLINE  
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[PMID]:28279980
[Au] Autor:McMillin SL; Schmidt DL; Kahn BB; Witczak CA
[Ad] Endereço:Department of Kinesiology, East Carolina University, Greenville, NC.
[Ti] Título:GLUT4 Is Not Necessary for Overload-Induced Glucose Uptake or Hypertrophic Growth in Mouse Skeletal Muscle.
[So] Source:Diabetes;66(6):1491-1500, 2017 Jun.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:GLUT4 is necessary for acute insulin- and contraction-induced skeletal muscle glucose uptake, but its role in chronic muscle loading (overload)-induced glucose uptake is unknown. Our goal was to determine whether GLUT4 is required for overload-induced glucose uptake. Overload was induced in mouse plantaris muscle by unilateral synergist ablation. After 5 days, muscle weights and ex vivo [ H]-2-deoxy-d-glucose uptake were assessed. Overload-induced muscle glucose uptake and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that GLUT4 is not necessary for these processes. To assess which transporters mediate overload-induced glucose uptake, chemical inhibitors were used. The facilitative GLUT inhibitor cytochalasin B, but not the sodium-dependent glucose cotransport inhibitor phloridzin, prevented overload-induced uptake demonstrating that GLUTs mediate this effect. To assess which GLUT, hexose competition experiments were performed. Overload-induced [ H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effect. To assess additional GLUTs, immunoblots were performed. Overload increased GLUT1, GLUT3, GLUT6, and GLUT10 protein levels twofold to fivefold. Collectively, these results demonstrate that GLUT4 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that GLUT1, GLUT3, GLUT6, and/or GLUT10 mediate overload-induced glucose uptake.
[Mh] Termos MeSH primário: Transportador de Glucose Tipo 4/genética
Glucose/metabolismo
Músculo Esquelético/metabolismo
Suporte de Carga
[Mh] Termos MeSH secundário: Animais
Citocalasina B/farmacologia
Desoxiglucose/metabolismo
Frutose/farmacologia
Proteínas Facilitadoras de Transporte de Glucose/metabolismo
Transportador de Glucose Tipo 1/metabolismo
Transportador de Glucose Tipo 2
Transportador de Glucose Tipo 4/metabolismo
Hipertrofia/genética
Immunoblotting
Camundongos
Camundongos Knockout
Músculo Esquelético/efeitos dos fármacos
Músculo Esquelético/patologia
Florizina/farmacologia
Trítio
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucose Transport Proteins, Facilitative); 0 (Glucose Transporter Type 1); 0 (Glucose Transporter Type 2); 0 (Glucose Transporter Type 4); 0 (Slc2A10 protein, mouse); 0 (Slc2a1 protein, mouse); 0 (Slc2a12 protein, mouse); 0 (Slc2a2 protein, mouse); 0 (Slc2a4 protein, mouse); 0 (Slc2a5 protein, mouse); 0 (Slc2a8 protein, mouse); 0 (Slc2a9 protein, mouse); 10028-17-8 (Tritium); 30237-26-4 (Fructose); 3CHI920QS7 (Cytochalasin B); 9G2MP84A8W (Deoxyglucose); CU9S17279X (Phlorhizin); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170311
[St] Status:MEDLINE
[do] DOI:10.2337/db16-1075


  7 / 1509 MEDLINE  
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[PMID]:28202581
[Au] Autor:Li SYT; Cheng STW; Zhang D; Leung PS
[Ad] Endereço:School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China.
[Ti] Título:Identification and Functional Implications of Sodium/ -Inositol Cotransporter 1 in Pancreatic ß-Cells and Type 2 Diabetes.
[So] Source:Diabetes;66(5):1258-1271, 2017 May.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:-inositol (MI), the precursor of the second messenger phosphoinositide (PI), mediates multiple cellular events. Rat islets exhibit active transport of MI, although the mechanism involved remains elusive. Here, we report, for the first time, the expression of sodium/ -inositol cotransporter 1 (SMIT1) in rat islets and, specifically, ß-cells. Genetic or pharmacological inhibition of SMIT1 impaired glucose-stimulated insulin secretion by INS-1E cells, probably via downregulation of PI signaling. In addition, SMIT1 expression in INS-1E cells and isolated islets was augmented by acute high-glucose exposure and reduced in chronic hyperglycemia conditions. In corroboration, chronic MI treatment improved the disease phenotypes of diabetic rats and islets. On the basis of our results, we postulate that the MI transporter SMIT1 is required to maintain a stable PI pool in ß-cells in order that PI remains available despite its rapid turnover.
[Mh] Termos MeSH primário: Glicemia/metabolismo
Diabetes Mellitus Tipo 2/metabolismo
Inositol/metabolismo
Células Secretoras de Insulina/metabolismo
Insulina/secreção
Fosfatidilinositóis/metabolismo
Simportadores/genética
[Mh] Termos MeSH secundário: Animais
Glicemia/efeitos dos fármacos
Western Blotting
Linhagem Celular
Regulação para Baixo
Técnicas de Silenciamento de Genes
Hiperglicemia
Imuno-Histoquímica
Células Secretoras de Insulina/efeitos dos fármacos
Células Secretoras de Insulina/secreção
Ilhotas Pancreáticas/efeitos dos fármacos
Ilhotas Pancreáticas/metabolismo
Masculino
Florizina/farmacologia
RNA Mensageiro/metabolismo
Ratos
Ratos Zucker
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais
Simportadores/antagonistas & inibidores
Simportadores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin); 0 (Phosphatidylinositols); 0 (RNA, Messenger); 0 (Symporters); 0 (sodium-myo-inositol cotransporter, rat); 4L6452S749 (Inositol); CU9S17279X (Phlorhizin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170217
[St] Status:MEDLINE
[do] DOI:10.2337/db16-0880


  8 / 1509 MEDLINE  
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[PMID]:28192456
[Au] Autor:Lieder B; Hoi JK; Holik AK; Geissler K; Hans J; Friedl B; Liszt K; Krammer GE; Ley JP; Somoza V
[Ad] Endereço:Christian Doppler Laboratory for Bioactive Aroma Compounds, Faculty of Chemistry, University of Vienna, Vienna, Austria.
[Ti] Título:The flavanone homoeriodictyol increases SGLT-1-mediated glucose uptake but decreases serotonin release in differentiated Caco-2 cells.
[So] Source:PLoS One;12(2):e0171580, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Flavanoids and related polyphenols, among them hesperitin, have been shown to modulate cellular glucose transport by targeting SGLT-1 and GLUT-2 transport proteins. We aimed to investigate whether homoeriodictyol, which is structurally related to hesperitin, affects glucose uptake in differentiated Caco-2 cells as a model for the intestinal barrier. The results revealed that, in contrast to other polyphenols, the flavanon homoeriodictyol promotes glucose uptake by 29.0 ± 3.83% at a concentration of 100 µM. The glucose uptake stimulating effect was sensitive to phloridzin, but not to phloretin, indicating an involvement of the sodium-coupled glucose transporter SGLT-1, but not of sodium-independent glucose transporters (GLUT). In addition, in contrast to the increased extracellular serotonin levels by stimulation with 500 mM D-(+)-glucose, treatment with 100 µM homoeriodictyol decreased serotonin release by -48.8 ± 7.57% in Caco-2 cells via a phloridzin-sensitive signaling pathway. Extracellular serotonin levels were also reduced by -57.1 ± 5.43% after application of 0.01 µM homoeriodictyol to human neural SH-SY5Y cells. In conclusion, we demonstrate that homoeriodictyol affects both the glucose metabolism and the serotonin system in Caco-2 cells via a SGLT-1-meditated pathway. Furthermore, the results presented here support the usage of Caco-2 cells as a model for peripheral serotonin release. Further investigations may address the value of homoeriodictyol in the treatment of anorexia and malnutrition through the targeting of SGLT-1.
[Mh] Termos MeSH primário: Flavonas/farmacologia
Glucose/metabolismo
Serotonina/secreção
Transportador 1 de Glucose-Sódio/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma/genética
Adenocarcinoma/metabolismo
Adenocarcinoma/patologia
Transporte Biológico/efeitos dos fármacos
Células CACO-2
Diferenciação Celular
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Neoplasias do Colo/genética
Neoplasias do Colo/metabolismo
Neoplasias do Colo/patologia
AMP Cíclico/metabolismo
Espaço Extracelular/efeitos dos fármacos
Espaço Extracelular/metabolismo
Expressão Gênica/efeitos dos fármacos
Glucose/farmacologia
Seres Humanos
Florizina/farmacologia
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/genética
Transportador 1 de Glucose-Sódio/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Flavones); 0 (SLC5A1 protein, human); 0 (Sodium-Glucose Transporter 1); 333DO1RDJY (Serotonin); CU9S17279X (Phlorhizin); E0399OZS9N (Cyclic AMP); EHE7H3705C (homoeriodictyol); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170214
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0171580


  9 / 1509 MEDLINE  
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[PMID]:28159283
[Au] Autor:Sun L; Sun J; Thavaraj P; Yang X; Guo Y
[Ad] Endereço:College of Food Engineering and Nutritional Science, Shaanxi Normal University, Xi'an 710062, PR China; Centre for Nutrition and Food Science, Queensland Alliance for Agricultural and Food Innovation, The University of Queensland, Brisbane 4072, Australia. Electronic address: l.sun1@uq.edu.au.
[Ti] Título:Effects of thinned young apple polyphenols on the quality of grass carp (Ctenopharyngodon idellus) surimi during cold storage.
[So] Source:Food Chem;224:372-381, 2017 Jun 01.
[Is] ISSN:0308-8146
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to investigate the effects of young apple polyphenols (YAP) on the quality of grass cap surimi (GCS) during storage at 4°C. The addition of YAP into GCS was found to be effective in delaying lipid oxidation, soluble myofibrillar protein (SMP) degradation and changes of L , a and b values of GCS. Chlorogenic acid was screened to be the primary component showing preservative effects. YAP was shown to protect the functional properties of SMP during cold storage, retarding both the decrease in emulsifying activity and stability, and the increase in surface hydrophobicity of SMP. Additionally, the loss of gel strength and texture of GCS with YAP were significantly (P<0.05) lower than that of GCS without YAP during cold storage. Therefore, YAP may be developed as a natural antioxidant to maintain the quality and to extend the shelf life of freshwater fish surimi.
[Mh] Termos MeSH primário: Carpas/metabolismo
Armazenamento de Alimentos
Malus/química
Polifenóis/química
Alimentos Marinhos/análise
[Mh] Termos MeSH secundário: Adulto
Animais
Antioxidantes/química
Catequina/química
Ácido Clorogênico/análise
Ácido Clorogênico/química
Feminino
Aditivos Alimentares
Conservação de Alimentos
Qualidade dos Alimentos
Seres Humanos
Metabolismo dos Lipídeos/efeitos dos fármacos
Masculino
Proteínas Musculares/metabolismo
Florizina/química
Paladar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Food Additives); 0 (Muscle Proteins); 0 (Polyphenols); 318ADP12RI (Chlorogenic Acid); 8R1V1STN48 (Catechin); CU9S17279X (Phlorhizin)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170205
[St] Status:MEDLINE


  10 / 1509 MEDLINE  
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[PMID]:27878313
[Au] Autor:Vallon V; Thomson SC
[Ad] Endereço:Division of Nephrology and Hypertension, Department of Medicine, University of California San Diego, La Jolla, CA, 92093, USA. vvallon@ucsd.edu.
[Ti] Título:Targeting renal glucose reabsorption to treat hyperglycaemia: the pleiotropic effects of SGLT2 inhibition.
[So] Source:Diabetologia;60(2):215-225, 2017 Feb.
[Is] ISSN:1432-0428
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Healthy kidneys filter ∼160 g/day of glucose (∼30% of daily energy intake) under euglycaemic conditions. To prevent valuable energy from being lost in the urine, the proximal tubule avidly reabsorbs filtered glucose up to a limit of ∼450 g/day. When blood glucose levels increase to the point that the filtered load exceeds this limit, the surplus is excreted in the urine. Thus, the kidney provides a safety valve that can prevent extreme hyperglycaemia as long as glomerular filtration is maintained. Most of the capacity for renal glucose reabsorption is provided by sodium glucose cotransporter (SGLT) 2 in the early proximal tubule. In the absence or with inhibition of SGLT2, the renal reabsorptive capacity for glucose declines to ∼80 g/day (the residual capacity of SGLT1), i.e. the safety valve opens at a lower threshold, which makes it relevant to glucose homeostasis from day-to-day. Several SGLT2 inhibitors are now approved glucose lowering agents for individuals with type 2 diabetes and preserved kidney function. By inducing glucosuria, these drugs improve glycaemic control in all stages of type 2 diabetes, while their risk of causing hypoglycaemia is low because they naturally stop working when the filtered glucose load falls below ∼80 g/day and they do not otherwise interfere with metabolic counterregulation. Through glucosuria, SGLT2 inhibitors reduce body weight and body fat, and shift substrate utilisation from carbohydrates to lipids and, possibly, ketone bodies. Because SGLT2 reabsorbs sodium along with glucose, SGLT2 blockers are natriuretic and antihypertensive. Also, because they work in the proximal tubule, SGLT2 inhibitors increase delivery of fluid and electrolytes to the macula densa, thereby activating tubuloglomerular feedback and increasing tubular back pressure. This mitigates glomerular hyperfiltration, reduces the kidney's demand for oxygen and lessens albuminuria. For reasons that are less well understood, SGLT2 inhibitors are also uricosuric. These pleiotropic effects of SGLT2 inhibitors are likely to have contributed to the results of the EMPA-REG OUTCOME trial in which the SGLT2 inhibitor, empagliflozin, slowed the progression of chronic kidney disease and reduced major adverse cardiovascular events in high-risk individuals with type 2 diabetes. This review discusses the role of SGLT2 in the physiology and pathophysiology of renal glucose reabsorption and outlines the unexpected logic of inhibiting SGLT2 in the diabetic kidney.
[Mh] Termos MeSH primário: Glucose/metabolismo
Hiperglicemia/metabolismo
Rim/metabolismo
Transportador 2 de Glucose-Sódio/antagonistas & inibidores
Transportador 2 de Glucose-Sódio/metabolismo
[Mh] Termos MeSH secundário: Diabetes Mellitus Tipo 2/tratamento farmacológico
Diabetes Mellitus Tipo 2/metabolismo
Seres Humanos
Hiperglicemia/tratamento farmacológico
Resistência à Insulina/fisiologia
Florizina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Sodium-Glucose Transporter 2); CU9S17279X (Phlorhizin); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161124
[St] Status:MEDLINE
[do] DOI:10.1007/s00125-016-4157-3



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