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[PMID]:29265781
[Au] Autor:Czekajlo A; Rózanska D; Mandecka A; Konikowska K; Madalinska M; Regulska-Ilow B
[Ad] Endereço:Wroclaw Medical University, Faculty of Health Sciences, Department of Dietetics, Wroclaw, Poland
[Ti] Título:Comparison of nutritional value of "fruit and vegetables" and "western" dietary patterns identified in a group of cancer patients
[So] Source:Rocz Panstw Zakl Hig;68(4):365-373, 2017.
[Is] ISSN:0035-7715
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Background: Dietary patterns (DPs) are defined as the amounts, types and combinations of various food products in habitual diets and the frequency of their consumption. Dietary pattern analysis is usually performed in order to assess the combined effect of consumed food products on health Objective: The aim of the study was to assess and compare the nutritional value of dietary patterns identified in a group of patients staying on the oncological ward Material and methods: The study group consisted of 100 patients (51 women and 49 men) aged 19-83 years. Dietary intake was assessed using a food frequency questionnaire (FFQ) validated for the population of Lower Silesian Voivodeship Results: Factor analysis identified two main dietary patterns explaining 25.6% of variance. The "fruit and vegetables" DP consisted of vegetables, fruits, juices, unrefined grains and nuts, seeds and raisins. Instead, the "Western" DP was characterized by the consumption of high-fat and processed meat and poultry, fried fish, refined grains, honey and sugar, fats, sweets, beverages and chips. While higher scores for "fruit and vegetables" pattern were associated with increased intake of dietary fiber, antioxidant vitamins, folic acid and decreased glycemic load per 1000 kcal and sodium intake, for "Western" pattern observed relationships were opposite. Women were more likely to have higher factor scores for "fruit and vegetables" DP and lower factor scores for "Western" DP than men Conclusions: Dietary patterns identified in the study group differed in terms of nutritional value, in spite of similar macronutrient content in the diet. "Western" DP was characterized by lower nutritional value than "fruit and vegetables" dietary pattern.
[Mh] Termos MeSH primário: Dieta Ocidental
Comportamento Alimentar
Frutas
Neoplasias/terapia
Valor Nutritivo
Verduras
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Ingestão de Energia
Análise Fatorial
Feminino
Seres Humanos
Masculino
Meia-Idade
Avaliação Nutricional
Polônia
Fatores Sexuais
Inquéritos e Questionários
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


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[PMID]:29244870
[Au] Autor:Cedó L; Santos D; Roglans N; Julve J; Pallarès V; Rivas-Urbina A; Llorente-Cortes V; Laguna JC; Blanco-Vaca F; Escolà-Gil JC
[Ad] Endereço:Institut d'Investigacions Biomèdiques (IIB) Sant Pau, Barcelona, Spain.
[Ti] Título:Human hepatic lipase overexpression in mice induces hepatic steatosis and obesity through promoting hepatic lipogenesis and white adipose tissue lipolysis and fatty acid uptake.
[So] Source:PLoS One;12(12):e0189834, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human hepatic lipase (hHL) is mainly localized on the hepatocyte cell surface where it hydrolyzes lipids from remnant lipoproteins and high density lipoproteins and promotes their hepatic selective uptake. Furthermore, hepatic lipase (HL) is closely associated with obesity in multiple studies. Therefore, HL may play a key role on lipid homeostasis in liver and white adipose tissue (WAT). In the present study, we aimed to evaluate the effects of hHL expression on hepatic and white adipose triglyceride metabolism in vivo. Experiments were carried out in hHL transgenic and wild-type mice fed a Western-type diet. Triglyceride metabolism studies included ß-oxidation and de novo lipogenesis in liver and WAT, hepatic triglyceride secretion, and adipose lipoprotein lipase (LPL)-mediated free fatty acid (FFA) lipolysis and influx. The expression of hHL promoted hepatic triglyceride accumulation and de novo lipogenesis without affecting triglyceride secretion, and this was associated with an upregulation of Srebf1 as well as the main genes controlling the synthesis of fatty acids. Transgenic mice also exhibited more adiposity and an increased LPL-mediated FFA influx into the WAT without affecting glucose tolerance. Our results demonstrate that hHL promoted hepatic steatosis in mice mainly by upregulating de novo lipogenesis. HL also upregulated WAT LPL and promoted triglyceride-rich lipoprotein hydrolysis and adipose FFA uptake. These data support the important role of hHL in regulating hepatic lipid homeostasis and confirm the broad cardiometabolic role of HL.
[Mh] Termos MeSH primário: Fígado Gorduroso/genética
Lipase/genética
Obesidade/genética
Proteína de Ligação a Elemento Regulador de Esterol 1/genética
[Mh] Termos MeSH secundário: Tecido Adiposo Branco/metabolismo
Tecido Adiposo Branco/patologia
Animais
Dieta Ocidental
Ácidos Graxos/metabolismo
Fígado Gorduroso/metabolismo
Fígado Gorduroso/patologia
Regulação Enzimológica da Expressão Gênica
Glucose/metabolismo
Seres Humanos
Lipase/biossíntese
Metabolismo dos Lipídeos/genética
Lipogênese/genética
Lipólise/genética
Camundongos
Camundongos Transgênicos
Obesidade/metabolismo
Obesidade/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids); 0 (Srebf1 protein, mouse); 0 (Sterol Regulatory Element Binding Protein 1); EC 3.1.1.3 (Lipase); EC 3.1.1.3 (hepatic lipase, human); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180102
[Lr] Data última revisão:
180102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189834


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[PMID]:28961281
[Au] Autor:Zhang M; Zhao H; Cai J; Li H; Wu Q; Qiao T; Li K
[Ad] Endereço:Department of Vascular Surgery, Drum Tower Clinical Medical College of Nanjing Medical University, Nanjing, P.R. China.
[Ti] Título:Chronic administration of mitochondrion-targeted peptide SS-31 prevents atherosclerotic development in ApoE knockout mice fed Western diet.
[So] Source:PLoS One;12(9):e0185688, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Oxidative stress and inflammatory factors are deeply involved in progression of atherosclerosis. Mitochondrion-targeted peptide SS-31, selectively targeting to mitochondrial inner membrane reacting with cardiolipin, has been reported to inhibit ROS generation and mitigate inflammation. The present study was designed to investigate whether SS-31 could suppress the development of atherosclerosis in vivo. METHODS: Male ApoE-/- mice (8 weeks old) fed with Western diet were treated with normal saline or SS-31 (1 mg/kg/d or 3 mg/kg/d) through subcutaneous injection for 12 weeks. Oil Red O staining was performed to evaluate area and sizes of the plaques. DHE staining and immunohistochemical staining of 8-OHDG was performed to assess the oxidative stress. The aorta ATP contents were assessed by the ATP bioluminescence assay kit. Immunohistochemical staining of CD68 and α-SMA and Masson's trichrome staining were performed to evaluate the composition of atherosclerotic plaque. Biochemical assays were performed to determine the protein level and activity of superoxide dismutase (SOD). The levels of CD36, LOX-1 and ABCA1 were immunohistochemically and biochemically determined to evaluate the cholesterol transport in aorta and peritoneal macrophages. Inflammatory factors, including ICAM-1, MCP-1, IL-6 and CRP in serum, were detected through ELISA. RESULTS: SS-31 administration reduced the area and sizes of western diet-induced atherosclerotic plaques and changed the composition of the plaques in ApoE-/- mice. Oxidative stress was suppressed, as evidenced by the reduced DHE stain, down-regulated 8-OHDG expression, and increased SOD activity after chronic SS-31 administration. Moreover, systemic inflammation was ameliorated as seen by decreasing serum ICAM-1, MCP-1, and IL-6 levels. Most importantly, SS-31 administration inhibited cholesterol influx by down-regulating expression of CD36 and LOX-1 to prevent lipid accumulation to further suppress the foam cell formation and atherosclerotic progression. CONCLUSION: Administration of SS-31 prevents against atherosclerotic formation in ApoE-/- mice suggesting that SS-31 might be considered to be a potential drug to prevent atherosclerotic progression.
[Mh] Termos MeSH primário: Apolipoproteínas E/genética
Aterosclerose/prevenção & controle
Dieta Ocidental
Mitocôndrias/efeitos dos fármacos
Oligopeptídeos/farmacologia
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/biossíntese
Animais
Células Cultivadas
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Estresse Oxidativo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Oligopeptides); 0 (arginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamide); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170930
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185688


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[PMID]:28935758
[Au] Autor:Marcovecchio PM; Thomas GD; Mikulski Z; Ehinger E; Mueller KAL; Blatchley A; Wu R; Miller YI; Nguyen AT; Taylor AM; McNamara CA; Ley K; Hedrick CC
[Ad] Endereço:From the Department of Medicine, University of California San Diego School of Medicine, La Jolla (P.M.M., Y.I.M.); Division of Inflammation Biology, La Jolla Institute for Allergy and Immunology, CA (P.M.M., G.D.T., Z.M., E.E., K.A.L.M., A.B., R.W., K.L., C.C.H.); Department of Cardiology and Circul
[Ti] Título:Scavenger Receptor CD36 Directs Nonclassical Monocyte Patrolling Along the Endothelium During Early Atherogenesis.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2043-2052, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Nonclassical monocytes (NCM) function to maintain vascular homeostasis by crawling or patrolling along the vessel wall. This subset of monocytes responds to viruses, tumor cells, and other pathogens to aid in protection of the host. In this study, we wished to determine how early atherogenesis impacts NCM patrolling in the vasculature. APPROACH AND RESULTS: To study the role of NCM in early atherogenesis, we quantified the patrolling behaviors of NCM in ApoE (apolipoprotein E) and C57BL/6J mice fed a Western diet. Using intravital imaging, we found that NCM from Western diet-fed mice display a 4-fold increase in patrolling activity within large peripheral blood vessels. Both human and mouse NCM preferentially engulfed OxLDL (oxidized low-density lipoprotein) in the vasculature, and we observed that OxLDL selectively induced NCM patrolling in vivo. Induction of patrolling during early atherogenesis required scavenger receptor CD36, as CD36 mice revealed a significant reduction in patrolling activity along the femoral vasculature. Mechanistically, we found that CD36-regulated patrolling was mediated by a SFK (src family kinase) through DAP12 (DNAX activating protein of 12KDa) adaptor protein. CONCLUSIONS: Our studies show a novel pathway for induction of NCM patrolling along the vascular wall during early atherogenesis. Mice fed a Western diet showed increased NCM patrolling activity with a concurrent increase in SFK phosphorylation. This patrolling activity was lost in the absence of either CD36 or DAP12. These data suggest that NCM function in an atheroprotective manner through sensing and responding to oxidized lipoprotein moieties via scavenger receptor engagement during early atherogenesis.
[Mh] Termos MeSH primário: Aterosclerose/metabolismo
Antígenos CD36/metabolismo
Células Endoteliais/metabolismo
Endotélio Vascular/metabolismo
Artéria Femoral/metabolismo
Migração e Rolagem de Leucócitos
Monócitos/metabolismo
[Mh] Termos MeSH secundário: Citoesqueleto de Actina/metabolismo
Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Animais
Apolipoproteínas E/deficiência
Apolipoproteínas E/genética
Aterosclerose/genética
Aterosclerose/patologia
Antígenos CD36/deficiência
Antígenos CD36/genética
Dieta Ocidental
Modelos Animais de Doenças
Células Endoteliais/patologia
Endotélio Vascular/patologia
Artéria Femoral/patologia
Predisposição Genética para Doença
Seres Humanos
Microscopia Intravital
Lipoproteínas LDL/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Knockout
Monócitos/patologia
Fenótipo
Transdução de Sinais
Fatores de Tempo
Quinases da Família src/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Apolipoproteins E); 0 (CD36 Antigens); 0 (Lipoproteins, LDL); 0 (Tyrobp protein, mouse); 0 (oxidized low density lipoprotein); EC 2.7.10.2 (src-Family Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309123


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[PMID]:28827412
[Au] Autor:Liu Z; Zhu H; Dai X; Wang C; Ding Y; Song P; Zou MH
[Ad] Endereço:From the Center for Molecular and Translational Medicine, Georgia State University, Atlanta.
[Ti] Título:Macrophage Liver Kinase B1 Inhibits Foam Cell Formation and Atherosclerosis.
[So] Source:Circ Res;121(9):1047-1057, 2017 Oct 13.
[Is] ISSN:1524-4571
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: LKB1 (liver kinase B1) is a serine/threonine kinase and tumor suppressor, which regulates the homeostasis of hematopoietic cells and immune responses. Macrophages transform into foam cells upon taking-in lipids. No role for LKB1 in foam cell formation has previously been reported. OBJECTIVE: We sought to establish the role of LKB1 in atherosclerotic foam cell formation. METHODS AND RESULTS: LKB1 expression was examined in human carotid atherosclerotic plaques and in western diet-fed atherosclerosis-prone Ldlr and ApoE mice. LKB1 expression was markedly reduced in human plaques when compared with nonatherosclerotic vessels. Consistently, time-dependent reduction of LKB1 levels occurred in atherosclerotic lesions in western diet-fed Ldlr and ApoE mice. Exposure of macrophages to oxidized low-density lipoprotein downregulated LKB1 in vitro. Furthermore, LKB1 deficiency in macrophages significantly increased the expression of SRA (scavenger receptor A), modified low-density lipoprotein uptake and foam cell formation, all of which were abolished by blocking SRA. Further, we found LKB1 phosphorylates SRA resulting in its lysosome degradation. To further investigate the role of macrophage LKB1 in vivo, ApoE LKB1 LysM and ApoE LKB1 mice were fed with western diet for 16 weeks. Compared with ApoE LKB1 wild-type control, ApoE LKB1 LysM mice developed more atherosclerotic lesions in whole aorta and aortic root area, with markedly increased SRA expression in aortic root lesions. CONCLUSIONS: We conclude that macrophage LKB1 reduction caused by oxidized low-density lipoprotein promotes foam cell formation and the progression of atherosclerosis.
[Mh] Termos MeSH primário: Aterosclerose/metabolismo
Células Espumosas/metabolismo
Macrófagos/metabolismo
Músculo Liso Vascular/metabolismo
Proteínas Serina-Treonina Quinases/deficiência
[Mh] Termos MeSH secundário: Animais
Aterosclerose/etiologia
Aterosclerose/patologia
Dieta Ocidental/efeitos adversos
Células Espumosas/patologia
Seres Humanos
Lipoproteínas LDL/metabolismo
Macrófagos/patologia
Masculino
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Músculo Liso Vascular/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipoproteins, LDL); EC 2.7.1.- (STK11 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCRESAHA.117.311546


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[PMID]:28764846
[Au] Autor:Aroor AR; Jia G; Habibi J; Sun Z; Ramirez-Perez FI; Brady B; Chen D; Martinez-Lemus LA; Manrique C; Nistala R; Whaley-Connell AT; Demarco VG; Meininger GA; Sowers JR
[Ad] Endereço:Diabetes and Cardiovascular Research Center, Department of Medicine, University of Missouri Columbia, School of Medicine, Columbia, MO 65212, USA; Research Service Harry S Truman Memorial Veterans Hospital, University of Missouri School of Medicine, Columbia, MO 65212, USA. Electronic address: aroor
[Ti] Título:Uric acid promotes vascular stiffness, maladaptive inflammatory responses and proteinuria in western diet fed mice.
[So] Source:Metabolism;74:32-40, 2017 Sep.
[Is] ISSN:1532-8600
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Aortic vascular stiffness has been implicated in the development of cardiovascular disease (CVD) and chronic kidney disease (CKD) in obese individuals. However, the mechanism promoting these adverse effects are unclear. In this context, promotion of obesity through consumption of a western diet (WD) high in fat and fructose leads to excess circulating uric acid. There is accumulating data implicating elevated uric acid in the promotion of CVD and CKD. Accordingly, we hypothesized that xanthine oxidase(XO) inhibition with allopurinol would prevent a rise in vascular stiffness and proteinuria in a translationally relevant model of WD-induced obesity. MATERIALS/METHODS: Four-week-old C57BL6/J male mice were fed a WD with excess fat (46%) and fructose (17.5%) with or without allopurinol (125mg/L in drinking water) for 16weeks. Aortic endothelial and extracellular matrix/vascular smooth muscle stiffness was evaluated by atomic force microscopy. Aortic XO activity, 3-nitrotyrosine (3-NT) and aortic endothelial sodium channel (EnNaC) expression were evaluated along with aortic expression of inflammatory markers. In the kidney, expression of toll like receptor 4 (TLR4) and fibronectin were assessed along with evaluation of proteinuria. RESULTS: XO inhibition significantly attenuated WD-induced increases in plasma uric acid, vascular XO activity and oxidative stress, in concert with reductions in proteinuria. Further, XO inhibition prevented WD-induced increases in aortic EnNaC expression and associated endothelial and subendothelial stiffness. XO inhibition also reduced vascular pro-inflammatory and maladaptive immune responses induced by consumption of a WD. XO inhibition also decreased WD-induced increases in renal TLR4 and fibronectin that associated proteinuria. CONCLUSIONS: Consumption of a WD leads to elevations in plasma uric acid, increased vascular XO activity, oxidative stress, vascular stiffness, and proteinuria all of which are attenuated with allopurinol administration.
[Mh] Termos MeSH primário: Dieta Ocidental
Inflamação/induzido quimicamente
Proteinúria/induzido quimicamente
Ácido Úrico/sangue
Rigidez Vascular/efeitos dos fármacos
[Mh] Termos MeSH secundário: Alopurinol/administração & dosagem
Alopurinol/farmacologia
Animais
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Ácido Úrico/farmacologia
Xantina Oxidase/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
268B43MJ25 (Uric Acid); 63CZ7GJN5I (Allopurinol); EC 1.17.3.2 (Xanthine Oxidase)
[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:170803
[St] Status:MEDLINE


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[PMID]:28739253
[Au] Autor:West G; Rodia C; Li D; Johnson Z; Dong H; Kohan AB
[Ad] Endereço:Department of Nutritional Sciences, University of Connecticut, 1392 Storrs Rd, Storrs, CT 06269-4017, United States.
[Ti] Título:Key differences between apoC-III regulation and expression in intestine and liver.
[So] Source:Biochem Biophys Res Commun;491(3):747-753, 2017 Sep 23.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ApoC-III is a critical cardiovascular risk factor, and humans expressing null mutations in apoC-III are robustly protected from cardiovascular disease. Because of its critical role in elevating plasma lipids and CVD risk, hepatic apoC-III regulation has been studied at length. Considerably less is known about the factors that regulate intestinal apoC-III. In this work, we use primary murine enteroids, Caco-2 cells, and dietary studies in wild-type mice to show that intestinal apoC-III expression does not change in response to fatty acids, glucose, or insulin administration, in contrast to hepatic apoC-III. Intestinal apoC-III is not sensitive to changes in FoxO1 expression (which is itself very low in the intestine, as is FoxO1 target IGFBP-1), nor is intestinal apoC-III responsive to western diet, a significant contrast to hepatic apoC-III stimulation during western diet. These data strongly suggest that intestinal apoC-III is not a FoxO1 target and support the idea that apoC-III is not regulated coordinately with hepatic apoC-III, and establishes another key aspect of apoC-III that is unique in the intestine from the liver.
[Mh] Termos MeSH primário: Apolipoproteína C-III/metabolismo
Proteína Forkhead Box O1/metabolismo
Regulação da Expressão Gênica/fisiologia
Intestinos/metabolismo
Metabolismo dos Lipídeos/fisiologia
Fígado/metabolismo
[Mh] Termos MeSH secundário: Animais
Células CACO-2
Dieta Ocidental
Feminino
Glucose/metabolismo
Seres Humanos
Técnicas In Vitro
Insulina/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Especificidade de Órgãos/fisiologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoprotein C-III); 0 (Forkhead Box Protein O1); 0 (Foxo1 protein, mouse); 0 (Insulin); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE


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[PMID]:28724546
[Au] Autor:Wang L; Jacobs JP; Lagishetty V; Yuan PQ; Wu SV; Million M; Reeve JR; Pisegna JR; Taché Y
[Ad] Endereço:CURE/Digestive Diseases Research Center and Center for Neurobiology of Stress and Resilience, Department of Medicine, Vatche and Tamar Manoukian Digestive Diseases Division, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California; and Lixinw@ucla.edu.
[Ti] Título:High-protein diet improves sensitivity to cholecystokinin and shifts the cecal microbiome without altering brain inflammation in diet-induced obesity in rats.
[So] Source:Am J Physiol Regul Integr Comp Physiol;313(4):R473-R486, 2017 Oct 01.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:High-protein diet (HPD) curtails obesity and/or fat mass, but it is unknown whether it reverses neuroinflammation or alters glucose levels, CCK sensitivity, and gut microbiome in rats fed a Western diet (WD)-induced obesity (DIO). Male rats fed a WD (high fat and sugar) for 12 wk were switched to a HPD for 6 wk. Body composition, food intake, meal pattern, sensitivity to intraperitoneal CCK-8S, blood glucose, brain signaling, and cecal microbiota were assessed. When compared with a normal diet, WD increased body weight (9.3%) and fat mass (73.4%). CCK-8S (1.8 or 5.2 nmol/kg) did not alter food intake and meal pattern in DIO rats. Switching to a HPD for 6 wk reduced fat mass (15.7%) with a nonsignificantly reduced body weight gain, normalized blood glucose, and decreased feeding after CCK-8S. DIO rats on the WD or switched to a HPD showed comparable microbial diversity. However, in HPD versus WD rats, there was enrichment of 114 operational taxonomic units (OTUs) and depletion of 188 OTUs. Of those, (enriched on a HPD), an unclassified Clostridiales, a member of the RF39 order, and a were significantly associated with fat mass. The WD increased cytokine expression in the hypothalamus and dorsal medulla that was unchanged by switching to HPD. These data indicate that HPD reduces body fat and restores glucose homeostasis and CCK sensitivity, while not modifying brain inflammation. In addition, expansion of cecal correlated to fat mass loss may represent a potential peripheral mechanism of HPD beneficial effects.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Ceco/efeitos dos fármacos
Colecistocinina/farmacologia
Proteínas na Dieta/farmacologia
Encefalite/metabolismo
Microbiota/efeitos dos fármacos
Obesidade/microbiologia
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
Composição Corporal/efeitos dos fármacos
Peso Corporal/efeitos dos fármacos
Encéfalo/metabolismo
Ceco/metabolismo
Ceco/microbiologia
Citocinas/metabolismo
Dieta Ocidental
Ingestão de Alimentos/efeitos dos fármacos
Masculino
Obesidade/metabolismo
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Cytokines); 0 (Dietary Proteins); 9011-97-6 (Cholecystokinin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00105.2017


  9 / 382 MEDLINE  
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[PMID]:28722707
[Au] Autor:Zitvogel L; Pietrocola F; Kroemer G
[Ad] Endereço:Gustave Roussy Cancer Campus, Villejuif, France.
[Ti] Título:Nutrition, inflammation and cancer.
[So] Source:Nat Immunol;18(8):843-850, 2017 Jul 19.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Quantitative and qualitative aspects of nutrition have a profound effect on leukocytes and thereby affect proinflammatory carcinogenic effects or anticancer immune responses. As a result, nutrition affects the incidence, natural progression and therapeutic response of malignant diseases, both in humans and in preclinical animal models. Here we discuss the molecular mechanisms through which alimentary cues modulate metabolic, microbial and neuroendocrine circuitries and thus affect the probability of developing premalignant lesions that progress to clinically manifested disease and the response to therapeutic intervention. We examine each of the connections that compose the triangle of nutrition, immunological and inflammatory reactions and cancer while focusing on the mechanistic aspects of these relationships.
[Mh] Termos MeSH primário: Inflamação/imunologia
Síndrome Metabólica/imunologia
Microbiota/imunologia
Neoplasias/imunologia
Obesidade/imunologia
[Mh] Termos MeSH secundário: Dieta
Dieta Ocidental
Seres Humanos
Hipernutrição/imunologia
Fatores de Risco
Vitaminas
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Vitamins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170720
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3754


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[PMID]:28711154
[Au] Autor:Jena PK; Sheng L; Liu HX; Kalanetra KM; Mirsoian A; Murphy WJ; French SW; Krishnan VV; Mills DA; Wan YY
[Ad] Endereço:Department of Medical Pathology and Laboratory Medicine, University of California, Davis, Sacramento, California.
[Ti] Título:Western Diet-Induced Dysbiosis in Farnesoid X Receptor Knockout Mice Causes Persistent Hepatic Inflammation after Antibiotic Treatment.
[So] Source:Am J Pathol;187(8):1800-1813, 2017 Aug.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Patients who have liver cirrhosis and liver cancer also have reduced farnesoid X receptor (FXR). The current study analyzes the effect of diet through microbiota that affect hepatic inflammation in FXR knockout (KO) mice. Wild-type and FXR KO mice were on a control (CD) or Western diet (WD) for 10 months. In addition, both CD- and WD-fed FXR KO male mice, which had hepatic lymphocyte and neutrophil infiltration, were treated by vancomycin, polymyxin B, and Abx (ampicillin, neomycin, metronidazole, and vancomycin). Mice were subjected to morphological analysis as well as gut microbiota and bile acid profiling. Male WD-fed FXR KO mice had the most severe steatohepatitis. FXR KO also had reduced Firmicutes and increased Proteobacteria, which could be reversed by Abx. In addition, Abx eliminated hepatic neutrophils and lymphocytes in CD-fed, but not WD-fed, FXR KO mice. Proteobacteria and Bacteroidetes persisted in WD-fed FXR KO mice even after Abx treatment. Only polymyxin B could reduce hepatic lymphocytes in WD-fed FXR KO mice. The reduced hepatic inflammation by antibiotics was accompanied by decreased free and conjugated secondary bile acids as well as changes in gut microbiota. Our data revealed that Lactococcus, Lactobacillus, and Coprococcus protect the liver from inflammation.
[Mh] Termos MeSH primário: Dieta Ocidental/efeitos adversos
Disbiose/patologia
Fígado Gorduroso/patologia
Inflamação/patologia
Fígado/patologia
Receptores Citoplasmáticos e Nucleares/metabolismo
[Mh] Termos MeSH secundário: Animais
Antibacterianos/farmacologia
Disbiose/etiologia
Disbiose/metabolismo
Disbiose/microbiologia
Fígado Gorduroso/etiologia
Fígado Gorduroso/metabolismo
Fígado Gorduroso/microbiologia
Inflamação/metabolismo
Inflamação/microbiologia
Fígado/efeitos dos fármacos
Fígado/metabolismo
Fígado/microbiologia
Linfócitos/efeitos dos fármacos
Linfócitos/metabolismo
Linfócitos/patologia
Masculino
Camundongos
Camundongos Knockout
Microbiota
Infiltração de Neutrófilos
Receptores Citoplasmáticos e Nucleares/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Receptors, Cytoplasmic and Nuclear); 0 (farnesoid X-activated receptor)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170717
[St] Status:MEDLINE



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