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[PMID]:29466360
[Au] Autor:Kaitu'u-Lino TJ; Brownfoot FC; Beard S; Cannon P; Hastie R; Nguyen TV; Binder NK; Tong S; Hannan NJ
[Ad] Endereço:Translational Obstetrics Group, The Department of Obstetrics and Gynaecology, University of Melbourne and Mercy Perinatal, Mercy Hospital for Women, Heidelberg, Victoria, Australia.
[Ti] Título:Combining metformin and esomeprazole is additive in reducing sFlt-1 secretion and decreasing endothelial dysfunction - implications for treating preeclampsia.
[So] Source:PLoS One;13(2):e0188845, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: The discovery of new treatments that prevent or treat preeclampsia would be a major advance. Antiangiogenic factors soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sENG) are secreted in excess from the placenta, causing hypertension, endothelial dysfunction, and multiorgan injury. We recently identified metformin and esomeprazole as potential treatments for preeclampsia. Both reduce placental and endothelial secretion of sFlt-1 and soluble endoglin, and reduce endothelial dysfunction. OBJECTIVES: We set out to assess whether combining metformin and esomeprazole would additively reduce sFlt-1 and soluble endoglin secretion and reduce endothelial dysfunction (verses drug alone). Metformin and esomeprazole were added to primary placental cells and tissues, and endothelial cells and their effects on sFlt-1 and soluble endoglin secretion were assessed in vitro. Tumor necrosis factor-α (TNF-α) was added to endothelial cells to induce dysfunction in vitro. We examined the ability of metformin + esomeprazole to rescue TNF-α induced vascular cell adhesion molecule-1 (VCAM-1) and Endothelin-1 (ET-1) expression, leukocyte adhesion (markers of endothelial dysfunction). RESULTS: Combining metformin and esomeprazole was additive at reducing sFlt-1 secretion and expression of sFlt-1 e15a mRNA isoform in primary cytotrophoblast, placental explants and endothelial cells. In contrast, no additive reduction in sENG was observed with combined metformin and esomeprazole. The low-dose combination of metformin + esomeprazole additively reduced TNF-α-induced VCAM-1 mRNA, but not VCAM-1 protein expression. There was no additive reduction when combining metformin and esomeprazole on TNF-α induced PBMC adhesion to endothelial cells. However, combining metformin and esomeprazole additively reduced ET-1 mRNA expression. CONCLUSIONS: In conclusion combining metformin and esomeprazole additively reduced secretion of sFlt-1, and markers of endothelial dysfunction. The combination of metformin and esomeprazole may provide a more effective treatment or prevention for preeclampsia compared to either as single agents.
[Mh] Termos MeSH primário: Endotélio Vascular/efeitos dos fármacos
Esomeprazol/administração & dosagem
Metformina/administração & dosagem
Pré-Eclâmpsia/tratamento farmacológico
Receptor 1 de Fatores de Crescimento do Endotélio Vascular/secreção
[Mh] Termos MeSH secundário: Endotélio Vascular/fisiopatologia
Feminino
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Gravidez
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
9100L32L2N (Metformin); EC 2.7.10.1 (FLT1 protein, human); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-1); N3PA6559FT (Esomeprazole)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180222
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188845


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[PMID]:28467723
[Au] Autor:Diaz-Morales N; Rovira-Llopis S; Bañuls C; Lopez-Domenech S; Escribano-Lopez I; Veses S; Jover A; Rocha M; Hernandez-Mijares A; Victor VM
[Ad] Endereço:1 Service of Endocrinology and Nutrition, University Hospital Doctor Peset , Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain .
[Ti] Título:Does Metformin Protect Diabetic Patients from Oxidative Stress and Leukocyte-Endothelium Interactions?
[So] Source:Antioxid Redox Signal;27(17):1439-1445, 2017 Dec 10.
[Is] ISSN:1557-7716
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Since metformin can exert beneficial vascular effects, we aimed at studying its effect on reactive oxygen species (ROS) production, antioxidant enzyme expression, levels of adhesion molecules, and leukocyte-endothelium interactions in the leukocytes from type 2 diabetic (T2D) patients. The study was carried out in 72 T2D patients (41 of whom were treated with metformin for at least 12 months at a dose of 1700 mg per day), and in 40 sex- and age-matched control subjects. Leukocytes from T2D patients exhibited enhanced levels of mitochondrial ROS and decreased mRNA levels of glutathione peroxidase 1 (gpx1) and sirtuin 3 (sirt3) with respect to controls, whereas metformin was shown to revert these effects. No changes were observed on total ROS production and the expression levels of superoxide dismutase 1 and catalase. Furthermore, increases in leukocyte-endothelial interactions and intercellular adhesion molecule-1 and P-selectin levels were found in T2D and were also restored in metformin-treated patients. Our findings raise the question of whether metformin could modulate the appearance of atherosclerosis in T2D patients and reduce vascular events by decreasing leukocyte oxidative stress through an increase in gpx1 and sirt3 expression, and undermining adhesion molecule levels and leukocyte-endothelium interactions. Antioxid. Redox Signal. 27, 1439-1445.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/tratamento farmacológico
Células Endoteliais/efeitos dos fármacos
Hipoglicemiantes/administração & dosagem
Leucócitos/efeitos dos fármacos
Metformina/administração & dosagem
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Idoso
Catalase
Adesão Celular
Diabetes Mellitus Tipo 2/genética
Diabetes Mellitus Tipo 2/metabolismo
Células Endoteliais/metabolismo
Feminino
Glutationa Peroxidase/genética
Seres Humanos
Hipoglicemiantes/farmacologia
Molécula 1 de Adesão Intercelular/metabolismo
Leucócitos/metabolismo
Masculino
Metformina/farmacologia
Meia-Idade
Selectina-P/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Sirtuína 3/genética
Superóxido Dismutase-1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypoglycemic Agents); 0 (ICAM1 protein, human); 0 (P-Selectin); 0 (Reactive Oxygen Species); 0 (SOD1 protein, human); 126547-89-5 (Intercellular Adhesion Molecule-1); 9100L32L2N (Metformin); EC 1.11.1.- (glutathione peroxidase GPX1); EC 1.11.1.6 (Catalase); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase-1); EC 3.5.1.- (SIRT3 protein, human); EC 3.5.1.- (Sirtuin 3)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1089/ars.2017.7122


  3 / 10308 MEDLINE  
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[PMID]:28453780
[Au] Autor:Billings LK; Jablonski KA; Warner AS; Cheng YC; McAteer JB; Tipton L; Shuldiner AR; Ehrmann DA; Manning AK; Dabelea D; Franks PW; Kahn SE; Pollin TI; Knowler WC; Altshuler D; Florez JC; Diabetes Prevention Program Research Group
[Ad] Endereço:Diabetes Unit, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114.
[Ti] Título:Variation in Maturity-Onset Diabetes of the Young Genes Influence Response to Interventions for Diabetes Prevention.
[So] Source:J Clin Endocrinol Metab;102(8):2678-2689, 2017 Aug 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Variation in genes that cause maturity-onset diabetes of the young (MODY) has been associated with diabetes incidence and glycemic traits. Objectives: This study aimed to determine whether genetic variation in MODY genes leads to differential responses to insulin-sensitizing interventions. Design and Setting: This was a secondary analysis of a multicenter, randomized clinical trial, the Diabetes Prevention Program (DPP), involving 27 US academic institutions. We genotyped 22 missense and 221 common variants in the MODY-causing genes in the participants in the DPP. Participants and Interventions: The study included 2806 genotyped DPP participants randomized to receive intensive lifestyle intervention (n = 935), metformin (n = 927), or placebo (n = 944). Main Outcome Measures: Association of MODY genetic variants with diabetes incidence at a median of 3 years and measures of 1-year ß-cell function, insulinogenic index, and oral disposition index. Analyses were stratified by treatment group for significant single-nucleotide polymorphism × treatment interaction (Pint < 0.05). Sequence kernel association tests examined the association between an aggregate of rare missense variants and insulinogenic traits. Results: After 1 year, the minor allele of rs3212185 (HNF4A) was associated with improved ß-cell function in the metformin and lifestyle groups but not the placebo group; the minor allele of rs6719578 (NEUROD1) was associated with an increase in insulin secretion in the metformin group but not in the placebo and lifestyle groups. Conclusions: These results provide evidence that genetic variation among MODY genes may influence response to insulin-sensitizing interventions.
[Mh] Termos MeSH primário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Diabetes Mellitus Tipo 2/genética
Terapia por Exercício
Fator 4 Nuclear de Hepatócito/genética
Programas de Redução de Peso
[Mh] Termos MeSH secundário: Diabetes Mellitus Tipo 2/prevenção & controle
Variação Genética
Glucoquinase/genética
Fator 1-alfa Nuclear de Hepatócito/genética
Fator 1-beta Nuclear de Hepatócito/genética
Proteínas de Homeodomínio/genética
Seres Humanos
Metformina/uso terapêutico
Mutação de Sentido Incorreto
Polimorfismo de Nucleotídeo Único
Comportamento de Redução do Risco
Transativadores/genética
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (HNF1A protein, human); 0 (HNF1B protein, human); 0 (HNF4A protein, human); 0 (Hepatocyte Nuclear Factor 1-alpha); 0 (Hepatocyte Nuclear Factor 4); 0 (Homeodomain Proteins); 0 (NEUROD1 protein, human); 0 (Trans-Activators); 0 (pancreatic and duodenal homeobox 1 protein); 138674-15-4 (Hepatocyte Nuclear Factor 1-beta); 9100L32L2N (Metformin); EC 2.7.1.2 (Glucokinase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2016-3429


  4 / 10308 MEDLINE  
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[PMID]:27778642
[Au] Autor:Garibay-Nieto N; Queipo-García G; Alvarez F; Bustos M; Villanueva E; Ramírez F; León M; Laresgoiti-Servitje E; Duggirala R; Macías T; Cuevas S; Jalife A; Fonseca-Sánchez M; Serratos F; López-Alvarenga JC
[Ad] Endereço:Children and Adolescent Obesity Clinic.
[Ti] Título:Effects of Conjugated Linoleic Acid and Metformin on Insulin Sensitivity in Obese Children: Randomized Clinical Trial.
[So] Source:J Clin Endocrinol Metab;102(1):132-140, 2017 Jan 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Insulin resistance precedes metabolic syndrome abnormalities and may promote cardiovascular disease and type 2 diabetes in children with obesity. Results of lifestyle modification programs have been discouraging, and the use of adjuvant strategies has been necessary. Objective: This study aimed to evaluate the effects of metformin and conjugated linoleic acid (CLA) on insulin sensitivity, measured via euglycemic-hyperinsulinemic clamp technique and insulin pathway expression molecules in muscle biopsies of children with obesity. Design: A randomized, double-blinded, placebo-controlled clinical trial was conducted. Setting: Children with obesity were randomly assigned to receive metformin, CLA, or placebo. Results: Intervention had a positive effect in all groups. For insulin sensitivity Rd value (mg/kg/min), there was a statistically significant difference between the CLA vs placebo (6.53 ± 2.54 vs 5.05 ± 1.46, P = 0.035). Insulinemia and homeostatic model assessment of insulin resistance significantly improved in the CLA group (P = 0.045). After analysis of covariance was performed and the influence of body mass index, age, Tanner stage, prescribed diet, and fitness achievement was controlled, a clinically relevant effect size on insulin sensitivity remained evident in the CLA group (37%) and exceeded lifestyle program benefits. Moreover, upregulated expression of the insulin receptor substrate 2 was evident in muscle biopsies of the CLA group. Conclusions: Improvement of insulin sensitivity, measured via euglycemic-hyperinsulinemic clamp and IRS2 upregulation, favored patients treated with CLA.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/prevenção & controle
Hipoglicemiantes/uso terapêutico
Resistência à Insulina
Ácidos Linoleicos Conjugados/uso terapêutico
Síndrome Metabólica/prevenção & controle
Metformina/uso terapêutico
Obesidade/tratamento farmacológico
[Mh] Termos MeSH secundário: Adolescente
Biomarcadores/análise
Glicemia/análise
Composição Corporal
Criança
Método Duplo-Cego
Quimioterapia Combinada
Feminino
Seguimentos
Seres Humanos
Insulina/sangue
Lipídeos/análise
Masculino
Obesidade/complicações
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Biomarkers); 0 (Blood Glucose); 0 (Hypoglycemic Agents); 0 (Insulin); 0 (Linoleic Acids, Conjugated); 0 (Lipids); 9100L32L2N (Metformin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2016-2701


  5 / 10308 MEDLINE  
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[PMID]:29489653
[Au] Autor:Xin WX; Fang L; Fang QL; Zheng XW; Ding HY; Huang P
[Ad] Endereço:Laboratory of Clinical Pharmacy.
[Ti] Título:Effect of hypoglycemic agents on survival outcomes of lung cancer patients with diabetes mellitus: A meta-analysis.
[So] Source:Medicine (Baltimore);97(9):e0035, 2018 Mar.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: To assess the association between hypoglycemic agents and prognosis of lung cancer patients with diabetes. METHODS: A comprehensive literature search was performed in PubMed, Web of Science, Embase, and Cochrane Library until May 2017. The search yielded 2593 unique citations, of which 18 articles met inclusion criteria. The hazard ratios (HRs) and 95% confidence intervals (95% CIs) were calculated by a fixed-effects or random-effects model. RESULTS: The pooled HRs favoring metformin users were 0.77 for overall survival (OS) (n = 15, 95% CI: 0.68-0.86) and 0.50 for disease-free survival (n = 5, 95% CI: 0.39-0.64). One study assessed the relationship between metformin and cancer-specific survival (CSS), reporting no significant results. No significant association between insulin and OS (n = 2, HR: 0.95, 95% CI: 0.79-1.13) or CSS (n = 2, HR: 1.03, 95% CI: 0.76-1.41) was noted. One study evaluated association of sulfonylureas with lung cancer survival and reported no clinical benefit (HR: 1.10, 95% CI: 0.87-1.40). One study reported no association of thiazolidinediones with lung cancer survival (HR: 1.04, 95% CI: 0.65-1.66). CONCLUSIONS: This meta-analysis demonstrated that metformin exposure might improve survival outcomes in lung cancer patients with diabetes.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 1/tratamento farmacológico
Diabetes Mellitus Tipo 2/tratamento farmacológico
Hipoglicemiantes/uso terapêutico
Neoplasias Pulmonares/mortalidade
[Mh] Termos MeSH secundário: Seres Humanos
Insulina/uso terapêutico
Metformina/uso terapêutico
Prognóstico
Compostos de Sulfonilureia/uso terapêutico
Tiazolidinedionas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Hypoglycemic Agents); 0 (Insulin); 0 (Sulfonylurea Compounds); 0 (Thiazolidinediones); 9100L32L2N (Metformin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180301
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000010035


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[PMID]:28464864
[Au] Autor:Shimazu K; Tada Y; Morinaga T; Shingyoji M; Sekine I; Shimada H; Hiroshima K; Namiki T; Tatsumi K; Tagawa M
[Ad] Endereço:Department of Respirology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.
[Ti] Título:Metformin produces growth inhibitory effects in combination with nutlin-3a on malignant mesothelioma through a cross-talk between mTOR and p53 pathways.
[So] Source:BMC Cancer;17(1):309, 2017 May 02.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Mesothelioma is resistant to conventional treatments and is often defective in p53 pathways. We then examined anti-tumor effects of metformin, an agent for type 2 diabetes, and combinatory effects of metformin and nutlin-3a, an inhibitor for ubiquitin-mediated p53 degradation, on human mesothelioma. METHODS: We examined the effects with a colorimetric assay and cell cycle analyses, and investigated molecular events in cells treated with metformin and/or nutlin-3a with Western blot analyses. An involvement of p53 was tested with siRNA for p53. RESULTS: Metformin suppressed cell growth of 9 kinds of mesothelioma including immortalized cells of mesothelium origin irrespective of the p53 functional status, whereas susceptibility to nutlin-3a was partly dependent on the p53 genotype. We investigated combinatory effects of metformin and nutlin-3a on, nutlin-3a sensitive MSTO-211H and NCI-H28 cells and insensitive EHMES-10 cells, all of which had the wild-type p53 gene. Knockdown of p53 expression with the siRNA demonstrated that susceptibility of MSTO-211H and NCI-H28 cells to nutlin-3a was p53-dependent, whereas that of EHMES-10 cells was not. Nevertheless, all the cells treated with both agents produced additive or synergistic growth inhibitory effects. Cell cycle analyses also showed that the combination increased sub-G1 fractions greater than metformin or nutlin-3a alone in MSTO-211H and EHMES-10 cells. Western blot analyses showed that metformin inhibited downstream pathways of the mammalian target of rapamycin (mTOR) but did not activate the p53 pathways, whereas nutlin-3a phosphorylated p53 and suppressed mTOR pathways. Cleaved caspase-3 and conversion of LC3A/B were also detected but it was dependent on cells and treatments. The combination of both agents in MSTO-211H cells rather suppressed the p53 pathways that were activated by nutrin-3a treatments, whereas the combination rather augmented the p53 actions in NCI-H28 and EHMES-10 cells. CONCLUSION: These data collectively indicated a possible interactions between mTOR and p53 pathways, and the combinatory effects were attributable to differential mechanisms induced by a cross-talk between the pathways.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Imidazóis/farmacologia
Neoplasias Pulmonares/metabolismo
Mesotelioma/metabolismo
Metformina/farmacologia
Piperazinas/farmacologia
Serina-Treonina Quinases TOR/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Seres Humanos
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Imidazoles); 0 (Piperazines); 0 (Tumor Suppressor Protein p53); 53IA0V845C (nutlin 3); 9100L32L2N (Metformin); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12885-017-3300-y


  7 / 10308 MEDLINE  
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[PMID]:29465545
[Au] Autor:Kim HJ; Lee S; Chun KH; Jeon JY; Han SJ; Kim DJ; Kim YS; Woo JT; Nam MS; Baik SH; Ahn KJ; Lee KW
[Ad] Endereço:Department of Endocrinology and Metabolism, Ajou University School of Medicine, Suwon.
[Ti] Título:Metformin reduces the risk of cancer in patients with type 2 diabetes: An analysis based on the Korean National Diabetes Program Cohort.
[So] Source:Medicine (Baltimore);97(8):e0036, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The epidemiological literature suggests that insulin resistance, hyperinsulinemia, and increased levels of insulin-like growth factors place patients with type 2 diabetes mellitus (T2DM) at greater risk of cancer. The association between cancer incidence and the use of antidiabetic medications in patients with T2DM has been recently examined. There have been conflicting reports regarding an association between metformin and cancer risk. The aim of this study was to investigate the relationship between metformin use and the incidence of cancer in Koreans with T2DM.Data from The Korean National Diabetes Program (KNDP, 2006-2014), a nationwide, large-scale, prospective, multicenter cohort study in Korea, were used to study patients with T2DM. Patients ≥30 years old whose complete medical records were available were included in this study. Patients with a history of any cancer on KNDP registration or those who had been diagnosed with any type of cancer within 1 year of metformin use were excluded. Survival curves with respect to the incidence of cancer were plotted using the Kaplan-Meier method. Hazard ratios and 95% confidence intervals for cancer were estimated in a Cox proportional hazards regression analysis.During a mean 5.8 years of follow-up, 164 of the 1918 study patients (335 metformin nonusers and 1583 metformin users) developed cancer. The incidence per 1000 person-years was 21.8 in metformin nonusers and 13.2 in metformin users. Metformin users had a reduced risk of cancer, even after adjustment for demographic characteristics, metabolic parameters, diabetic complications, and other antidiabetic medications (hazard ratio 0.513, 95% confidence interval 0.318-0.826, P = .0060). Subgroup analysis of metformin users showed a reduced risk of cancer in males, patients < 65 years of age, patients with a T2DM duration < 5 years, nonobese patients, nonsmokers, and good glycemic control group.This large-scale, prospective, multicenter cohort study demonstrated an association between metformin use and reduced cancer risk in patients with T2DM.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/tratamento farmacológico
Hipoglicemiantes/uso terapêutico
Metformina/uso terapêutico
Neoplasias/etiologia
Comportamento de Redução do Risco
[Mh] Termos MeSH secundário: Diabetes Mellitus Tipo 2/complicações
Feminino
Seres Humanos
Incidência
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Neoplasias/epidemiologia
Modelos de Riscos Proporcionais
Estudos Prospectivos
República da Coreia/epidemiologia
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Hypoglycemic Agents); 9100L32L2N (Metformin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180222
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000010036


  8 / 10308 MEDLINE  
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[PMID]:29441996
[Au] Autor:Ayoub BM; Abdel-Aziz O
[Ti] Título:A guide for using experimental design in chromatographic method development: applied to the analysis of selected anti-diabetic pharmaceutical combinations.
[So] Source:Pharmazie;71(12):683-690, 2016 Dec 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:A guide experimental design in chromatographic method development was described and applied successfully to the analysis of different recently approved anti-diabetic pharmaceutical combinations. Enhancement of UHPLC analysis of alogliptin benzoate either with pioglitazone hydrochloride or with metformin hydrochloride was achieved. The optimal chromatographic conditions were not attained by trial and error that requires a large number of experiments. Alternatively, a computer program was used as a systematic optimization strategy for the design of the experiment which accurately predicts the combined effect of different factors simultaneously. Resolution between peaks was studied by the proposed fractional factorial design approach performed by the Minitab® Program using screening and optimization steps. Application of the central composite design was implemented. A Pareto chart was used to exclude the insignificant variables. Linearity ranges were found to be 0.5-40 µg ml-1, 1-20 µg ml-1 and 1-32 µg ml-1 for alogliptin benzoate, pioglitazone hydrochloride and metformin hydrochloride, respectively. The proposed method is applicable for the analysis of six pharmaceutical dosage forms namely, Nesina®, Actos®, Glucophage®, Oseni®, Kazano® and Actoplus MET® tablets.
[Mh] Termos MeSH primário: Cromatografia Líquida de Alta Pressão/métodos
Hipoglicemiantes/análise
[Mh] Termos MeSH secundário: Formas de Dosagem
Combinação de Medicamentos
Desenho de Equipamento
Metformina/análise
Piperidinas/análise
Padrões de Referência
Reprodutibilidade dos Testes
Soluções
Comprimidos/análise
Tiazolidinedionas/análise
Uracila/análogos & derivados
Uracila/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dosage Forms); 0 (Drug Combinations); 0 (Hypoglycemic Agents); 0 (Piperidines); 0 (Solutions); 0 (Tablets); 0 (Thiazolidinediones); 56HH86ZVCT (Uracil); 9100L32L2N (Metformin); JHC049LO86 (alogliptin); X4OV71U42S (pioglitazone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6095


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[PMID]:29355545
[Au] Autor:Ma YR; Zhou Y; Huang J; Qin HY; Wang P; Wu XA
[Ad] Endereço:Department of Pharmacy, The First Hospital of Lanzhou University, Lanzhou 730000, China.
[Ti] Título:The urinary excretion of metformin, ceftizoxime and ofloxacin in high serum creatinine rats: Can creatinine predict renal tubular elimination?
[So] Source:Life Sci;196:110-117, 2018 Mar 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The renal excretion of creatinine and most drugs are the net result of glomerular filtration and tubular secretion, and their tubular secretions are mediated by individual transporters. Thus, we hypothesized that the increase of serum creatinine (SCr) levels attributing to inhibiting tubular transporters but not glomerular filtration rate (GFR) could be used to evaluate the tubular excretion of drugs mediated by identical or partial overlap transporter with creatinine. In this work, we firstly developed the creatinine excretion inhibition model with normal GFR by competitively inhibiting tubular transporters, and investigated the renal excretion of metformin, ceftizoxime and ofloxacin in vivo and in vitro. The results showed that the 24-hour urinary excretion of metformin and ceftizoxime in model rats were decreased by 25% and 17% compared to that in control rats, respectively. The uptake amount and urinary excretion of metformin and ceftizoxime could be inhibited by creatinine in renal cortical slices and isolated kidney perfusion. However, the urinary excretion of ofloxacin was not affected by high SCr. These results showed that the inhibition of tubular creatinine transporters by high SCr resulted to the decrease of urinary excretion of metformin and ceftizoxime, but not ofloxacin, which implied that the increase of SCr could also be used to evaluate the tubular excretion of drugs mediated by identical or partial overlap transporter with creatinine in normal GFR rats.
[Mh] Termos MeSH primário: Ceftizoxima/urina
Creatinina/sangue
Túbulos Renais/metabolismo
Metformina/urina
Ofloxacino/urina
[Mh] Termos MeSH secundário: Animais
Proteínas de Transporte/metabolismo
Ceftizoxima/farmacocinética
Taxa de Filtração Glomerular
Técnicas In Vitro
Testes de Função Renal
Masculino
Metformina/farmacocinética
Ofloxacino/farmacocinética
Valor Preditivo dos Testes
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 9100L32L2N (Metformin); A4P49JAZ9H (Ofloxacin); AYI8EX34EU (Creatinine); C43C467DPE (Ceftizoxime)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180123
[St] Status:MEDLINE


  10 / 10308 MEDLINE  
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Fotocópia
[PMID]:29284782
[Au] Autor:Pyaskovskaya ON; Kolesnik DL; Fedorchuk AG; Gorbik GV; Solyanik GI
[Ad] Endereço:R.E. Kavetsky Institute of Experimental Pathology, Oncology and Radiobiology, NAS of Ukraine, Kyiv 03022, Ukraine.
[Ti] Título:Cytotoxic activity of metformin in vitro does not correlate with its antitumor action in vivo.
[So] Source:Exp Oncol;39(4):264-268, 2017 Dec.
[Is] ISSN:1812-9269
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:It is known that metformin is a hypoglycemic drug used to treat type II diabetes mellitus. Recently active studies of its antitumor activity in relation to different types of malignant cells are conducted. AIM: To determine the relationship between cytotoxic activity of metformin in vitro and its antitumor activity in vivo. MATERIALS AND METHODS: The rat C6 glioma cell line and mouse Lewis lung carcinoma cells (LLC) were used in this work. The number of living cells in the cytotoxic test was evaluated using sulforhodamine B. Parameters of tumor cell susceptibility to metformin activity in vitro were calculated using nonlinear and linear regression of experimental data. The antitumor action of metformin in vivo was evaluated routinely by the extension of survival time (ST) (in rats with intracerebral C6 glioma) and its effect on the volume of the primary tumor, the number and volume of metastases (in mice with LLC). RESULTS: In cultured LLC cells in vitro, the proportions of metformin-resistant (A , %) and metformin-sensitive (A , %) subpopulations were 10.0 ± 2.2% and 92.0 ± 3.5%, respectively, in terms of the total number of living cells. Parameter t, which characterizes the sensitivity of cancer cells to metformin action (the lower is the value of this parameter the higher is sensitivity of cells to metformin cytotoxicity), for metformin-resistant and metformin-sensitive subpopulations was: t (mM) = ∞ and t (mM) = 2.9 ± 0.3, correspondingly. For metformin-sensitive subpopulation of LLC cells IC50 (mM) = 2.42 ± 0.34. The volume of the primary tumor, the amount and volume of metastases in mice receiving metformin at a dose of D (0.15 g/kg) and D (0.3 g/kg) values did not significantly differ from those in the control. However, in the case of Dmin, there was a tendency to increased volume of the primary tumor, in the case of Dmax, there was a tendency to increased volume of metastases. The analogical parameters (A , A , b , b , IC50 (1), IC50 (2)) characterizing cell sensitivity to the action of metformin in vitro were obtained in relation to C6 glioma cells. In metformin-resistant subpopulation, these parameters were: A (%) = 72.3 ± 1.4; b (%/mM) = 0.43 ± 0.005; IC50 (1) (mM) = 84.1 ± 2.4. For metformin-sensitive subpopulation, these parameters were: A (%) = 30.8 ± 2.3; b (%/mM) = 2.87 ± 0.4; IC50 (2) (mM) = 5.37 ± 0.45. In vivo, a statistically significant anti-glioma effect of metformin was observed: at a dose of D (5.2 g/kg) administration of this preparation resulted in a prolongation of the mean ST of tumor-bearing rats by 23% (p < 0.05) compared with that in the control. CONCLUSIONS: We found no correlation between the cytotoxic/cytostatic action of metformin in vitro and its antitumor activity in vivo on the two types of tumor cells; these results indicate a significant contribution of the tumor microenvironment to the implementation of the antitumor activity of the drug.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Carcinoma Pulmonar de Lewis/tratamento farmacológico
Metformina/farmacologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Feminino
Camundongos
Camundongos Endogâmicos C57BL
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 9100L32L2N (Metformin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE



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