Base de dados : MEDLINE
Pesquisa : D04.210.500.247.808.197.225 [Categoria DeCS]
Referências encontradas : 8021 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 803 ir para página                         

  1 / 8021 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29352300
[Au] Autor:Wang Z; Koonen D; Hofker M; Bao Z
[Ad] Endereço:Department of Geriatrics and Gastroenterology, Huadong Hospital, Shanghai Medical College, Fudan University, Shanghai Key Laboratory of Clinical Geriatric Medicine, Shanghai, P.R. China.
[Ti] Título:5-aminosalicylic acid improves lipid profile in mice fed a high-fat cholesterol diet through its dual effects on intestinal PPARγ and PPARα.
[So] Source:PLoS One;13(1):e0191485, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Obesity is associated with a series of metabolic complications, including dyslipidemia and insulin resistance (IR) that lack effective therapies. In recent years, intestinal inflammation has been suggested to contribute to obesity related metabolic syndrome and targeting gut inflammation with 5-ASA improves diet induced IR, however, its role in dyslipidemia is unknown and has never been explored. In the present study, we reported for the first time that administration of 5-ASA for 12 weeks significantly improved lipid profile by repressing plasma triglycerides and free cholesterol levels in mice fed high-fat cholesterol diet (HFC). In addition, liver lipids were significantly reduced by 5-ASA treatment in HFC-fed mice. Mechanistically, anti-inflammatory genes peroxisome proliferator-activated receptor-γ (Pparγ) and M2 marker, such as Mrc1 and Ym1, were remarkably upregulated, while pro-inflammation gene monocyte chemoattractant protein-1 (Mcp-1) were downregulated in small intestine of mice treated by 5-ASA. Further, 5-ASA improved gastrointestinal barrier by increasing the expression of the tight junction marker ZO-1. 5-ASA also enhanced cholesterol translocation by elevating genes expression of Npc1l1 and Abcg5/8. Moreover, mice fed HFC 5-ASA expressed increased Pparα in small intestinal and its target genes function in lipid oxidation and hydrolysis were remarkable elevated. Taken together, we reported a novel role of 5-ASA which may serve as a therapy target intestinal inflammation induced dyslipidemia.
[Mh] Termos MeSH primário: Colesterol na Dieta/administração & dosagem
Dieta Hiperlipídica/efeitos adversos
Intestinos/efeitos dos fármacos
Intestinos/metabolismo
Metabolismo dos Lipídeos/efeitos dos fármacos
Mesalamina/farmacologia
PPAR alfa/metabolismo
PPAR gama/metabolismo
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios não Esteroides/farmacologia
Dislipidemias/tratamento farmacológico
Dislipidemias/genética
Dislipidemias/metabolismo
Ácidos Graxos/metabolismo
Hipolipemiantes/farmacologia
Inflamação/tratamento farmacológico
Inflamação/genética
Inflamação/metabolismo
Metabolismo dos Lipídeos/genética
Lipídeos/sangue
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
PPAR gama/genética
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cholesterol, Dietary); 0 (Fatty Acids); 0 (Hypolipidemic Agents); 0 (Lipids); 0 (PPAR alpha); 0 (PPAR gamma); 0 (RNA, Messenger); 4Q81I59GXC (Mesalamine)
[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:180121
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191485


  2 / 8021 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28882873
[Au] Autor:Trigueros-Motos L; van Capelleveen JC; Torta F; Castaño D; Zhang LH; Chai EC; Kang M; Dimova LG; Schimmel AWM; Tietjen I; Radomski C; Tan LJ; Thiam CH; Narayanaswamy P; Wu DH; Dorninger F; Yakala GK; Barhdadi A; Angeli V; Dubé MP; Berger J; Dallinga-Thie GM; Tietge UJF; Wenk MR; Hayden MR; Hovingh GK; Singaraja RR
[Ad] Endereço:From the Translational Laboratory in Genetic Medicine, A*STAR Institute, and Yong Loo Lin School of Medicine, National University of Singapore (L.T.-M., D.C., E.C.C., L.J.T., D.H.W., G.K.Y., M.R.H., R.R.S.); Departments of Vascular Medicine and Experimental Vascular Medicine, Academic Medical Centre
[Ti] Título:ABCA8 Regulates Cholesterol Efflux and High-Density Lipoprotein Cholesterol Levels.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2147-2155, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: High-density lipoproteins (HDL) are considered to protect against atherosclerosis in part by facilitating the removal of cholesterol from peripheral tissues. However, factors regulating lipid efflux are incompletely understood. We previously identified a variant in adenosine triphosphate-binding cassette transporter A8 ( ) in an individual with low HDL cholesterol (HDLc). Here, we investigate the role of ABCA8 in cholesterol efflux and in regulating HDLc levels. APPROACH AND RESULTS: We sequenced in individuals with low and high HDLc and identified, exclusively in low HDLc probands, 3 predicted deleterious heterozygous mutations (p.Pro609Arg [P609R], IVS17-2 A>G and p.Thr741Stop [T741X]). HDLc levels were lower in heterozygous mutation carriers compared with first-degree family controls (0.86±0.34 versus 1.17±0.26 mmol/L; =0.005). HDLc levels were significantly decreased by 29% ( =0.01) in mice on a high-cholesterol diet compared with wild-type mice, whereas hepatic overexpression of human in mice resulted in significant increases in plasma HDLc and the first steps of macrophage-to-feces reverse cholesterol transport. Overexpression of wild-type but not mutant ABCA8 resulted in a significant increase (1.8-fold; =0.01) of cholesterol efflux to apolipoprotein AI in vitro. ABCA8 colocalizes and interacts with adenosine triphosphate-binding cassette transporter A1 and further potentiates adenosine triphosphate-binding cassette transporter A1-mediated cholesterol efflux. CONCLUSIONS: ABCA8 facilitates cholesterol efflux and modulates HDLc levels in humans and mice.
[Mh] Termos MeSH primário: Transportadores de Cassetes de Ligação de ATP/metabolismo
Colesterol na Dieta/sangue
HDL-Colesterol/sangue
[Mh] Termos MeSH secundário: Transportadores de Cassetes de Ligação de ATP/deficiência
Transportadores de Cassetes de Ligação de ATP/genética
Adulto
Idoso
Animais
Apolipoproteína A-I/sangue
Apolipoproteína B-100/sangue
Transporte Biológico
Biomarcadores/sangue
Células COS
Estudos de Casos e Controles
Cercopithecus aethiops
Análise Mutacional de DNA
Dieta Hiperlipídica
Fezes/química
Feminino
Células HEK293
Hereditariedade
Heterozigoto
Seres Humanos
Fígado/metabolismo
Macrófagos/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Meia-Idade
Mutação
Linhagem
Fenótipo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABCA8 protein, human); 0 (APOA1 protein, human); 0 (APOB protein, human); 0 (Abca8b protein, mouse); 0 (Apolipoprotein A-I); 0 (Apolipoprotein B-100); 0 (Biomarkers); 0 (Cholesterol, Dietary); 0 (Cholesterol, HDL)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309574


  3 / 8021 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28666194
[Au] Autor:Gu X; Fu H; Sun S; Qiao H; Zhang W; Jiang S; Xiong Y; Jin S; Gong Y; Wu Y
[Ad] Endereço:Wuxi Fisheries College, Nanjing Agricultural University, Wuxi 214081, China; Key Laboratory of Freshwater Fisheries and Germplasm Resources Utilization, Ministry of Agriculture, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi 214081, China.
[Ti] Título:Dietary cholesterol-induced transcriptome differences in the intestine, hepatopancreas, and muscle of Oriental River prawn Macrobrachium nipponense.
[So] Source:Comp Biochem Physiol Part D Genomics Proteomics;23:39-48, 2017 Sep.
[Is] ISSN:1878-0407
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Cholesterol is an important nutrient for crustaceans. In this study, we performed comparative transcriptome analyses to explore the transcriptome differences in the intestine, hepatopancreas, and muscle of Macrobrachium nipponense fed either a low cholesterol (LC) or high cholesterol (HC) diet (2.8 or 17.1g cholesterol per kg diet). High-throughput RNA-Seq was conducted, resulting in 7.65, 5.88, and 7.59G clean bases from the intestine, hepatopancreas, and muscle of the LC group, respectively, and 7.59, 6.73, and 6.70G clean bases from the same tissues of the HC group. Assembly of clean reads resulted in 230,946 unigenes. The following enriched pathways were identified: xenobiotic and drug metabolism by cytochrome P450; chloroalkane and chloroalkene degradation; metabolic and biosynthetic pathways; fatty acid metabolism and biosynthesis; and immune-related pathways. To the best of our knowledge, this is the first study to describe how functional unigenes and biosynthetic and metabolic pathways are affected by dietary cholesterol in aquatic crustaceans. Thus, these results contribute to our understanding of the molecular mechanisms underlying the cholesterol requirement of crustaceans.
[Mh] Termos MeSH primário: Colesterol na Dieta/metabolismo
Dieta
Palaemonidae/genética
Palaemonidae/metabolismo
Transcriptoma
[Mh] Termos MeSH secundário: Animais
Biblioteca Gênica
Hepatopâncreas/metabolismo
Intestinos/metabolismo
Músculos/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Rios
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholesterol, Dietary)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170701
[St] Status:MEDLINE


  4 / 8021 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28659302
[Au] Autor:Ikezaki H; Furusyo N; Jacques PF; Shimizu M; Murata M; Schaefer EJ; Urita Y; Hayashi J
[Ad] Endereço:Department of General Internal Medicine, Kyushu University Hospital, Fukuoka, Japan; hiroaki.ikezaki@tufts.edu.
[Ti] Título:Higher dietary cholesterol and ω-3 fatty acid intakes are associated with a lower success rate of eradication therapy in Japan.
[So] Source:Am J Clin Nutr;106(2):581-588, 2017 Aug.
[Is] ISSN:1938-3207
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:infection is a known risk factor for duodenal ulcers, gastritis, and gastric cancer. The eradication of is successful in treating these disorders; however, the success rate of eradication therapy is declining. There may be an interaction with nutrient intake to account for this decline. We investigated the influence of food and nutrient intake on eradication therapy. In this study, 4014 subjects underwent endoscopy, were tested for serum antibodies to (2046 positive; 51.0%), and had their food intake assessed with the use of a food-frequency questionnaire (FFQ). Of the positive subjects, endoscopies showed that 389 (19.0%) had gastritis and/or duodenal ulcers and were also positive for a C-urea breath test (UBT). These 389 subjects received 1-wk eradication therapy with lansoprazole, amoxicillin, and clarithromycin and a second UBT 8 wk after treatment. Complete demographic characteristics, serum lipid, insulin, glycated hemoglobin, C-reactive protein (CRP), and creatinine concentrations as well as complete FFQs were available for 352 subjects. Multivariate logistic regression analyses were performed to determine factors that were associated with successful eradication therapy. The success rate of eradication therapy was 60.4% (235 of 389). Factors associated with the failure of eradication therapy included increased age ( = 0.02), higher CRP concentrations ( < 0.01), higher dietary cholesterol ( < 0.01) or egg intake ( < 0.01), higher ω-3 (n-3) fatty acid ( = 0.02) or fish intake ( = 0.01), and higher vitamin D intake ( = 0.02). Moreover, the higher vitamin D intake was strongly linked to higher fish intake. A limitation of the study is that we did not assess the antibiotic resistance of Our results indicate that higher egg and fish intake may be negatively correlated with successful eradication therapy in -positive subjects with gastritis and/or duodenal ulcers.
[Mh] Termos MeSH primário: Antibacterianos/uso terapêutico
Colesterol na Dieta/efeitos adversos
Dieta
Ácidos Graxos Ômega-3/efeitos adversos
Comportamento Alimentar
Infecções por Helicobacter/tratamento farmacológico
Helicobacter pylori/efeitos dos fármacos
[Mh] Termos MeSH secundário: Fatores Etários
Idoso
Animais
Antibacterianos/farmacologia
Proteína C-Reativa/metabolismo
Colesterol na Dieta/administração & dosagem
Úlcera Duodenal/tratamento farmacológico
Úlcera Duodenal/microbiologia
Ovos
Ácidos Graxos Ômega-3/administração & dosagem
Feminino
Peixes
Gastrite/tratamento farmacológico
Gastrite/microbiologia
Infecções por Helicobacter/microbiologia
Seres Humanos
Japão
Masculino
Meia-Idade
Alimentos Marinhos
Falha de Tratamento
Vitamina D/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Cholesterol, Dietary); 0 (Fatty Acids, Omega-3); 1406-16-2 (Vitamin D); 9007-41-4 (C-Reactive Protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170630
[St] Status:MEDLINE
[do] DOI:10.3945/ajcn.116.144873


  5 / 8021 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28546217
[Au] Autor:Wang C; Nishijima K; Kitajima S; Niimi M; Yan H; Chen Y; Ning B; Matsuhisa F; Liu E; Zhang J; Chen YE; Fan J
[Ad] Endereço:From the Department of Molecular Pathology, Faculty of Medicine, Graduate Faculty of Interdisciplinary Research, Graduate School, University of Yamanashi, Japan (C.W., M.N., B.N., H.Y., Y.C., J.F.); Department of Pathology, Xi'an Medical University, China (B.N., J.F.); Animal Research Laboratory, Bi
[Ti] Título:Increased Hepatic Expression of Endothelial Lipase Inhibits Cholesterol Diet-Induced Hypercholesterolemia and Atherosclerosis in Transgenic Rabbits.
[So] Source:Arterioscler Thromb Vasc Biol;37(7):1282-1289, 2017 Jul.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Endothelial lipase (EL) is a key determinant in plasma high-density lipoprotein-cholesterol. However, functional roles of EL on the development of atherosclerosis have not been clarified. We investigated whether hepatic expression of EL affects plasma lipoprotein metabolism and cholesterol diet-induced atherosclerosis. APPROACH AND RESULTS: We generated transgenic (Tg) rabbits expressing the human EL gene in the liver and then examined the effects of EL expression on plasma lipids and lipoproteins and compared the susceptibility of Tg rabbits with cholesterol diet-induced atherosclerosis with non-Tg littermates. On a chow diet, hepatic expression of human EL in Tg rabbits led to remarkable reductions in plasma levels of total cholesterol, phospholipids, and high-density lipoprotein-cholesterol compared with non-Tg controls. On a cholesterol-rich diet for 16 weeks, Tg rabbits exhibited significantly lower hypercholesterolemia and less atherosclerosis than non-Tg littermates. In Tg rabbits, gross lesion area of aortic atherosclerosis was reduced by 52%, and the lesions were characterized by fewer macrophages and smooth muscle cells compared with non-Tg littermates. CONCLUSIONS: Increased hepatic expression of EL attenuates cholesterol diet-induced hypercholesterolemia and protects against atherosclerosis.
[Mh] Termos MeSH primário: Doenças da Aorta/prevenção & controle
Aterosclerose/prevenção & controle
Colesterol na Dieta
Hipercolesterolemia/prevenção & controle
Lipase/metabolismo
Fígado/enzimologia
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Aorta/metabolismo
Aorta/patologia
Doenças da Aorta/enzimologia
Doenças da Aorta/genética
Doenças da Aorta/patologia
Aterosclerose/enzimologia
Aterosclerose/genética
Aterosclerose/patologia
Biomarcadores/sangue
Colesterol na Dieta/sangue
HDL-Colesterol/sangue
Modelos Animais de Doenças
Feminino
Predisposição Genética para Doença
Seres Humanos
Hipercolesterolemia/enzimologia
Hipercolesterolemia/genética
Hipercolesterolemia/patologia
Lipase/genética
Macrófagos/metabolismo
Macrófagos/patologia
Masculino
Músculo Liso Vascular/metabolismo
Músculo Liso Vascular/patologia
Miócitos de Músculo Liso/metabolismo
Miócitos de Músculo Liso/patologia
Fenótipo
Fosfolipídeos/sangue
Placa Aterosclerótica
Coelhos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cholesterol, Dietary); 0 (Cholesterol, HDL); 0 (Phospholipids); EC 3.1.1.3 (LIPG protein, human); EC 3.1.1.3 (Lipase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309139


  6 / 8021 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28472600
[Au] Autor:Vázquez-Velasco M; González-Torres L; García-Fernández RA; Méndez MT; Bastida S; Benedí J; González-Muñoz MJ; Sánchez-Muniz FJ
[Ad] Endereço:1 Department of Nutrition and Food Science (I) Nutrition, School of Pharmacy, Complutense University , Madrid, Spain .
[Ti] Título:Glucomannan or Glucomannan Plus Spirulina-Enriched Squid-Surimi Diets Reduce Histological Damage to Liver and Heart in Zucker fa/fa Rats Fed a Cholesterol-Enriched and Non-Cholesterol-Enriched Atherogenic Diet.
[So] Source:J Med Food;20(6):618-625, 2017 Jun.
[Is] ISSN:1557-7600
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glucomannan-enriched squid surimi improves cholesterolemia and liver antioxidant status. The effect of squid surimi enriched with glucomannan or glucomannan plus spirulina on liver and heart structures and cell damage markers was tested in fa/fa rats fed highly saturated-hyper-energetic diets. Animals were fed 70% AIN-93M rodent diet plus six versions of 30% squid surimi for 7 weeks: control (C), glucomannan (G), and glucomannan plus spirulina (GS). The cholesterol-control (HC), cholesterol-glucomannan (HG), and cholesterol-glucomannan plus spirulina (HGS) groups were given similar diets that were enriched with 2% cholesterol and 0.4% cholic acid. G and GS diets versus C diet significantly inhibited weight gain and lowered plasma alanine aminotransferase and aspartate aminotransferase, liver steatosis, lipogranulomas, and total inflammation and alteration scores. The hypercholesterolemic agent significantly increased the harmful effects of the C diet. Liver weight, the hepatosomatic index, all damage markers, and total histological scoring rose for HC versus C (at least P < .05). The addition of glucomannan (HG vs. HC) improved these biomarkers, and non-additional effects from spirulina were observed except for the total liver alteration score. In conclusion, glucomannan and glucomannan plus spirulina blocked the highly saturated-hyper-energetic diet negative effects both with and without added cholesterol. Results suggest the usefulness of including these functional ingredients in fish products.
[Mh] Termos MeSH primário: Antioxidantes/metabolismo
Colesterol na Dieta/efeitos adversos
Dieta Aterogênica/efeitos adversos
Produtos Pesqueiros/efeitos adversos
Fígado/metabolismo
Mananas/metabolismo
Miocárdio/metabolismo
Spirulina/metabolismo
[Mh] Termos MeSH secundário: Animais
Decapodiformes/metabolismo
Produtos Pesqueiros/análise
Coração/anatomia & histologia
Histologia
Fígado/anatomia & histologia
Masculino
Ratos
Ratos Zucker
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Cholesterol, Dietary); 0 (Mannans); 36W3E5TAMG ((1-6)-alpha-glucomannan)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1089/jmf.2016.0157


  7 / 8021 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28446627
[Au] Autor:Garcimartín A; López-Oliva ME; Sántos-López JA; García-Fernández RA; Macho-González A; Bastida S; Benedí J; Sánchez-Muniz FJ
[Ad] Endereço:Department of Pharmacology.
[Ti] Título:Silicon Alleviates Nonalcoholic Steatohepatitis by Reducing Apoptosis in Aged Wistar Rats Fed a High-Saturated Fat, High-Cholesterol Diet.
[So] Source:J Nutr;147(6):1104-1112, 2017 Jun.
[Is] ISSN:1541-6100
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lipoapoptosis has been identified as a key event in the progression of nonalcoholic fatty liver disease (NAFLD), and hence, antiapoptotic agents have been recommended as a possible effective treatment for nonalcoholic steatohepatitis (NASH). Silicon, included in meat as a functional ingredient, improves lipoprotein profiles and liver antioxidant defenses in aged rats fed a high-saturated fat, high-cholesterol diet (HSHCD). However, to our knowledge, the antiapoptotic effect of this potential functional meat on the liver has never been tested. This study was designed to evaluate the effect of silicon on NASH development and the potential antiapoptotic properties of silicon in aged rats. One-year-old male Wistar rats weighing ∼500 g were fed 3 experimental diets containing restructured pork (RP) for 8 wk: ) a high-saturated fat diet, as an NAFLD control, with 16.9% total fat, 0.14 g cholesterol/kg diet, and 46.8 mg SiO /kg (control); ) the HSHCD as a model of NASH, with 16.6% total fat, 16.3 g cholesterol/kg diet, and 46.8 mg SiO /kg [high-cholesterol diet (Chol-C)]; and ) the HSHCD with silicon-supplemented RP with amounts of fat and cholesterol identical to those in the Chol-C diet, but with 750 mg SiO /kg (Chol-Si). Detailed histopathological assessments were performed, and the NAFLD activity score (NAS) was calculated. Liver apoptosis and damage markers were evaluated by Western blotting and immunohistochemical staining. Chol-C rats had a higher mean NAS (7.4) than did control rats (1.9; < 0.001). The score in Chol-Si rats (5.4) was intermediate and different from that in both other groups ( < 0.05). Several liver apoptosis markers-including hepatocyte terminal deoxynucleotidyl transferase 2'-deoxyuridine 5'-triphosphate (dUTP) nick end labeling, cytosolic cytochrome c, apoptosis-inducing factor, caspases 9 and 3, and the mitochondrial Bcl-2-associated X protein (BAX)-to-B-cell lymphoma 2 (BCL2) ratio-were 9-45% lower in Chol-Si than in Chol-C rats ( 0.05) and did not differ from values in the control group. Supplemental silicon substantially affects NASH development in aged male Wistar rats fed an HSHCD by partially blocking apoptosis. These results suggest that silicon-enriched RP could be used as an effective nutritional strategy in preventing NASH.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Colesterol na Dieta/administração & dosagem
Dieta Hiperlipídica
Fígado/efeitos dos fármacos
Hepatopatia Gordurosa não Alcoólica/prevenção & controle
Carne Vermelha
Silício/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Colesterol na Dieta/metabolismo
Fígado/metabolismo
Fígado/patologia
Masculino
Hepatopatia Gordurosa não Alcoólica/etiologia
Hepatopatia Gordurosa não Alcoólica/metabolismo
Hepatopatia Gordurosa não Alcoólica/patologia
Ratos Wistar
Silício/farmacologia
Dióxido de Silício/farmacologia
Dióxido de Silício/uso terapêutico
Suínos
Oligoelementos/farmacologia
Oligoelementos/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cholesterol, Dietary); 0 (Trace Elements); 7631-86-9 (Silicon Dioxide); Z4152N8IUI (Silicon)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170705
[Lr] Data última revisão:
170705
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.3945/jn.116.243204


  8 / 8021 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28438611
[Au] Autor:Dimova LG; de Boer JF; Plantinga J; Plösch T; Hoekstra M; Verkade HJ; Tietge UJF
[Ad] Endereço:Department of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
[Ti] Título:Inhibiting Cholesterol Absorption During Lactation Programs Future Intestinal Absorption of Cholesterol in Adult Mice.
[So] Source:Gastroenterology;153(2):382-385.e3, 2017 Aug.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In nematodes, the intestine senses and integrates early life dietary cues that lead to lifelong epigenetic adaptations to a perceived nutritional environment-it is not clear whether this process occurs in mammals. We aimed to establish a mouse model of reduced dietary cholesterol availability from maternal milk and investigate the consequences of decreased milk cholesterol availability, early in life, on the metabolism of cholesterol in adult mice. We blocked intestinal absorption of cholesterol in milk fed to newborn mice by supplementing the food of dams (for 3 weeks between birth and weaning) with ezetimibe, which is secreted into milk. Ezetimibe interacts with the intestinal cholesterol absorption transporter NPC1l1 to block cholesterol uptake into enterocytes. Characterization of these offspring at 24 weeks of age showed a 27% decrease in cholesterol absorption (P < .001) and reduced levels of Npc1l1 messenger RNA and protein, but not other cholesterol transporters, in the proximal small intestine. We observed increased histone H3K9me3 methylation at positions -423 to -607 of the proximal Npc1l1 promoter in small intestine tissues from 24-week-old offspring fed ezetimibe during lactation, compared with controls. These findings show that the early postnatal mammalian intestine functions as an environmental sensor of nutritional conditions, responding to conditions such as low cholesterol levels by epigenetic modifications of genes. Further studies are needed to determine how decreased sterol absorption for a defined period might activate epigenetic regulators; the findings of our study might have implications for human infant nutrition and understanding and preventing cardiometabolic disease.
[Mh] Termos MeSH primário: Adaptação Fisiológica
Colesterol na Dieta/metabolismo
Colesterol/metabolismo
Absorção Intestinal/fisiologia
Intestinos/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticolesterolemiantes/farmacologia
Disponibilidade Biológica
Transporte Biológico
Enterócitos/metabolismo
Epigênese Genética
Ezetimiba/farmacologia
Feminino
Histonas/metabolismo
Absorção Intestinal/efeitos dos fármacos
Intestino Delgado/metabolismo
Intestinos/citologia
Lactação/fisiologia
Proteínas de Membrana Transportadoras/efeitos dos fármacos
Proteínas de Membrana Transportadoras/genética
Camundongos
Leite/química
Modelos Animais
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticholesteremic Agents); 0 (Cholesterol, Dietary); 0 (Histones); 0 (Membrane Transport Proteins); 0 (Npc1l1 protein, mouse); 0 (RNA, Messenger); 97C5T2UQ7J (Cholesterol); EOR26LQQ24 (Ezetimibe)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170831
[Lr] Data última revisão:
170831
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170426
[St] Status:MEDLINE


  9 / 8021 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28428219
[Au] Autor:Zhang J; Niimi M; Yang D; Liang J; Xu J; Kimura T; Mathew AV; Guo Y; Fan Y; Zhu T; Song J; Ackermann R; Koike Y; Schwendeman A; Lai L; Pennathur S; Garcia-Barrio M; Fan J; Chen YE
[Ad] Endereço:From the Center for Advanced Models for Translational Sciences and Therapeutics, Department of Internal Medicine (J.Z., D.Y., J.L., J.X., Y.G., Y.F., T.Z., J.S., Y.K., M.G.-B., Y.E.C.), Department of Internal Medicine, Nephrology (A.V.M., S.P.), University of Michigan Medical Center, Ann Arbor; Depa
[Ti] Título:Deficiency of Cholesteryl Ester Transfer Protein Protects Against Atherosclerosis in Rabbits.
[So] Source:Arterioscler Thromb Vasc Biol;37(6):1068-1075, 2017 Jun.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: CETP (cholesteryl ester transfer protein) plays an important role in lipoprotein metabolism; however, whether inhibition of CETP activity can prevent cardiovascular disease remains controversial. APPROACH AND RESULTS: We generated CETP knockout (KO) rabbits by zinc finger nuclease gene editing and compared their susceptibility to cholesterol diet-induced atherosclerosis to that of wild-type (WT) rabbits. On a chow diet, KO rabbits showed higher plasma levels of high-density lipoprotein (HDL) cholesterol than WT controls, and HDL particles of KO rabbits were essentially rich in apolipoprotein AI and apolipoprotein E contents. When challenged with a cholesterol-rich diet for 18 weeks, KO rabbits not only had higher HDL cholesterol levels but also lower total cholesterol levels than WT rabbits. Analysis of plasma lipoproteins revealed that reduced plasma total cholesterol in KO rabbits was attributable to decreased apolipoprotein B-containing particles, while HDLs remained higher than that in WT rabbits. Both aortic and coronary atherosclerosis was significantly reduced in KO rabbits compared with WT rabbits. Apolipoprotein B-depleted plasma isolated from CETP KO rabbits showed significantly higher capacity for cholesterol efflux from macrophages than that from WT rabbits. Furthermore, HDLs isolated from CETP KO rabbits suppressed tumor necrosis factor-α-induced vascular cell adhesion molecule 1 and E-selectin expression in cultured endothelial cells. CONCLUSIONS: These results provide evidence that genetic ablation of CETP activity protects against cholesterol diet-induced atherosclerosis in rabbits.
[Mh] Termos MeSH primário: Doenças da Aorta/prevenção & controle
Aterosclerose/prevenção & controle
Proteínas de Transferência de Ésteres de Colesterol/deficiência
Colesterol na Dieta
Doença da Artéria Coronariana/prevenção & controle
Erros Inatos do Metabolismo Lipídico/metabolismo
Macrófagos/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Doenças da Aorta/genética
Doenças da Aorta/metabolismo
Doenças da Aorta/patologia
Apolipoproteína A-I/sangue
Apolipoproteínas B/sangue
Apolipoproteínas E/sangue
Aterosclerose/genética
Aterosclerose/metabolismo
Aterosclerose/patologia
Linhagem Celular
Proteínas de Transferência de Ésteres de Colesterol/sangue
Proteínas de Transferência de Ésteres de Colesterol/genética
Proteínas de Transferência de Ésteres de Colesterol/metabolismo
HDL-Colesterol/sangue
Doença da Artéria Coronariana/genética
Doença da Artéria Coronariana/metabolismo
Doença da Artéria Coronariana/patologia
Modelos Animais de Doenças
Selectina E/metabolismo
Feminino
Edição de Genes
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana/metabolismo
Erros Inatos do Metabolismo Lipídico/sangue
Erros Inatos do Metabolismo Lipídico/genética
Masculino
Camundongos
Coelhos
Fatores de Tempo
Fator de Necrose Tumoral alfa/farmacologia
Molécula 1 de Adesão de Célula Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoprotein A-I); 0 (Apolipoproteins B); 0 (Apolipoproteins E); 0 (Cholesterol Ester Transfer Proteins); 0 (Cholesterol, Dietary); 0 (Cholesterol, HDL); 0 (E-Selectin); 0 (SELE protein, human); 0 (Tumor Necrosis Factor-alpha); 0 (Vascular Cell Adhesion Molecule-1)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170422
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309114


  10 / 8021 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28414328
[Au] Autor:Nus M; Sage AP; Lu Y; Masters L; Lam BYH; Newland S; Weller S; Tsiantoulas D; Raffort J; Marcus D; Finigan A; Kitt L; Figg N; Schirmbeck R; Kneilling M; Yeo GSH; Binder CJ; de la Pompa JL; Mallat Z
[Ad] Endereço:Division of Cardiovascular Medicine, University of Cambridge, Cambridge, UK.
[Ti] Título:Marginal zone B cells control the response of follicular helper T cells to a high-cholesterol diet.
[So] Source:Nat Med;23(5):601-610, 2017 May.
[Is] ISSN:1546-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Splenic marginal zone B (MZB) cells, positioned at the interface between circulating blood and lymphoid tissue, detect and respond to blood-borne antigens. Here we show that MZB cells in mice activate a homeostatic program in response to a high-cholesterol diet (HCD) and regulate both the differentiation and accumulation of T follicular helper (T ) cells. Feeding mice an HCD resulted in upregulated MZB cell surface expression of the immunoregulatory ligand PDL1 in an ATF3-dependent manner and increased the interaction between MZB cells and pre-T cells, leading to PDL1-mediated suppression of T cell motility, alteration of T cell differentiation, reduced T abundance and suppression of the proatherogenic T response. Our findings reveal a previously unsuspected role for MZB cells in controlling the T -germinal center response to a cholesterol-rich diet and uncover a PDL1-dependent mechanism through which MZB cells use their innate immune properties to limit an exaggerated adaptive immune response.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Antígeno B7-H1/imunologia
Colesterol na Dieta/imunologia
Dieta
Centro Germinativo/imunologia
Tecido Linfoide/imunologia
Linfócitos T Auxiliares-Indutores/imunologia
[Mh] Termos MeSH secundário: Fator 3 Ativador da Transcrição/genética
Fator 3 Ativador da Transcrição/imunologia
Animais
Aterosclerose/imunologia
Diferenciação Celular/imunologia
Movimento Celular/imunologia
Colesterol/sangue
HDL-Colesterol/sangue
Citometria de Fluxo
Homeostase
Seres Humanos
Contagem de Linfócitos
Tecido Linfoide/citologia
Camundongos
Placa Aterosclerótica/sangue
Placa Aterosclerótica/imunologia
Placa Aterosclerótica/patologia
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Baço/citologia
Baço/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Activating Transcription Factor 3); 0 (Atf3 protein, mouse); 0 (B7-H1 Antigen); 0 (Cd274 protein, mouse); 0 (Cholesterol, Dietary); 0 (Cholesterol, HDL); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE
[do] DOI:10.1038/nm.4315



página 1 de 803 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