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[PMID]:28657399
[Au] Autor:Busch RS; Kane MP
[Ad] Endereço:a Albany Medical Center Division of Community Endocrinology , Albany , NY , USA.
[Ti] Título:Combination SGLT2 inhibitor and GLP-1 receptor agonist therapy: a complementary approach to the treatment of type 2 diabetes.
[So] Source:Postgrad Med;129(7):686-697, 2017 Sep.
[Is] ISSN:1941-9260
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Among persons with type 2 diabetes (t2d), the development of glucose intolerance involves dysfunction in several organs and tissues, including the muscle, liver, pancreas, kidney, gastrointestinal tract, adipose tissue, and brain. individuals with t2d typically have a number of comorbidities, including hypertension, hyperlipidemia, and being overweight or obese, and are, consequently, at high cardiovascular risk. guidelines recommend a comprehensive care strategy that includes treatment of diabetes-related complications and comorbidities beyond those related to hyperglycemia. use of glucose-lowering therapies with complementary activities that address multiple facets of the disease may improve long-term outcomes for patients with t2d. two recent drug classes developed for use in t2d, glucagon-like peptide-1 receptor agonists (glp-1ras) and sodium glucose cotransporter 2 (sglt2) inhibitors, have been shown in clinical trials to have beneficial effects on glycemic control, body weight, cardiovascular risk factors, and (for liraglutide, semaglutide, and empagliflozin) cardiovascular outcomes, while having an acceptable safety profile. between them, these drug classes directly or indirectly affect many of the organs and tissues involved in the pathogenesis of t2d, and their beneficial effects on glycemic- and cardiovascular-related parameters are likely to be complementary and potentially additive. in the largest clinical trial of a glp-1ra and an sglt2 inhibitor in combination (duration-8), patients with t2d (n = 685) who received exenatide plus dapagliflozin added to their treatment regimen for 28 weeks had significantly greater reductions from baseline in glycated hemoglobin, body weight, and systolic blood pressure compared with patients who received either drug as monotherapy. this review summarizes the complementary aspects of these drug classes and presents the available data among patients receiving dual therapy with a glp-1ra and an sglt2 inhibitor.
[Mh] Termos MeSH primário: Complicações do Diabetes/tratamento farmacológico
Diabetes Mellitus Tipo 2/tratamento farmacológico
Receptor do Peptídeo Semelhante ao Glucagon 1/agonistas
Receptor do Peptídeo Semelhante ao Glucagon 1/uso terapêutico
Hipoglicemiantes/uso terapêutico
Proteínas de Transporte de Sódio-Glucose/agonistas
Proteínas de Transporte de Sódio-Glucose/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Terapias Complementares
Complicações do Diabetes/etiologia
Diabetes Mellitus Tipo 2/complicações
Feminino
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucagon-Like Peptide-1 Receptor); 0 (Hypoglycemic Agents); 0 (Sodium-Glucose Transport Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE
[do] DOI:10.1080/00325481.2017.1342509


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[PMID]:28611037
[Au] Autor:Abdul-Ghani M; Al Jobori H; Daniele G; Adams J; Cersosimo E; Triplitt C; DeFronzo RA
[Ad] Endereço:Diabetes Division, The University of Texas Health Science Center at San Antonio, San Antonio, TX.
[Ti] Título:Inhibition of Renal Sodium-Glucose Cotransport With Empagliflozin Lowers Fasting Plasma Glucose and Improves ß-Cell Function in Subjects With Impaired Fasting Glucose.
[So] Source:Diabetes;66(9):2495-2502, 2017 Sep.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The objective of this study was to examine the effect of renal sodium-glucose cotransporter inhibition with empagliflozin on the fasting plasma glucose (FPG) concentration and ß-cell function in subjects with impaired fasting glucose (IFG). Eight subjects with normal fasting glucose (NFG) and eight subjects with IFG received empagliflozin (25 mg/day) for 2 weeks. FPG concentration and ß-cell function was measured with a nine-step hyperglycemic clamp before and 48 h and 14 days after the start of empagliflozin. Empagliflozin caused 50 ± 4 and 45 ± 4 g glucosuria on day 2 in subjects with IFG and NFG, respectively, and the glucosuria was maintained for 2 weeks in both groups. The FPG concentration decreased only in subjects with IFG from 110 ± 2 to 103 ± 3 mg/dL ( < 0.01) after 14 days. The FPG concentration remained unchanged (95 ± 2 to 94 ± 2 mg/dL) in subjects with NFG. Empagliflozin enhanced ß-cell function only in subjects with IFG. The incremental area under the plasma C-peptide concentration curve during the hyperglycemic clamp increased by 22 ± 4 and 23 ± 4% after 48 h and 14 days, respectively ( < 0.01); the plasma C-peptide response remained unchanged in subjects with NFG. Insulin sensitivity during the hyperglycemic clamp was not affected by empagliflozin in either IFG or NFG. Thus, ß-cell function measured with the insulin secretion/insulin sensitivity (disposition) index increased significantly in IFG, but not in subjects with normal glucose tolerance. Inhibition of renal sodium-glucose cotransport with empagliflozin in subjects with IFG and NFG produces comparable glucosuria but lowers the plasma glucose concentration and improves ß-cell function only in subjects with IFG.
[Mh] Termos MeSH primário: Compostos Benzidrílicos/farmacologia
Glicemia
Glucosídeos/farmacologia
Células Secretoras de Insulina/efeitos dos fármacos
Proteínas de Transporte de Sódio-Glucose/metabolismo
[Mh] Termos MeSH secundário: Estudos de Casos e Controles
Feminino
Seres Humanos
Hipoglicemiantes/farmacologia
Células Secretoras de Insulina/fisiologia
Rim/metabolismo
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzhydryl Compounds); 0 (Blood Glucose); 0 (Glucosides); 0 (Hypoglycemic Agents); 0 (Sodium-Glucose Transport Proteins); HDC1R2M35U (empagliflozin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170615
[St] Status:MEDLINE
[do] DOI:10.2337/db17-0055


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[PMID]:28472796
[Au] Autor:Zhou Y; Wu W
[Ti] Título:The Sodium-Glucose Co-Transporter 2 Inhibitor, Empagliflozin, Protects against Diabetic Cardiomyopathy by Inhibition of the Endoplasmic Reticulum Stress Pathway.
[So] Source:Cell Physiol Biochem;41(6):2503-2512, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: This study aimed to determine whether or not the sodium-glucose co-transporter 2 inhibitor, empagliflozin (EMPA), can protect against diabetic cardiomyopathy (DCM) and to elucidate the related mechanism. METHODS: Rats were divided into the following four groups: a non-diabetic group; diabetic cardiomyopathy rats without EMPA treatment; and diabetic cardiomyopathy rats with EMPA treatment (low- and high-dose EMPA). Hemodynamic measurements were performed to evaluate left ventricular systolic and diastolic function. The histopathology of the heart was examined with hematoxylin-eosin staining. Expression of glucose-regulated protein (GRP)78, enhancer-binding protein homologous protein (CHOP), and caspase-12 was detected by Western blot, and the mRNA levels of XBP1, ATF4, and TRAF2 were analysed by real-time PCR. RESULTS: EMPA significantly decreased the blood glucose level when compared with vehicle. EMPA strongly improved cardiac function based on hemodynamic and histopathologic analyses. Moreover, EMPA can significantly down-regulate the expression of GRP78, CHOP, and caspase-12 (P < 0.01). Additionally, the mRNA levels of XBP1, ATF4, and TRAF2 were markedly decreased by administration of EMPA (P < 0.01). CONCLUSION: EMPA protects against DCM by inactivating the endoplasmic reticulum stress pathway.
[Mh] Termos MeSH primário: Compostos Benzidrílicos/farmacologia
Cardiomiopatias Diabéticas/prevenção & controle
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Glucosídeos/farmacologia
Proteínas de Transporte de Sódio-Glucose/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Glicemia/análise
Diabetes Mellitus Experimental/induzido quimicamente
Diabetes Mellitus Experimental/patologia
Cardiomiopatias Diabéticas/patologia
Regulação para Baixo/efeitos dos fármacos
Proteínas de Choque Térmico/metabolismo
Hemodinâmica/efeitos dos fármacos
Masculino
Miocárdio/metabolismo
Miocárdio/patologia
Miócitos Cardíacos/citologia
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/metabolismo
Substâncias Protetoras/farmacologia
Ratos
Ratos Wistar
Proteínas de Transporte de Sódio-Glucose/metabolismo
Fator 2 Associado a Receptor de TNF/genética
Fator 2 Associado a Receptor de TNF/metabolismo
Fator de Transcrição CHOP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzhydryl Compounds); 0 (Blood Glucose); 0 (Glucosides); 0 (Heat-Shock Proteins); 0 (Protective Agents); 0 (Sodium-Glucose Transport Proteins); 0 (TNF Receptor-Associated Factor 2); 0 (molecular chaperone GRP78); 147336-12-7 (Transcription Factor CHOP); HDC1R2M35U (empagliflozin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1159/000475942


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[PMID]:28356283
[Au] Autor:Shepard BD; Pluznick JL
[Ad] Endereço:Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
[Ti] Título:Saving the sweetness: renal glucose handling in health and disease.
[So] Source:Am J Physiol Renal Physiol;313(1):F55-F61, 2017 Jul 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glucose homeostasis is highly controlled, and the function of the kidney plays an integral role in this process. The exquisite control of blood glucose relies, in part, on renal glucose filtration, renal glucose reabsorption, and renal gluconeogenesis. Particularly critical to maintaining glucose homeostasis is the renal reabsorption of glucose; with ~162 g of glucose filtered by the kidney per day, it is imperative that the kidney have the ability to efficiently reabsorb nearly 100% of this glucose back in the bloodstream. In this review, we focus on this central process, highlighting the renal transporters and regulators involved in both the physiology and pathophysiology of glucose reabsorption.
[Mh] Termos MeSH primário: Glicemia/metabolismo
Nefropatias/metabolismo
Rim/metabolismo
Reabsorção Renal
[Mh] Termos MeSH secundário: Animais
Biomarcadores/sangue
Gluconeogênese
Proteínas Facilitadoras de Transporte de Glucose/metabolismo
Homeostase
Seres Humanos
Rim/fisiopatologia
Nefropatias/sangue
Nefropatias/fisiopatologia
Proteínas de Transporte de Sódio-Glucose/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (Blood Glucose); 0 (Glucose Transport Proteins, Facilitative); 0 (Sodium-Glucose Transport Proteins)
[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:170331
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00046.2017


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[PMID]:28303514
[Au] Autor:Pfützner A; Klonoff D; Heinemann L; Ejskjaer N; Pickup J
[Ad] Endereço:Pfützner Science & Health Institute, Mainz, UK. Andreas.pfuetzner@pfuetzner-mainz.com.
[Ti] Título:Euglycemic ketosis in patients with type 2 diabetes on SGLT2-inhibitor therapy-an emerging problem and solutions offered by diabetes technology.
[So] Source:Endocrine;56(1):212-216, 2017 Apr.
[Is] ISSN:1559-0100
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Diabetic ketoacidosis is an infrequent but life-threatening acute complication of diabetes, affecting predominantly patients with type 1 diabetes, children, and pregnant women, where ketosis is usually associated with marked hyperglycemia. Recently, an increasing number of cases have been reported of euglycemic diabetic ketoacidosis in patients with type 2 diabetes receiving sodium-glucose cotransporter 2 inhibitor treatment in routine practice. There is a minor, but not negligible diabetic ketoacidosis risk associated with this drug class, which was not seen in randomized clinical trials. However, sodium-glucose cotransporter2 inhibitors increase the risk of ketosis by increasing glucagon secretion in the pancreas and decreasing the renal excretion of 3-hydroxybutyrate and acetoacetate. When used in addition to insulin, any insulin dose reduction required to avoid hypoglycemia may lead to insufficient suppression of lipolysis and ketogenesis. sodium-glucose cotransporter2 inhibitor-induced loss of urinary glucose encourages euglycemia. Normo-glycemic or near-normoglycemic diabetic ketoacidosis represents a major threat to the health and well-being of a patient, because it may occur undetected and without any indicative hyperglycemia. In consequence, patients on sodium-glucose cotransporter2 inhibitors are recommended to perform regular blood ketone tests since they are not alerted to incipient diabetic ketoacidosis by glucose testing alone. This option is offered by several blood glucose meters that can also measure ketones with a separate ketone strip or in one case by an automatic parallel ketone assessment from the same strip. The need for extra testing and the associated costs may be a barrier to patient acceptance of this risk mitigation procedure. However, patients who are at risk for euglycemic diabetic ketoacidosis when being treated with sodium-glucose cotransporter2 inhibitors should be specially advised to monitor blood ketone levels on a regular basis.
[Mh] Termos MeSH primário: Compostos Benzidrílicos/efeitos adversos
Canagliflozina/efeitos adversos
Diabetes Mellitus Tipo 2/tratamento farmacológico
Cetoacidose Diabética/etiologia
Glucosídeos/efeitos adversos
Hipoglicemiantes/efeitos adversos
Proteínas de Transporte de Sódio-Glucose/antagonistas & inibidores
[Mh] Termos MeSH secundário: Compostos Benzidrílicos/uso terapêutico
Canagliflozina/uso terapêutico
Glucosídeos/uso terapêutico
Seres Humanos
Hipoglicemiantes/uso terapêutico
[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 (Hypoglycemic Agents); 0 (Sodium-Glucose Transport Proteins); 0SAC974Z85 (Canagliflozin); HDC1R2M35U (empagliflozin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170318
[St] Status:MEDLINE
[do] DOI:10.1007/s12020-017-1264-y


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[PMID]:28192604
[Au] Autor:Åstrand A; Wingren C; Benjamin A; Tregoning JS; Garnett JP; Groves H; Gill S; Orogo-Wenn M; Lundqvist AJ; Walters D; Smith DM; Taylor JD; Baker EH; Baines DL
[Ad] Endereço:Respiratory, Inflammation and Autoimmunity Innovative Medicines Research Unit, AstraZeneca Gothenburg, Mölndal, Sweden.
[Ti] Título:Dapagliflozin-lowered blood glucose reduces respiratory Pseudomonas aeruginosa infection in diabetic mice.
[So] Source:Br J Pharmacol;174(9):836-847, 2017 May.
[Is] ISSN:1476-5381
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Hyperglycaemia increases glucose concentrations in airway surface liquid and increases the risk of pulmonary Pseudomonas aeruginosa infection. We determined whether reduction of blood and airway glucose concentrations by the anti-diabetic drug dapagliflozin could reduce P. aeruginosa growth/survival in the lungs of diabetic mice. EXPERIMENTAL APPROACH: The effect of dapagliflozin on blood and airway glucose concentration, the inflammatory response and infection were investigated in C57BL/6J (wild type, WT) or leptin receptor-deficient (db/db) mice, treated orally with dapagliflozin prior to intranasal dosing with LPS or inoculation with P. aeruginosa. Pulmonary glucose transport and fluid absorption were investigated in Wistar rats using the perfused fluid-filled lung technique. KEY RESULTS: Fasting blood, airway glucose and lactate concentrations were elevated in the db/db mouse lung. LPS challenge increased inflammatory cells in bronchoalveolar lavage fluid from WT and db/db mice with and without dapagliflozin treatment. P. aeruginosa colony-forming units (CFU) were increased in db/db lungs. Pretreatment with dapagliflozin reduced blood and bronchoalveolar lavage glucose concentrations and P. aeruginosa CFU in db/db mice towards those seen in WT. Dapagliflozin had no adverse effects on the inflammatory response in the mouse or pulmonary glucose transport or fluid absorption in the rat lung. CONCLUSION AND IMPLICATIONS: Pharmacological lowering of blood glucose with dapagliflozin effectively reduced P. aeruginosa infection in the lungs of diabetic mice and had no adverse pulmonary effects in the rat. Dapagliflozin has potential to reduce the use, or augment the effect, of antimicrobials in the prevention or treatment of pulmonary infection.
[Mh] Termos MeSH primário: Compostos Benzidrílicos/uso terapêutico
Glicemia/efeitos dos fármacos
Diabetes Mellitus Experimental/tratamento farmacológico
Glucosídeos/uso terapêutico
Infecções por Pseudomonas/sangue
Infecções por Pseudomonas/tratamento farmacológico
Pseudomonas aeruginosa/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Compostos Benzidrílicos/farmacologia
Glicemia/metabolismo
Líquido da Lavagem Broncoalveolar
Diabetes Mellitus Experimental/sangue
Glucosídeos/farmacologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Ratos
Ratos Wistar
Proteínas de Transporte de Sódio-Glucose/farmacologia
Proteínas de Transporte de Sódio-Glucose/uso terapêutico
[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 (Blood Glucose); 0 (Glucosides); 0 (Sodium-Glucose Transport Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170214
[St] Status:MEDLINE
[do] DOI:10.1111/bph.13741


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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]:28086872
[Au] Autor:Hayashi T; Fukui T; Nakanishi N; Yamamoto S; Tomoyasu M; Osamura A; Ohara M; Yamamoto T; Ito Y; Hirano T
[Ad] Endereço:Division of Diabetes, Metabolism, and Endocrinology, Department of Medicine, Showa University School of Medicine, 1-5-8, Hatanodai, Shinagawa-ku, Tokyo, 142-8666, Japan. t-hayashi@med.showa-u.ac.jp.
[Ti] Título:Dapagliflozin decreases small dense low-density lipoprotein-cholesterol and increases high-density lipoprotein 2-cholesterol in patients with type 2 diabetes: comparison with sitagliptin.
[So] Source:Cardiovasc Diabetol;16(1):8, 2017 Jan 13.
[Is] ISSN:1475-2840
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The sodium-glucose co-transporter-2 (SGLT-2) inhibitors have been reported to increase both low-density lipoprotein (LDL) and high-density lipoprotein (HDL)-cholesterol (C). This study aimed to determine how SGLT-2 inhibitors affect LDL and HDL-C subspecies. METHODS: This single center, open-label, randomized, prospective study included 80 patients with type 2 diabetes taking prescribed oral hypoglycemic agents. Patients were allocated to receive dapagliflozin (n = 40) or sitagliptin (n = 40) as add-on treatment. Fasting blood samples were collected before and 12 weeks after this intervention. Small dense (sd) LDL-C, large buoyant (lb) LDL-C, HDL2-C, and HDL3-C levels were determined using our established homogeneous assays. Statistical comparison of blood parameters before and after treatment was performed using the paired t test. RESULTS: Dapagliflozin and sitagliptin comparably decreased HbA1c (0.75 and 0.63%, respectively). Dapagliflozin significantly decreased body weight, systolic blood pressure, plasma triglycerides and liver transaminases, and increased adiponectin; sitagliptin did not alter these measurements. LDL-C and apolipoprotein (apo) B were not significantly changed by dapagliflozin, whereas HDL-C and apo AI were increased. Dapagliflozin did not alter concentrations of LDL-C, but sd LDL-C decreased by 20% and lb LDL-C increased by 18%. Marked elevation in lb LDL-C (53%) was observed in individuals (n = 20) whose LDL-C was elevated by dapagliflozin. However, sd LDL-C remained suppressed (20%). Dapagliflozin increased HDL2-C by 18% without affecting HDL3-C. Sitagliptin did not alter plasma lipids or lipoprotein subspecies. CONCLUSIONS: A SGLT-2 inhibitor, dapagliflozin suppresses potent atherogenic sd LDL-C and increased HDL2-C, a favorable cardiometabolic marker. Although LDL-C levels are elevated by treatment with dapagliflozin, this was due to increased concentrations of the less atherogenic lb LDL-C. However, these findings were not observed after treatment with dipeptidyl peptidase-4 inhibitor, sitagliptin. Trial registration UMIN Clinical Trials Registry (UMIN000020984).
[Mh] Termos MeSH primário: Compostos Benzidrílicos/administração & dosagem
LDL-Colesterol/sangue
Diabetes Mellitus Tipo 2/sangue
Glucosídeos/administração & dosagem
Lipoproteínas HDL2/sangue
Fosfato de Sitagliptina/administração & dosagem
Proteínas de Transporte de Sódio-Glucose/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adulto
LDL-Colesterol/antagonistas & inibidores
Diabetes Mellitus Tipo 2/tratamento farmacológico
Quimioterapia Combinada
Feminino
Seres Humanos
Hipoglicemiantes/administração & dosagem
Lipoproteínas HDL2/agonistas
Masculino
Meia-Idade
Estudos Prospectivos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (2-(3-(4-ethoxybenzyl)-4-chlorophenyl)-6-hydroxymethyltetrahydro-2H-pyran-3,4,5-triol); 0 (Benzhydryl Compounds); 0 (Cholesterol, LDL); 0 (Glucosides); 0 (Hypoglycemic Agents); 0 (Lipoproteins, HDL2); 0 (Sodium-Glucose Transport Proteins); TS63EW8X6F (Sitagliptin Phosphate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171121
[Lr] Data última revisão:
171121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170115
[St] Status:MEDLINE
[do] DOI:10.1186/s12933-016-0491-5


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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]:27429292
[Au] Autor:Melo IS; Santos YMO; Costa MA; Pacheco ALD; Silva NKGT; Cardoso-Sousa L; Pereira UP; Goulart LR; Garcia-Cairasco N; Duzzioni M; Gitaí DLG; Tilelli CQ; Sabino-Silva R; Castro OW
[Ad] Endereço:Institute of Biological Sciences and Health, Federal University of Alagoas (UFAL), Maceio, AL, Brazil.
[Ti] Título:Inhibition of sodium glucose cotransporters following status epilepticus induced by intrahippocampal pilocarpine affects neurodegeneration process in hippocampus.
[So] Source:Epilepsy Behav;61:258-268, 2016 Aug.
[Is] ISSN:1525-5069
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Temporal lobe epilepsy (TLE) is characterized by spontaneous recurrent seizures, starting from secondary functional disorders due to several insults, including self-sustaining continuous seizures identified as status epilepticus (SE). Although hypoglycemia has been associated with SE, the effect of inhibition of the Na(+)/glucose cotransporters (SGLTs) on hippocampus during SE is still unknown. Here we evaluated the functional role of SGLT in the pattern of limbic seizures and neurodegeneration process after pilocarpine (PILO)-induced SE. Vehicle (VEH, 1µL) or phlorizin, a specific SGLT inhibitor (PZN, 1µL, 50µg/µL), was administered in the hippocampus of rats 30min before PILO (VEH+PILO or PZN+PILO, respectively). The limbic seizures were classified using the Racine's scale, and the amount of wet dog shakes (WDS) was quantified before and during SE. Neurodegeneration process was evaluated by Fluoro-Jade C (FJ-C), and FJ-C-positive neurons (FJ-C+) were counted 24h and 15days after SE. The PZN-treated rats showed higher (p<0.05) number of WDS when compared with VEH+PILO. There was no difference in seizure severity between PZN+PILO and VEH+PILO groups. However, the pattern of limbic seizures significantly changed in PZN+PILO. Indeed, the class 5 seizures repeated themselves more times (p<0.05) than the other classes in the PZN group at 50min after SE induction. The PZN+PILO animals had a higher (p<0.05) number of FJ-C+ cells in the dentate gyrus (DG), hilus, and CA3 and CA1 of hippocampus, when compared with VEH+PILO. The PZN+PILO animals had a decreased number (p<0.05) of FJ-C+ cells in CA1 compared with VEH+PILO 15days after SE induction. Taken together, our data suggest that SGLT inhibition with PZN increased the severity of limbic seizures during SE and increased neurodegeneration in hippocampus 24h after SE, suggesting that SGLT1 and SGLT2 could participate in the modulation of earlier stages of epileptogenic processes.
[Mh] Termos MeSH primário: Hipocampo/efeitos dos fármacos
Degeneração Neural/patologia
Neurônios/efeitos dos fármacos
Florizina/farmacologia
Convulsões/patologia
Proteínas de Transporte de Sódio-Glucose/antagonistas & inibidores
Estado Epiléptico/patologia
[Mh] Termos MeSH secundário: Animais
Hipocampo/metabolismo
Hipocampo/patologia
Masculino
Degeneração Neural/induzido quimicamente
Degeneração Neural/metabolismo
Neurônios/metabolismo
Neurônios/patologia
Pilocarpina
Ratos
Ratos Wistar
Convulsões/induzido quimicamente
Convulsões/metabolismo
Estado Epiléptico/induzido quimicamente
Estado Epiléptico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Sodium-Glucose Transport Proteins); 01MI4Q9DI3 (Pilocarpine); CU9S17279X (Phlorhizin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170815
[Lr] Data última revisão:
170815
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160719
[St] Status:MEDLINE



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