Base de dados : MEDLINE
Pesquisa : D27.505.519.186.071.601 [Categoria DeCS]
Referências encontradas : 387 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 39 ir para página                         

  1 / 387 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28137899
[Au] Autor:Woods E; Dawson C; Senthil L; Geberhiwot T
[Ad] Endereço:QE Hospital Birmingham, Birmingham, UK.
[Ti] Título:Cerebral venous thrombosis as the first presentation of classical homocystinuria in an adult patient.
[So] Source:BMJ Case Rep;2017, 2017 Jan 30.
[Is] ISSN:1757-790X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A 30-year-old woman presented with severe headache, dysarthria and right hemiparesis. She was treated for suspected viral encephalopathy and recovered over the following weeks although the headaches persisted. Two months later she was treated in-hospital for pulmonary embolism. The following year she was readmitted for increased frequency of headaches and was given a diagnosis of migraine. A subsequent MRI head scan was suggestive of longstanding venous sinus infarcts and neuroradiology review concluded that encephalitis had been the incorrect initial diagnosis. Subsequent investigations for an underlying cause of the two episodes of venous thrombosis revealed a total homocysteine level of >350 µmol/L (<15 µmol/L). An underlying diagnosis of homocystinuria secondary to cystathionine ß-synthase deficiency was made although this metabolic condition is normally recognised in childhood. Treatment with pyridoxine and betaine normalised her homocysteine levels and she has had no further thrombotic event since.
[Mh] Termos MeSH primário: Erros de Diagnóstico
Encefalite Viral/diagnóstico
Homocistinúria/diagnóstico
Transtornos de Enxaqueca/diagnóstico
Trombose dos Seios Intracranianos/diagnóstico por imagem
[Mh] Termos MeSH secundário: Adulto
Betaína/uso terapêutico
Angiografia Cerebral
Angiografia por Tomografia Computadorizada
Disartria/etiologia
Feminino
Cefaleia/etiologia
Homocistinúria/complicações
Homocistinúria/tratamento farmacológico
Seres Humanos
Lipotrópicos/uso terapêutico
Angiografia por Ressonância Magnética
Imagem por Ressonância Magnética
Paresia/etiologia
Flebografia
Embolia Pulmonar/etiologia
Piridoxina/uso terapêutico
Trombose dos Seios Intracranianos/etiologia
Complexo Vitamínico B/uso terapêutico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipotropic Agents); 12001-76-2 (Vitamin B Complex); 3SCV180C9W (Betaine); KV2JZ1BI6Z (Pyridoxine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170306
[Lr] Data última revisão:
170306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170201
[St] Status:MEDLINE


  2 / 387 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27980239
[Au] Autor:Takase T; Nakamura A; Miyoshi H; Yamamoto C; Atsumi T
[Ad] Endereço:Division of Rheumatology, Endocrinology and Nephrology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
[Ti] Título:Amelioration of fatty liver index in patients with type 2 diabetes on ipragliflozin: an association with glucose-lowering effects.
[So] Source:Endocr J;64(3):363-367, 2017 Mar 31.
[Is] ISSN:1348-4540
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:In this study, we investigated the ameliorating effects of ipragliflozin on fatty liver in patients with type 2 diabetes. The factors that influenced the amelioration of fatty liver were also examined. Analysis included data of 21 Japanese patients with type 2 diabetes obtained from our prospective observational study. After obtaining patients' informed consent, once-daily ipragliflozin (50 mg/day) was given for 16 weeks. In addition to several clinical parameters, body composition was also compared before and after 16 weeks of treatment. The extent of fatty liver was estimated using a fatty liver index (FLI). After 16 weeks, FLI significantly decreased, from 70.1 ± 19.4 to 60.3 ± 25.5 (p = 0.0009) as well as levels of fasting plasma glucose (FPG), HbA1c, body weight, visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT) and fat mass. To reveal the factors influencing the FLI changes observed on ipragliflozin treatment, correlations between changes in FLI and several other measured parameters were examined. Changes in FPG (correlation coefficient = 0.4683, p = 0.0323) and HbA1c (correlation coefficient = 0.4383, p = 0.0469) showed significant positive correlations with changes in FLI. On the other hand, no correlations of changes in FLI were observed with body weight, VAT, SAT nor fat mass. In conclusion, ipragliflozin ameliorated FLI in Japanese patients with type 2 diabetes. Improvement in FLI was associated with that of glucose intolerance.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/tratamento farmacológico
Glucosídeos/uso terapêutico
Hipoglicemiantes/uso terapêutico
Lipotrópicos/uso terapêutico
Fígado/efeitos dos fármacos
Hepatopatia Gordurosa não Alcoólica/prevenção & controle
Transportador 2 de Glucose-Sódio/antagonistas & inibidores
Tiofenos/uso terapêutico
[Mh] Termos MeSH secundário: Adiposidade/efeitos dos fármacos
Adulto
Diabetes Mellitus Tipo 2/sangue
Diabetes Mellitus Tipo 2/complicações
Diabetes Mellitus Tipo 2/metabolismo
Feminino
Hemoglobina A Glicada/análise
Seres Humanos
Hiperglicemia/prevenção & controle
Japão
Fígado/metabolismo
Masculino
Meia-Idade
Hepatopatia Gordurosa não Alcoólica/complicações
Hepatopatia Gordurosa não Alcoólica/fisiopatologia
Estudos Prospectivos
Índice de Gravidade de Doença
Transportador 2 de Glucose-Sódio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Glucosides); 0 (Glycated Hemoglobin A); 0 (Hypoglycemic Agents); 0 (Lipotropic Agents); 0 (SLC5A2 protein, human); 0 (Sodium-Glucose Transporter 2); 0 (Thiophenes); 0 (hemoglobin A1c protein, human); 3N2N8OOR7X (ipragliflozin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161217
[St] Status:MEDLINE
[do] DOI:10.1507/endocrj.EJ16-0295


  3 / 387 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27424611
[Au] Autor:Al Humayed S
[Ad] Endereço:a Department of Medicine , College of Medicine, King Khalid University , Abha , Saudi Arabia.
[Ti] Título:Protective and therapeutic effects of Crataegus aronia in non-alcoholic fatty liver disease.
[So] Source:Arch Physiol Biochem;123(1):23-30, 2017 Feb.
[Is] ISSN:1744-4160
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIM: We evaluated the potential preventive and therapeutic effects of Crataegus aronia (C. aronia) in NAFLD induced by high-fat diet (HFD) in rat models. METHODS: Protective effect of Crataegus aronia or simvastatin was investigated in Wistar rats fed either low-fat diet (LFD) or HFD. RESULTS: Liver histopathological examinations confirmed the development of NAFLD in rats fed HFD. In both protective and therapeutic treatments, C. aronia significantly reduced liver index (3.85 ± 0.21% in HFD plus aronia group versus 6.22 ± 0.58% in HFD model group), increased the HDL-cholesterol and reduced the LDL-cholesterol in blood. The hawthorn plant also significantly ameliorated oxidative stress biomarker (p < 0.002) and liver enzymes (p < 0.0001) that indicate liver damage. CONCLUSION: C. aronia exhibits therapeutic and protective effects on NAFLD in an animal model possibly by its lipid lowering and antioxidant effects; thus, may offer therapeutic potential in humans.
[Mh] Termos MeSH primário: Anticolesterolemiantes/uso terapêutico
Antioxidantes/uso terapêutico
Lipotrópicos/uso terapêutico
Fígado/efeitos dos fármacos
Hepatopatia Gordurosa não Alcoólica/prevenção & controle
Estresse Oxidativo/efeitos dos fármacos
Extratos Vegetais/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Anticolesterolemiantes/efeitos adversos
Anticolesterolemiantes/isolamento & purificação
Antioxidantes/efeitos adversos
Antioxidantes/isolamento & purificação
Biomarcadores/sangue
Biomarcadores/metabolismo
HDL-Colesterol/agonistas
HDL-Colesterol/sangue
LDL-Colesterol/antagonistas & inibidores
LDL-Colesterol/sangue
Crataegus/efeitos adversos
Crataegus/química
Crataegus/crescimento & desenvolvimento
Dieta com Restrição de Gorduras
Dieta Hiperlipídica/efeitos adversos
Jordânia
Lipotrópicos/efeitos adversos
Lipotrópicos/isolamento & purificação
Fígado/metabolismo
Fígado/patologia
Fígado/fisiopatologia
Masculino
Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico
Hepatopatia Gordurosa não Alcoólica/patologia
Hepatopatia Gordurosa não Alcoólica/fisiopatologia
Componentes Aéreos da Planta/química
Componentes Aéreos da Planta/crescimento & desenvolvimento
Extratos Vegetais/efeitos adversos
Extratos Vegetais/isolamento & purificação
Distribuição Aleatória
Ratos Wistar
Sinvastatina/efeitos adversos
Sinvastatina/uso terapêutico
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticholesteremic Agents); 0 (Antioxidants); 0 (Biomarkers); 0 (Cholesterol, HDL); 0 (Cholesterol, LDL); 0 (Lipotropic Agents); 0 (Plant Extracts); 6OM09RPY36 (crataegus extract); AGG2FN16EV (Simvastatin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170206
[Lr] Data última revisão:
170206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160719
[St] Status:MEDLINE
[do] DOI:10.1080/13813455.2016.1205097


  4 / 387 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27046515
[Au] Autor:Couser NL; McClure J; Evans MW; Haines NR; Burden SK; Muenzer J
[Ad] Endereço:a Department of Ophthalmology , University of North Carolina School of Medicine , Chapel Hill , NC , USA.
[Ti] Título:Homocysteinemia due to MTHFR deficiency in a young adult presenting with bilateral lens subluxations.
[So] Source:Ophthalmic Genet;38(1):91-94, 2017 Jan-Feb.
[Is] ISSN:1744-5094
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The most common cause of isolated inherited homocysteinemia is a deficiency of the enzyme cystathionine ß-synthase (CBS). Clinical manifestations of CBS deficiency can include ectopia lentis, thromboembolism, marfanoid habits, and intellectual disability. CBS deficiency, which affects the transsulfuration pathway, is marked biochemically by elevated serum homocysteine and plasma methionine. We report a patient with homocysteinemia, low plasma methionine, and no significant neurological abnormalities who presented with bilateral subluxated crystalline lenses due to a 5,10-methylenetetrahydrofolate reductase (MTHFR) deficiency. MTHFR deficiency, a disorder in the remethylation pathway, can cause mild to severe disease, although most presentations include neurological involvement. MTHFR deficiency has not been previously associated with lens subluxation or complete dislocation. Prolonged exposure to elevated serum homocysteine levels is most likely the explanation for her ectopia lentis. This case expands the differential diagnosis of homocysteinemia and highlights the need for a correct diagnosis to optimize the clinical outcome of patients with this condition.
[Mh] Termos MeSH primário: Homocistinúria/complicações
Hiper-Homocisteinemia/etiologia
Subluxação do Cristalino/etiologia
Metilenotetra-Hidrofolato Redutase (NADPH2)/deficiência
Espasticidade Muscular/complicações
Tetra-Hidrofolatos/deficiência
[Mh] Termos MeSH secundário: Adulto
Betaína/uso terapêutico
Quimioterapia Combinada
Feminino
Homocisteína/sangue
Homocistinúria/diagnóstico
Homocistinúria/tratamento farmacológico
Seres Humanos
Hiper-Homocisteinemia/diagnóstico
Hiper-Homocisteinemia/tratamento farmacológico
Subluxação do Cristalino/diagnóstico
Leucovorina/uso terapêutico
Lipotrópicos/uso terapêutico
Metionina/sangue
Espasticidade Muscular/diagnóstico
Espasticidade Muscular/tratamento farmacológico
Polimorfismo de Nucleotídeo Único
Transtornos Psicóticos/complicações
Transtornos Psicóticos/diagnóstico
Transtornos Psicóticos/tratamento farmacológico
Tetra-Hidrofolatos/genética
Complexo Vitamínico B/uso terapêutico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipotropic Agents); 0 (Tetrahydrofolates); 0LVT1QZ0BA (Homocysteine); 0SXY5ET48B (5,10-methylenetetrahydrofolic acid); 12001-76-2 (Vitamin B Complex); 3SCV180C9W (Betaine); AE28F7PNPL (Methionine); EC 1.5.1.20 (Methylenetetrahydrofolate Reductase (NADPH2)); Q573I9DVLP (Leucovorin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160406
[St] Status:MEDLINE
[do] DOI:10.3109/13816810.2016.1143017


  5 / 387 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:27646125
[Au] Autor:Yilmaz Z; Eralp Inan O; Kocaturk M; Baykal AT; Hacariz O; Hatipoglu I; Tvarijonaviciute A; Cansev M; Ceron J; Ulus IH
[Ad] Endereço:Department of Internal Medicine, Faculty of Veterinary Medicine, Uludag University, 16059, Bursa, Turkey. zyilmaz@uludag.edu.tr.
[Ti] Título:Changes in serum proteins after endotoxin administration in healthy and choline-treated calves.
[So] Source:BMC Vet Res;12:210, 2016 Sep 20.
[Is] ISSN:1746-6148
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: This study aimed to investigate the possible serum protein changes after endotoxin administration in healthy and choline-treated calves using proteomics. These results are expected to contribute to the understanding of the pathophysiological mechanisms of endotoxemia and the beneficial effect of choline administration in this clinical situation. METHODS: Healthy-calves (n = 20) were divided into 4 groups: Control, Choline treated (C), Lipopolysaccharide administered (LPS), and LPS + C. Control calves received 0.9 % NaCl injection. Calves in C and LPS + C groups received choline chloride (1 mg/kg/iv). Endotoxin (LPS) was injected (2 µg/kg/iv) to the calves in LPS and LPS + C groups. Serum samples were collected before and after the treatments. Differentially expressed proteins (> 1.5 fold-change relative to controls) were identified by LC-MS/MS. RESULTS: After LPS administration, 14 proteins increased, and 13 proteins decreased within 48 h as compared to controls. In the LPS group, there were significant increases in serum levels of ragulator complex protein (189-fold) and galectin-3-binding protein (10-fold), but transcription factor MafF and corticosteroid binding globulin were down regulated (≥ 5 fold). As compared with the LPS group, in LPS + C group, fibrinogen gamma-B-chain and antithrombin were up-regulated, while hemopexin and histone H4 were down-regulated. Choline treatment attenuated actin alpha cardiac muscle-1 overexpression after LPS. CONCLUSIONS: LPS administration produces changes in serum proteins associated with lipid metabolism, immune and inflammatory response, protein binding/transport, cell adhesion, venous thrombosis, cardiac contractility and blood coagulation. The administration of choline is associated with changes in proteins which can be related with its beneficial effect in this clinical situation.
[Mh] Termos MeSH primário: Proteínas Sanguíneas/metabolismo
Bovinos/sangue
Colina/farmacologia
Endotoxinas/toxicidade
Proteômica
[Mh] Termos MeSH secundário: Animais
Colina/administração & dosagem
Regulação para Baixo
Regulação da Expressão Gênica/efeitos dos fármacos
Lipotrópicos/química
Lipotrópicos/farmacologia
Projetos Piloto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Blood Proteins); 0 (Endotoxins); 0 (Lipotropic Agents); N91BDP6H0X (Choline)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160921
[St] Status:MEDLINE
[do] DOI:10.1186/s12917-016-0837-y


  6 / 387 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26880573
[Au] Autor:Yamamoto H; Kanno K; Ikuta T; Arihiro K; Sugiyama A; Kishikawa N; Tazuma S
[Ad] Endereço:Department of General Internal Medicine, Hiroshima University Hospital, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8551, Japan.
[Ti] Título:Enhancing hepatic fibrosis in spontaneously hypertensive rats fed a choline-deficient diet: a follow-up report on long-term effects of oxidative stress in non-alcoholic fatty liver disease.
[So] Source:J Hepatobiliary Pancreat Sci;23(5):260-9, 2016 May.
[Is] ISSN:1868-6982
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: We previously reported a model of non-alcoholic fatty liver disease (NAFLD) using spontaneously hypertensive rats (SHRs), fed a choline-deficient (CD) diet for 5 weeks, that hepatic steatosis but not fibrosis is developed through oxidative stress. To determine the relationship between hypertension and hepatic fibrosis in NAFLD, we examined whether long-term CD diet leads to hepatic fibrosis through oxidative stress. METHODS: Eight-week-old male SHR and normotensive Wistar Kyoto rats (WKYs) were fed a CD diet for 5 or 20 weeks, then liver histology and hepatic expression of genes related to lipid metabolism, fibrosis, and oxidative stress were assessed. Oxidative stress was assessed by hepatic thiobarbituric acid reactive substance (TBARS) levels. RESULTS: After 5 weeks on CD diet, prominent hepatic steatosis and decrease in expression of genes for lipid metabolism were observed in SHRs as compared with WKYs. SHRs on a CD diet demonstrated a downregulated expression of genes for antioxidants, along with significant increases in hepatic TBARS. After 20 weeks on CD diet, SHRs demonstrated severe liver fibrosis and upregulated expressions of genes for fibrosis when compared with WKY. CONCLUSION: Hypertension precipitated hepatic steatosis, and further, acts as an enhancer in NAFLD progression to liver fibrosis through oxidative stress.
[Mh] Termos MeSH primário: Colina/farmacologia
Dieta
Hepatopatia Gordurosa não Alcoólica/metabolismo
Estresse Oxidativo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Seguimentos
Lipotrópicos/farmacologia
Fígado/patologia
Masculino
Hepatopatia Gordurosa não Alcoólica/diagnóstico
Hepatopatia Gordurosa não Alcoólica/dietoterapia
Ratos
Ratos Endogâmicos SHR
Ratos Endogâmicos WKY
Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Lipotropic Agents); 0 (Thiobarbituric Acid Reactive Substances); N91BDP6H0X (Choline)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170126
[Lr] Data última revisão:
170126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160217
[St] Status:MEDLINE
[do] DOI:10.1002/jhbp.333


  7 / 387 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26804769
[Au] Autor:Geng T; Yang B; Li F; Xia L; Wang Q; Zhao X; Gong D
[Ad] Endereço:College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu 225009, China. Electronic address: tygeng@yzu.edu.cn.
[Ti] Título:Identification of protective components that prevent the exacerbation of goose fatty liver: Characterization, expression and regulation of adiponectin receptors.
[So] Source:Comp Biochem Physiol B Biochem Mol Biol;194-195:32-8, 2016 Apr-May.
[Is] ISSN:1879-1107
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Fat accumulation in the liver is a natural process in goose, which prepares goose for long-distance migration. In contrast to mammalian fatty liver that usually progresses into an irreversible status, steatohepatitis, goose fatty liver can return to normal without obvious pathological damage, suggesting a protective system exists in goose liver. This study was to identify the components of this system. We first focused on goose adiponectin receptor 1 and 2 (Adipor1/2) as they have ceramidase activity, and can cleave ceramide, a group of proinflammatory signaling lipid species. Quantitative analysis indicated that tumor necrosis factor alpha (Tnfα), a key proinflammatory cytokine, was down-regulated in goose fatty liver by overfeeding. This inhibition of Tnfα was accompanied with reduced adiponectin and increased Adipor1/2 in the adipose tissues and in the livers of the overfed geese, respectively. To investigate the regulation of goose Adipor2 in the context of fatty liver, we treated goose primary hepatocytes with fatty liver associated factors. Data indicated that Adipor2 was upregulated by glucose and oleate but not palmitate. Its expression was even suppressed by high level of insulin. The regulation of Adipor1 by these factors was quite similar to that of Adipor2 except that glucose did not induce Adipor1. Together, these findings suggest the upregulation of Adipor1/2 may, at least partially, contribute to the inhibition of inflammation in goose fatty liver, and the expression of Adipor1/2 can be regulated by fatty liver-associated factors.
[Mh] Termos MeSH primário: Proteínas Aviárias/metabolismo
Fígado Gorduroso/veterinária
Gansos
Regulação da Expressão Gênica
Fígado/metabolismo
Doenças das Aves Domésticas/metabolismo
Receptores de Adiponectina/metabolismo
[Mh] Termos MeSH secundário: Gordura Abdominal/imunologia
Gordura Abdominal/metabolismo
Adiponectina/genética
Adiponectina/metabolismo
Animais
Animais Endogâmicos
Proteínas Aviárias/agonistas
Proteínas Aviárias/genética
Células Cultivadas
China
Progressão da Doença
Embrião não Mamífero/citologia
Nutrição Enteral/efeitos adversos
Nutrição Enteral/veterinária
Fígado Gorduroso/etiologia
Fígado Gorduroso/metabolismo
Fígado Gorduroso/fisiopatologia
Regulação da Expressão Gênica/efeitos dos fármacos
Glucose/efeitos adversos
Glucose/metabolismo
Insulina/farmacologia
Lipotrópicos/farmacologia
Fígado/efeitos dos fármacos
Fígado/imunologia
Fígado/patologia
Masculino
Ácido Oleico/efeitos adversos
Ácido Oleico/metabolismo
Doenças das Aves Domésticas/etiologia
Doenças das Aves Domésticas/imunologia
Doenças das Aves Domésticas/fisiopatologia
Isoformas de Proteínas/agonistas
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Receptores de Adiponectina/agonistas
Receptores de Adiponectina/genética
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adiponectin); 0 (Avian Proteins); 0 (Insulin); 0 (Lipotropic Agents); 0 (Protein Isoforms); 0 (Receptors, Adiponectin); 0 (Tumor Necrosis Factor-alpha); 2UMI9U37CP (Oleic Acid); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160126
[St] Status:MEDLINE


  8 / 387 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26794269
[Au] Autor:Musso G; Cassader M; Gambino R
[Ad] Endereço:Gradenigo Hospital, Corso Regina Margherita 8, 10132 Turin, Italy.
[Ti] Título:Non-alcoholic steatohepatitis: emerging molecular targets and therapeutic strategies.
[So] Source:Nat Rev Drug Discov;15(4):249-74, 2016 Apr.
[Is] ISSN:1474-1784
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Non-alcoholic fatty liver disease - the most common chronic liver disease - encompasses a histological spectrum ranging from simple steatosis to non-alcoholic steatohepatitis (NASH). Over the next decade, NASH is projected to be the most common indication for liver transplantation. The absence of an effective pharmacological therapy for NASH is a major incentive for research into novel therapeutic approaches for this condition. The current focus areas for research include the modulation of nuclear transcription factors; agents that target lipotoxicity and oxidative stress; and the modulation of cellular energy homeostasis, metabolism and the inflammatory response. Strategies to enhance resolution of inflammation and fibrosis also show promise to reverse the advanced stages of liver disease.
[Mh] Termos MeSH primário: Hepatopatia Gordurosa não Alcoólica
Estresse Oxidativo/efeitos dos fármacos
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Autofagia/efeitos dos fármacos
Metabolismo Energético/efeitos dos fármacos
Seres Humanos
Imunidade Celular/efeitos dos fármacos
Inflamação/tratamento farmacológico
Inflamação/imunologia
Inflamação/metabolismo
Lipotrópicos/farmacologia
Fígado/efeitos dos fármacos
Fígado/metabolismo
Fígado/patologia
Cirrose Hepática/tratamento farmacológico
Cirrose Hepática/metabolismo
Conduta do Tratamento Medicamentoso
Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico
Hepatopatia Gordurosa não Alcoólica/imunologia
Hepatopatia Gordurosa não Alcoólica/metabolismo
Hepatopatia Gordurosa não Alcoólica/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Lipotropic Agents); 0 (Transcription Factors)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160123
[St] Status:MEDLINE
[do] DOI:10.1038/nrd.2015.3


  9 / 387 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26732065
[Au] Autor:Kusat Ol K; Kanbak G; Oglakci Ilhan A; Burukoglu D; Yücel F
[Ad] Endereço:Department of Biochemistry, Faculty of Medicine, University of Eskisehir Osmangazi, 26480, Eskisehir, Turkey. kkusat@hotmail.com.
[Ti] Título:The investigation of the prenatal and postnatal alcohol exposure-induced neurodegeneration in rat brain: protection by betaine and/or omega-3.
[So] Source:Childs Nerv Syst;32(3):467-74, 2016 Mar.
[Is] ISSN:1433-0350
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: We aim to study the effect of neurodegeneration on the brain of rat pups caused by prenatal and postnatal ethanol exposure with modified liquid diet to elucidate protective effects of betaine and omega-3 supplementation. When ethanol is consumed during prenatal and postnatal periods, it may result in fetal alcohol syndrome (FAS) in the offspring. METHODS: Rats were divided into control, ethanol, ethanol + betaine, ethanol + omega-3, ethanol + omega-3 + betaine groups. The effect of betaine and omega-3 in response to ethanol-induced changes on the brain, by biochemical analyses cytochrome c, caspase-3, calpain, cathepsin B and L, DNA fragmentation, histological and morfometric methods were evaluated. RESULTS: Caspase-3, calpain, cathepsin B, and cytochrome c levels in ethanol group were significantly higher than control. Caspase-3, calpain levels were decreased in ethanol + betaine, ethanol + omega-3, and ethanol + omega-3 + betaine groups compared to ethanol group. Cathepsin B in ethanol + omega-3 + betaine group was decreased compared to ethanol, ethanol + betaine groups. Cathepsin L and DNA fragmentation were found not statistically significant. We found similar results in histological and morfometric parameters. CONCLUSION: We found that pre- and postnatal ethanol exposure is capable of triggering necrotic cell death in rat brains, omega-3, and betaine reduce neurodegeneration. Omega-3 and betaine may prove beneficial for neurodegeneration, particularly in preventing FAS.
[Mh] Termos MeSH primário: Betaína/farmacologia
Depressores do Sistema Nervoso Central/toxicidade
Etanol/toxicidade
Ácidos Graxos Ômega-3/farmacologia
Degeneração Neural/induzido quimicamente
Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente
[Mh] Termos MeSH secundário: Animais
Encéfalo/efeitos dos fármacos
Modelos Animais de Doenças
Feminino
Lipotrópicos/farmacologia
Degeneração Neural/prevenção & controle
Gravidez
Efeitos Tardios da Exposição Pré-Natal/prevenção & controle
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Central Nervous System Depressants); 0 (Fatty Acids, Omega-3); 0 (Lipotropic Agents); 3K9958V90M (Ethanol); 3SCV180C9W (Betaine)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160107
[St] Status:MEDLINE
[do] DOI:10.1007/s00381-015-2990-1


  10 / 387 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26646265
[Au] Autor:Yang W; Gao J; Tai Y; Chen M; Huang L; Wen S; Huang Z; Liu R; Li J; Tang C
[Ad] Endereço:From the *Department of Gastroenterology, West China Hospital, Sichuan University, Chengdu; and †Division of Peptides Related with Human Diseases, State Key Laboratory of Biotherapy, Chengdu, P.R. China.
[Ti] Título:Betaine Attenuates Alcohol-Induced Pancreatic Steatosis.
[So] Source:Pancreas;45(6):836-45, 2016 07.
[Is] ISSN:1536-4828
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To explore the effect of betaine on alcoholic pancreatic steatosis and its mechanism. METHODS: Rats were randomly assigned to control, ethanol, or ethanol + betaine groups. Changes in pancreatic morphology; serum lipid levels; and pancreatic lipid, amylase and lipase levels were determined. The serum and adipose tissue adiponectin level was measured by an enzyme-linked immunoassay. Adiponectin receptor-1 (AdipoR1), AdipoR2, sterol regulatory element binding protein-1c (SREBP-1c), SREBP-2, and fatty acid synthetase expression levels were quantified. The SREBP-1c expression in SW1990 cells treated with various concentrations of ethanol or ethanol plus betaine and/or adiponectin was assessed. RESULTS: Alcohol-induced changes in pancreatic morphology were attenuated by betaine. Pancreatic triglyceride, free fatty acid and expression levels of SREBP-1c and fatty acid synthetase were elevated after ethanol feeding but remained at control levels after betaine supplementation. Alcohol-induced decreases in serum and adipose tissue adiponectin, pancreatic AdipoR1, amylase, and lipase were attenuated by betaine. Serum triglyceride and free fatty acid levels were elevated after alcohol consumption and remained higher after betaine supplementation compared with controls. Betaine and/or adiponectin suppressed alcohol-induced SREBP-1c upregulation in vitro. CONCLUSIONS: Betaine attenuated alcoholic-induced pancreatic steatosis most likely by suppressing pancreatic SREBP-1c both directly and through the restoration of adiponectin signaling.
[Mh] Termos MeSH primário: Betaína/farmacologia
Etanol/administração & dosagem
Pâncreas/efeitos dos fármacos
Pancreatopatias/prevenção & controle
[Mh] Termos MeSH secundário: Adiponectina/metabolismo
Amilases/metabolismo
Animais
Western Blotting
Linhagem Celular Tumoral
Depressores do Sistema Nervoso Central/administração & dosagem
Depressores do Sistema Nervoso Central/toxicidade
Etanol/toxicidade
Insuficiência Pancreática Exócrina/sangue
Insuficiência Pancreática Exócrina/induzido quimicamente
Insuficiência Pancreática Exócrina/prevenção & controle
Seres Humanos
Imuno-Histoquímica
Lipase/metabolismo
Lipídeos/análise
Lipídeos/sangue
Lipotrópicos/farmacologia
Masculino
Pâncreas/metabolismo
Pâncreas/patologia
Pancreatopatias/sangue
Pancreatopatias/induzido quimicamente
Substâncias Protetoras/farmacologia
Ratos Wistar
Receptores de Adiponectina/genética
Receptores de Adiponectina/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Proteína de Ligação a Elemento Regulador de Esterol 1/genética
Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo
Proteína de Ligação a Elemento Regulador de Esterol 2/genética
Proteína de Ligação a Elemento Regulador de Esterol 2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adiponectin); 0 (Central Nervous System Depressants); 0 (Lipids); 0 (Lipotropic Agents); 0 (Protective Agents); 0 (Receptors, Adiponectin); 0 (Sterol Regulatory Element Binding Protein 1); 0 (Sterol Regulatory Element Binding Protein 2); 0 (adiponectin receptor 1, rat); 0 (adiponectin receptor 2, rat); 3K9958V90M (Ethanol); 3SCV180C9W (Betaine); EC 3.1.1.3 (Lipase); EC 3.2.1.- (Amylases)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170328
[Lr] Data última revisão:
170328
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151210
[St] Status:MEDLINE
[do] DOI:10.1097/MPA.0000000000000557



página 1 de 39 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde