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  1 / 139 MEDLINE  
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[PMID]:27350110
[Au] Autor:Futatsugi A; Masuo Y; Kawabata S; Nakamichi N; Kato Y
[Ad] Endereço:Faculty of Pharmacy, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Japan.
[Ti] Título:L503F variant of carnitine/organic cation transporter 1 efficiently transports metformin and other biguanides.
[So] Source:J Pharm Pharmacol;68(9):1160-9, 2016 Sep.
[Is] ISSN:2042-7158
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Carnitine/organic cation transporter 1 (OCTN1) is involved in gastrointestinal absorption and mitochondrial toxicity of biguanides in rodents, but its pharmacokinetic roles in humans are largely unknown. The purpose of this study was to clarify the transport activities of two major OCTN1 variants, L503F and I306T, for gabapentin and three biguanide drugs, metformin, buformin and phenformin. METHODS: HEK293 cells were transfected with OCTN1 gene, its variants, or vector alone, and the uptake and cytotoxicity of each drug were examined. KEY FINDINGS: Buformin was identified to be an OCTN1 substrate. Uptake of biguanides, especially metformin, mediated by OCTN1 variant L503F, which is commonly found in Caucasians, was much higher than that by the wild-type transporter (WT-OCTN1). Cytotoxicity of metformin was also greater in HEK293 cells expressing the L503F variant, compared with WT-OCTN1. Uptake of gabapentin mediated by OCTN1 variant I306T, which is commonly found in both Asians and Caucasians, was lower than that by WT-OCTN1, although uptake of the typical OCTN1 substrate ergothioneine was similar. CONCLUSION: Organic cation transporter 1 variant L503F transports biguanides, especially metformin, more efficiently than WT-OCTN1, whereas the I306T variant transports gabapentin less efficiently than WT-OCTN1, suggesting that the common OCTN1 variants may alter pharmacokinetics of these drugs.
[Mh] Termos MeSH primário: Absorção Intestinal
Metformina/farmacocinética
Transportador 1 de Cátions Orgânicos/genética
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Aminas/metabolismo
Aminas/farmacocinética
Grupo com Ancestrais do Continente Asiático
Biguanidas/metabolismo
Biguanidas/farmacocinética
Transporte Biológico Ativo
Buformina/metabolismo
Buformina/farmacocinética
Carnitina/metabolismo
Ácidos Cicloexanocarboxílicos/metabolismo
Ácidos Cicloexanocarboxílicos/farmacocinética
Ergotioneína/metabolismo
Ergotioneína/farmacocinética
Grupo com Ancestrais do Continente Europeu
Células HEK293
Seres Humanos
Metformina/metabolismo
Transportador 1 de Cátions Orgânicos/metabolismo
Ácido gama-Aminobutírico/metabolismo
Ácido gama-Aminobutírico/farmacocinética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amines); 0 (Biguanides); 0 (Cyclohexanecarboxylic Acids); 0 (Organic Cation Transporter 1); 56-12-2 (gamma-Aminobutyric Acid); 6CW7F3G59X (gabapentin); 9100L32L2N (Metformin); BDZ3DQM98W (Ergothioneine); S7UI8SM58A (Carnitine); W2115E9C7B (Buformin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160629
[St] Status:MEDLINE
[do] DOI:10.1111/jphp.12574


  2 / 139 MEDLINE  
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[PMID]:27328723
[Au] Autor:Ohnishi S; Mizutani H; Kawanishi S
[Ad] Endereço:a Faculty of Pharmaceutical Sciences , Suzuka University of Medical Science , Suzuka , Mie , Japan ;
[Ti] Título:The enhancement of oxidative DNA damage by anti-diabetic metformin, buformin, and phenformin, via nitrogen-centered radicals.
[So] Source:Free Radic Res;50(8):929-37, 2016 Aug.
[Is] ISSN:1029-2470
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Metformin (N,N-dimethylbiguanide), buformin (1-butylbiguanide), and phenformin (1-phenethylbiguanide) are anti-diabetic biguanide drugs, expected to having anti-cancer effect. The mechanism of anti-cancer effect by these drugs is not completely understood. In this study, we demonstrated that these drugs dramatically enhanced oxidative DNA damage under oxidative condition. Metformin, buformin, and phenformin enhanced generation of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) in isolated DNA reacted with hydrogen peroxide (H2O2) and Cu(II), although these drugs did not form 8-oxodG in the absence of H2O2 or Cu(II). An electron paramagnetic resonance (EPR) study, utilizing alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone and 3,3,5,5-tetramethyl-1-pyrroline-N-oxide as spin trapping agents, showed that nitrogen-centered radicals were generated from biguanides in the presence of Cu(II) and H2O2, and that these radicals were decreased by the addition of DNA. These results suggest that biguanides enhance Cu(II)/H2O2-mediated 8-oxodG generation via nitrogen-centered radical formation. The enhancing effect on oxidative DNA damage may play a role on anti-cancer activity.
[Mh] Termos MeSH primário: Buformina/farmacologia
Dano ao DNA/efeitos dos fármacos
Hipoglicemiantes/farmacologia
Metformina/farmacologia
Fenformin/farmacologia
[Mh] Termos MeSH secundário: Animais
Buformina/administração & dosagem
Bovinos
Dano ao DNA/genética
Seres Humanos
Hipoglicemiantes/administração & dosagem
Metformina/administração & dosagem
Oxirredução
Fenformin/administração & dosagem
Espécies Reativas de Oxigênio
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypoglycemic Agents); 0 (Reactive Oxygen Species); 9100L32L2N (Metformin); DD5K7529CE (Phenformin); W2115E9C7B (Buformin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170224
[Lr] Data última revisão:
170224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160623
[St] Status:MEDLINE
[do] DOI:10.1080/10715762.2016.1204651


  3 / 139 MEDLINE  
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[PMID]:25804611
[Au] Autor:Zhu Z; Jiang W; Thompson MD; Echeverria D; McGinley JN; Thompson HJ
[Ad] Endereço:Cancer Prevention Laboratory, Colorado State University, Fort Collins, Colorado.
[Ti] Título:Effects of metformin, buformin, and phenformin on the post-initiation stage of chemically induced mammary carcinogenesis in the rat.
[So] Source:Cancer Prev Res (Phila);8(6):518-27, 2015 Jun.
[Is] ISSN:1940-6215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Metformin is a widely prescribed drug for the treatment of type II diabetes. Although epidemiologic data have provided a strong rationale for investigating the potential of this biguanide for use in cancer prevention and control, uncertainty exists whether metformin should be expected to have an impact in nondiabetic patients. Furthermore, little attention has been given to the possibility that other biguanides may have anticancer activity. In this study, the effects of clinically relevant doses of metformin (9.3 mmol/kg diet), buformin (7.6 mmol/kg diet), and phenformin (5.0 mmol/kg diet) were compared with rats fed control diet (AIN93-G) during the post-initiation stage of 1-methyl-1-nitrosourea-induced (50 mg/kg body weight) mammary carcinogenesis (n = 30/group). Plasma, liver, skeletal muscle, visceral fat, mammary gland, and mammary carcinoma concentrations of the biguanides were determined. In comparison with the control group, buformin decreased cancer incidence, multiplicity, and burden, whereas metformin and phenformin had no statistically significant effect on the carcinogenic process relative to the control group. Buformin did not alter fasting plasma glucose or insulin. Within mammary carcinomas, evidence was obtained that buformin treatment perturbed signaling pathways related to energy sensing. However, further investigation is needed to determine the relative contributions of host systemic and cell autonomous mechanisms to the anticancer activity of biguanides such as buformin.
[Mh] Termos MeSH primário: Buformina/farmacologia
Transformação Celular Neoplásica/efeitos dos fármacos
Hipoglicemiantes/farmacologia
Neoplasias Mamárias Experimentais/tratamento farmacológico
Metformina/farmacologia
Fenformin/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Western Blotting
Carcinógenos/toxicidade
Proliferação Celular/efeitos dos fármacos
Transformação Celular Neoplásica/patologia
Feminino
Neoplasias Mamárias Experimentais/induzido quimicamente
Neoplasias Mamárias Experimentais/patologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Carcinogens); 0 (Hypoglycemic Agents); 9100L32L2N (Metformin); DD5K7529CE (Phenformin); W2115E9C7B (Buformin)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150326
[St] Status:MEDLINE
[do] DOI:10.1158/1940-6207.CAPR-14-0121


  4 / 139 MEDLINE  
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[PMID]:24796485
[Au] Autor:Isono T; Chano T; Kitamura A; Yuasa T
[Ad] Endereço:Central Reseach Laboratory, Shiga University of Medical Science, Otsu, Shiga, Japan.
[Ti] Título:Glucose deprivation induces G2/M transition-arrest and cell death in N-GlcNAc2-modified protein-producing renal carcinoma cells.
[So] Source:PLoS One;9(5):e96168, 2014.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Some cancer cells can survive under glucose deprivation within the microenvironment of a tumor. Recently, we reported that N-linked (ß-N-acetylglucosamine)2 [N-GlcNAc2]-modified proteins induce G2/M arrest and cell death under glucose deprivation. Here, we investigated whether such a response to glucose deprivation contributes to the survival of renal cell carcinomas, which are sensitive to nutritional stress. Specifically, we analyzed seven renal carcinoma cell lines. Four of these cell lines produced N-GlcNAc2-modified proteins and led G2/M-phase arrest under glucose deprivation, leading to cell death. The remaining three cell lines did not produce N-GlcNAc2-modified proteins and undergo G1/S-phase arrest under glucose deprivation, leading to survival. The four dead cell lines displayed significant up-regulation in the UDP-GlcNAc biosynthesis pathway as well as increased phosphorylation of p53, which was not observed in the surviving three cell lines. In addition, the four dead cell lines showed prolonged up-regulated expression of ATF3, which is related to unfolded protein response (UPR), while the surviving three cell lines showed only transient up-regulation of ATF3. In this study, we demonstrated that the renal carcinoma cells which accumulate N-GlcNAc2-modified proteins under glucose deprivation do not survive with abnormaly prolonged UPR pathway. By contrast, renal carcinoma cells that do not accumulate N-GlcNAc2-modified proteins under these conditions survive. Morover, we demonstrated that buformin, a UPR inhibitor, efficiently reduced cell survival under conditions of glucose deprivation for both sensitive and resistant phenotypes. Further studies to clarify these findings will lead to the development of novel chemotherapeutic treatments for renal cancer.
[Mh] Termos MeSH primário: Acetilglucosamina/metabolismo
Pontos de Checagem da Fase G2 do Ciclo Celular
Glucose
Glicoproteínas/metabolismo
Pontos de Checagem da Fase M do Ciclo Celular
Microambiente Tumoral
[Mh] Termos MeSH secundário: Fator 3 Ativador da Transcrição/biossíntese
Buformina/farmacologia
Morte Celular
Linhagem Celular Tumoral
Regulação da Expressão Gênica/efeitos dos fármacos
Glicosilação
Seres Humanos
Hipoglicemiantes/farmacologia
Neoplasias Renais
Proteína Supressora de Tumor p53/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ATF3 protein, human); 0 (Activating Transcription Factor 3); 0 (Glycoproteins); 0 (Hypoglycemic Agents); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); IY9XDZ35W2 (Glucose); V956696549 (Acetylglucosamine); W2115E9C7B (Buformin)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140507
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0096168


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[PMID]:18817800
[Au] Autor:Dykens JA; Jamieson J; Marroquin L; Nadanaciva S; Billis PA; Will Y
[Ad] Endereço:Drug Safety Research and Development, Pfizer, Inc., Ramsgate Rd. Sandwich, CT13 9NJ, UK. jamesdykens@pfizer.com
[Ti] Título:Biguanide-induced mitochondrial dysfunction yields increased lactate production and cytotoxicity of aerobically-poised HepG2 cells and human hepatocytes in vitro.
[So] Source:Toxicol Appl Pharmacol;233(2):203-10, 2008 Dec 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:As a class, the biguanides induce lactic acidosis, a hallmark of mitochondrial impairment. To assess potential mitochondrial impairment, we evaluated the effects of metformin, buformin and phenformin on: 1) viability of HepG2 cells grown in galactose, 2) respiration by isolated mitochondria, 3) metabolic poise of HepG2 and primary human hepatocytes, 4) activities of immunocaptured respiratory complexes, and 5) mitochondrial membrane potential and redox status in primary human hepatocytes. Phenformin was the most cytotoxic of the three with buformin showing moderate toxicity, and metformin toxicity only at mM concentrations. Importantly, HepG2 cells grown in galactose are markedly more susceptible to biguanide toxicity compared to cells grown in glucose, indicating mitochondrial toxicity as a primary mode of action. The same rank order of potency was observed for isolated mitochondrial respiration where preincubation (40 min) exacerbated respiratory impairment, and was required to reveal inhibition by metformin, suggesting intramitochondrial bio-accumulation. Metabolic profiling of intact cells corroborated respiratory inhibition, but also revealed compensatory increases in lactate production from accelerated glycolysis. High (mM) concentrations of the drugs were needed to inhibit immunocaptured respiratory complexes, supporting the contention that bioaccumulation is involved. The same rank order was found when monitoring mitochondrial membrane potential, ROS production, and glutathione levels in primary human hepatocytes. In toto, these data indicate that biguanide-induced lactic acidosis can be attributed to acceleration of glycolysis in response to mitochondrial impairment. Indeed, the desired clinical outcome, viz., decreased blood glucose, could be due to increased glucose uptake and glycolytic flux in response to drug-induced mitochondrial dysfunction.
[Mh] Termos MeSH primário: Buformina/toxicidade
Hipoglicemiantes/toxicidade
Metformina/toxicidade
Mitocôndrias Hepáticas/efeitos dos fármacos
Fenformin/toxicidade
[Mh] Termos MeSH secundário: Acidose Láctica/induzido quimicamente
Animais
Glicemia/efeitos dos fármacos
Buformina/administração & dosagem
Linhagem Celular
Respiração Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Meios de Cultura
Glutationa/efeitos dos fármacos
Glutationa/metabolismo
Glicólise/efeitos dos fármacos
Hepatócitos/efeitos dos fármacos
Hepatócitos/metabolismo
Seres Humanos
Hipoglicemiantes/administração & dosagem
Ácido Láctico/metabolismo
Masculino
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Metformina/administração & dosagem
Oxirredução/efeitos dos fármacos
Fenformin/administração & dosagem
Ratos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Culture Media); 0 (Hypoglycemic Agents); 0 (Reactive Oxygen Species); 33X04XA5AT (Lactic Acid); 9100L32L2N (Metformin); DD5K7529CE (Phenformin); GAN16C9B8O (Glutathione); W2115E9C7B (Buformin)
[Em] Mês de entrada:0812
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080927
[St] Status:MEDLINE
[do] DOI:10.1016/j.taap.2008.08.013


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[PMID]:16799926
[Au] Autor:Tahara K; Yonemoto A; Yoshiyama Y; Nakamura T; Aizawa M; Fujita Y; Nishikawa T
[Ad] Endereço:Kyoritsu University of Pharmacy, 1-5-30, Shibakoen, Minato-ku, Tokyo 105-8512, Japan.
[Ti] Título:Determination of antihyperglycemic biguanides in serum and urine using an ion-pair solid-phase extraction technique followed by HPLC-UV on a pentafluorophenylpropyl column and on an octadecyl column.
[So] Source:Biomed Chromatogr;20(11):1200-5, 2006 Nov.
[Is] ISSN:0269-3879
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:An HPLC-UV method was established for the determination of metformin and buformin in biological fluids. Metformin was not retained on particles packed in conventional solid-phase extraction cartridges; in contrast, buformin was retained too firmly and not eluted with a solvent for recovery. However, both drugs were retained on particles that had been treated with an ion-pair reagent of heptanesulfonate or dodecylsulfate and recovered almost completely. The recovered fraction was subjected to HPLC on a pentafluorophenylpropyl column which was suitable for the determination of both biguanides in serum and in urine. Limits of quantitation were low enough for clinical use, and reproducibility was high with an RSD of 0.9-2.3%. HPLC on a conventional octadecyl column was suitable only for the determination of buformin in serum since interfering peaks appeared on the chromatograms of urine samples. The method was applied to analysis of some clinical specimens.
[Mh] Termos MeSH primário: Buformina/sangue
Buformina/urina
Cromatografia Líquida de Alta Pressão/métodos
Hipoglicemiantes/sangue
Hipoglicemiantes/urina
Metformina/sangue
Metformina/urina
Extração em Fase Sólida/métodos
[Mh] Termos MeSH secundário: Alcanos
Métodos Analíticos de Preparação de Amostras
Seres Humanos
Raios Ultravioleta
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Alkanes); 0 (Hypoglycemic Agents); 9100L32L2N (Metformin); N102P6HAIU (octadecane); W2115E9C7B (Buformin)
[Em] Mês de entrada:0701
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:060627
[St] Status:MEDLINE


  7 / 139 MEDLINE  
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[PMID]:16651735
[Au] Autor:Yano A; Kubota M; Iguchi K; Usui S; Hirano K
[Ad] Endereço:Department of Pharmaceutics, Gifu Pharmaceutical University, Japan.
[Ti] Título:Buformin suppresses the expression of glyceraldehyde 3-phosphate dehydrogenase.
[So] Source:Biol Pharm Bull;29(5):1006-9, 2006 May.
[Is] ISSN:0918-6158
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The biguanides metformin and buformin, which are clinically used for diabetes mellitus, are known to improve resistance to insulin in patients. Biguanides were reported to cause lactic acidosis as a side effect. Since the mechanism of the side effect still remains obscure, we have examined genes whose expression changes by treating HepG2 cells with buformin in order to elucidate the mechanisms of the side effect. A subtraction cDNA library was constructed by the method of suppressive subtractive hybridization and the screening of the library was performed with cDNA probes prepared from HepG2 cells treated with or without buformin for 12 h. The expression of the gene and the protein obtained by the screening was monitored by real-time RT-PCR with specific primers and Western blotting with specific antibody. The amounts of ATP and NAD+ were determined with luciferase and alcohol dehydrogenase, respectively. We found that expression of the glyceraldehyde 3-phosphate dehydrogenase (GAPD) gene was suppressed by treating HepG2 cells with 0.25 mM buformin for 12 h as a result of the library screening. The decrease in the expression depended on the treatment period. The amount of GAPD protein also decreased simultaneously with the suppression of the gene expression by the treatment with buformin. The amount of ATP and NAD+ in the HepG2 cells treated with buformin decreased to 10 and 20% of the control, respectively. These observations imply that the biguanide causes deactivation of the glycolytic pathway and subsequently the accumulation of pyruvate and NADH and a decrease in NAD+. Therefore, the reaction equilibrium catalyzed by lactate dehydrogenase leans towards lactate production and this may result in lactic acidosis.
[Mh] Termos MeSH primário: Buformina/farmacologia
Gliceraldeído-3-Fosfato Desidrogenases/antagonistas & inibidores
Gliceraldeído-3-Fosfato Desidrogenases/biossíntese
Hipoglicemiantes/farmacologia
[Mh] Termos MeSH secundário: Acidose Láctica/induzido quimicamente
Acidose Láctica/metabolismo
Trifosfato de Adenosina/biossíntese
Western Blotting
Linhagem Celular
DNA Complementar/biossíntese
Seres Humanos
NAD/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (Hypoglycemic Agents); 0U46U6E8UK (NAD); 8L70Q75FXE (Adenosine Triphosphate); EC 1.2.1.- (Glyceraldehyde-3-Phosphate Dehydrogenases); W2115E9C7B (Buformin)
[Em] Mês de entrada:0607
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:060503
[St] Status:MEDLINE


  8 / 139 MEDLINE  
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[PMID]:15946656
[Au] Autor:Kiho T; Kato M; Usui S; Hirano K
[Ad] Endereço:Gifu Prefectural Institute of Health and Environmental Sciences, 1-1 Naka-fudogaoka, Kakamigahara 504-0838, Japan. kiho-tadashi@pref.gifu.lg.jp
[Ti] Título:Effect of buformin and metformin on formation of advanced glycation end products by methylglyoxal.
[So] Source:Clin Chim Acta;358(1-2):139-45, 2005 Aug.
[Is] ISSN:0009-8981
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The formation and accumulation of advanced glycation end products (AGE) in various tissues are known to be involved in the aging process and complications of long-term diabetes. Aminoguanidine as AGE inhibitors was first studied, and metformin as biguanide compounds have been reported to react with reactive dicarbonyl precursors such as methylglyoxal. METHODS: We studied the effects of the biguanides of buformin and metformin on AGE formation by the methods of specific fluorescence, and enzyme-linked immunosorbent assay and a Western blot analysis using the anti-AGE antibody after incubating BSA or RNase with methylglyoxal. RESULTS: Buformin is a more potent inhibitor of AGE formation than metformin, and suggests that the amino group of buformin trap the carbonyl group of methylglyoxal to suppress formation of AGE. CONCLUSION: In addition to that of metformin, buformin may be clinically useful to prevent diabetic complications.
[Mh] Termos MeSH primário: Buformina/química
Produtos Finais de Glicação Avançada/síntese química
Metformina/química
Aldeído Pirúvico/química
[Mh] Termos MeSH secundário: Animais
Bovinos
Ensaio de Imunoadsorção Enzimática
Produtos Finais de Glicação Avançada/análise
Guanidinas/química
Ribonucleases/química
Ribonucleases/farmacologia
Soroalbumina Bovina/química
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycation End Products, Advanced); 0 (Guanidines); 27432CM55Q (Serum Albumin, Bovine); 722KLD7415 (Pyruvaldehyde); 9100L32L2N (Metformin); EC 3.1.- (Ribonucleases); SCQ4EZQ113 (pimagedine); W2115E9C7B (Buformin)
[Em] Mês de entrada:0512
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:050611
[St] Status:MEDLINE


  9 / 139 MEDLINE  
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[PMID]:15898889
[Au] Autor:Martínez Laso A
[Ti] Título:[A new case of lactic acidosis caused by buformin].
[Ti] Título:Un nuevo caso de acidosis láctica por buformina..
[So] Source:An Med Interna;22(2):91, 2005 Feb.
[Is] ISSN:0212-7199
[Cp] País de publicação:Spain
[La] Idioma:spa
[Mh] Termos MeSH primário: Acidose Láctica/induzido quimicamente
Buformina/efeitos adversos
Hipoglicemiantes/efeitos adversos
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Feminino
Seres Humanos
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Nm] Nome de substância:
0 (Hypoglycemic Agents); W2115E9C7B (Buformin)
[Em] Mês de entrada:0511
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:050519
[St] Status:MEDLINE


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Fotocópia
[PMID]:15852659
[Au] Autor:Matsuura T; Miyao M; Mizuno Y
[Ad] Endereço:Division of Endocrinology and Metabolism, Kanto Central Hospital.
[Ti] Título:[A case of lactic acidosis caused by buformin in an oldest elderly diabetic patient].
[So] Source:Nihon Ronen Igakkai Zasshi;42(2):235-40, 2005 Mar.
[Is] ISSN:0300-9173
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:A 93-year-old male was urgently admitted to our hospital with dyspnea and disturbance of consciousness. The patient had been visiting a general physician regularly for ten years, for treatment of type 2 diabetes. He had been treated with glibenclamide and voglibose, until voglibose was replaced with buformin 3 months before admission. During pre-admission treatment, his HbA1c was 10-12% and serum Cr level was around 2mg/dL, but insulin therapy had never been considered because of "being too old". The patient had started taking furosemide one year before admission, because of edema of the lower legs, and also spironolactone two months before admission. Anorexia had continued for one month before admission on May 29, 2003. On admission, his laboratory data were; blood glucose 87mg/dL, HbA1c 12.5%, BUN 75mg/dL, Cr 3.9mg/dL, lactate 253.1 mg/dL, and blood gas analysis; pH 6.97, anion gap 45.3mmol/L breathing room air, suggesting marked lactic acidosis with renal failure. Intensive care with bicarbonate and fluid therapy was successful, and his glycemic control improved markedly with insulin. On the other hand, his activity of daily living (ADL) severely deteriorated while in hospital Home follow-up was therefore not indicated, and he had to change a hospital for further follow-up. This case report gives rise to the question of how we should manage diabetes in the oldest elderly, including the use of insulin and biguanides. In addition, complications of biguanides in the elderly are reviewed.
[Mh] Termos MeSH primário: Acidose Láctica/induzido quimicamente
Buformina/efeitos adversos
Diabetes Mellitus Tipo 2/tratamento farmacológico
Hipoglicemiantes/efeitos adversos
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Diabetes Mellitus Tipo 2/complicações
Seres Humanos
Masculino
Insuficiência Renal/etiologia
[Pt] Tipo de publicação:CASE REPORTS; ENGLISH ABSTRACT; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Hypoglycemic Agents); W2115E9C7B (Buformin)
[Em] Mês de entrada:0506
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:050428
[St] Status:MEDLINE



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