Base de dados : MEDLINE
Pesquisa : D10.351.303 [Categoria DeCS]
Referências encontradas : 7113 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 712 ir para página                         

  1 / 7113 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28460635
[Au] Autor:Chen I; Mathews-Greiner L; Li D; Abisoye-Ogunniyan A; Ray S; Bian Y; Shukla V; Zhang X; Guha R; Thomas C; Gryder B; Zacharia A; Beane JD; Ravichandran S; Ferrer M; Rudloff U
[Ad] Endereço:Thoracic and Gastrointestinal Oncology Branch, National Cancer Institute, National Institutes for Health, CCR 4 West/4-3740, 10 Center Drive, Bethesda, MD, 20892-0001, USA.
[Ti] Título:Transcriptomic profiling and quantitative high-throughput (qHTS) drug screening of CDH1 deficient hereditary diffuse gastric cancer (HDGC) cells identify treatment leads for familial gastric cancer.
[So] Source:J Transl Med;15(1):92, 2017 May 01.
[Is] ISSN:1479-5876
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Patients with hereditary diffuse gastric cancer (HDGC), a cancer predisposition syndrome associated with germline mutations of the CDH1 (E-cadherin) gene, have few effective treatment options. Despite marked differences in natural history, histopathology, and genetic profile to patients afflicted by sporadic gastric cancer, patients with HDGC receive, in large, identical systemic regimens. The lack of a robust preclinical in vitro system suitable for effective drug screening has been one of the obstacles to date which has hampered therapeutic advances in this rare disease. METHODS: In order to identify therapeutic leads selective for the HDGC subtype of gastric cancer, we compared gene expression profiles and drug phenotype derived from an oncology library of 1912 compounds between gastric cancer cells established from a patient with metastatic HDGC harboring a c.1380delA CDH1 germline variant and sporadic gastric cancer cells. RESULTS: Unsupervised hierarchical cluster analysis shows select gene expression alterations in c.1380delA CDH1 SB.mhdgc-1 cells compared to a panel of sporadic gastric cancer cell lines with enrichment of ERK1-ERK2 (extracellular signal regulated kinase) and IP3 (inositol trisphosphate)/DAG (diacylglycerol) signaling as the top networks in c.1380delA SB.mhdgc-1 cells. Intracellular phosphatidylinositol intermediaries were increased upon direct measure in c.1380delA CDH1 SB.mhdgc-1 cells. Differential high-throughput drug screening of c.1380delA CDH1 SB.mhdgc-1 versus sporadic gastric cancer cells identified several compound classes with enriched activity in c.1380 CDH1 SB.mhdgc-1 cells including mTOR (Mammalian Target Of Rapamycin), MEK (Mitogen-Activated Protein Kinase), c-Src kinase, FAK (Focal Adhesion Kinase), PKC (Protein Kinase C), or TOPO2 (Topoisomerase II) inhibitors. Upon additional drug response testing, dual PI3K (Phosphatidylinositol 3-Kinase)/mTOR and topoisomerase 2A inhibitors displayed up to >100-fold increased activity in hereditary c.1380delA CDH1 gastric cancer cells inducing apoptosis most effectively in cells with deficient CDH1 function. CONCLUSION: Integrated pharmacological and transcriptomic profiling of hereditary diffuse gastric cancer cells with a loss-of-function c.1380delA CDH1 mutation implies various pharmacological vulnerabilities selective to CDH1-deficient familial gastric cancer cells and suggests novel treatment leads for future preclinical and clinical treatment studies of familial gastric cancer.
[Mh] Termos MeSH primário: Caderinas/deficiência
Avaliação Pré-Clínica de Medicamentos
Perfilação da Expressão Gênica
Ensaios de Triagem em Larga Escala
Neoplasias Gástricas/tratamento farmacológico
Neoplasias Gástricas/genética
[Mh] Termos MeSH secundário: Adulto
Caderinas/genética
Linhagem Celular Tumoral
Diglicerídeos/metabolismo
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Feminino
Regulação Neoplásica da Expressão Gênica
Predisposição Genética para Doença
Mutação em Linhagem Germinativa/genética
Seres Humanos
Fosfatos de Inositol/metabolismo
Masculino
Linhagem
Reprodutibilidade dos Testes
Neoplasias Gástricas/patologia
Regulação para Cima/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDH1 protein, human); 0 (Cadherins); 0 (Diglycerides); 0 (Inositol Phosphates); 0 (inositol 3,4,5-trisphosphate); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1186/s12967-017-1197-5


  2 / 7113 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29261777
[Au] Autor:Noll F; Behnke J; Leiting S; Troidl K; Alves GT; Müller-Redetzky H; Preissner KT; Fischer S
[Ad] Endereço:Institute of Biochemistry, Medical School, Justus-Liebig-University, Giessen, Germany.
[Ti] Título:Self-extracellular RNA acts in synergy with exogenous danger signals to promote inflammation.
[So] Source:PLoS One;12(12):e0190002, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Self-extracellular RNA (eRNA), released from stressed or injured cells upon various pathological situations such as ischemia-reperfusion-injury, has been shown to act as an alarmin by inducing procoagulatory and proinflammatory responses. In particular, M1-polarization of macrophages by eRNA resulted in the expression and release of a variety of cytokines, including tumor necrosis factor (TNF)-α or interleukin-6 (IL-6). The present study now investigates in which way self-eRNA may influence the response of macrophages towards various Toll-like receptor (TLR)-agonists. Isolated agonists of TLR2 (Pam2CSK4), TLR3 (PolyIC), TLR4 (LPS), or TLR7 (R848) induced the release of TNF-α in a concentration-dependent manner in murine macrophages, differentiated from bone marrow-derived stem cells by mouse colony stimulating factor. Here, the presence of eRNA shifted the dose-response curve for Pam2CSK4 (Pam) considerably to the left, indicating that eRNA synergistically enhanced the cytokine liberation from macrophages even at very low Pam-levels. The synergistic activation of TLR2 by eRNA/Pam was duplicated by other TLR2-agonists such as FSL-1 or Pam3CSK4. In contrast, for TLR4-agonists such as LPS a synergistic effect of eRNA was much weaker, and was not existent for TLR3-, or TLR7-agonists. The synergistic eRNA/Pam action was dependent on the NFκB-signaling pathway as well as on p38MAP- and MEK1/ERK-kinases and was prevented by predigestion of eRNA with RNase1 or by antibodies against TLR2. Thus, the presence of self-eRNA as alarming molecule sensitizes innate immune responses towards pathogen-associated molecular patterns (PAMPs) in a synergistic way and may thereby contribute to the differentiated outcome of inflammatory responses.
[Mh] Termos MeSH primário: Espaço Extracelular/metabolismo
Inflamação/metabolismo
RNA/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Citocinas/metabolismo
Diglicerídeos/farmacologia
Lipopeptídeos/farmacologia
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Camundongos Endogâmicos C57BL
Oligopeptídeos/farmacologia
Padrões Moleculares Associados a Patógenos/metabolismo
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
Receptores Toll-Like/antagonistas & inibidores
Receptores Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Diglycerides); 0 (FSL-1 lipoprotein, synthetic); 0 (Lipopeptides); 0 (Oligopeptides); 0 (Pam2CSK4 lipopeptide); 0 (Pathogen-Associated Molecular Pattern Molecules); 0 (Toll-Like Receptors); 63231-63-0 (RNA)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190002


  3 / 7113 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28465188
[Au] Autor:Honda H; Kawamoto T; Doi Y; Matsumura S; Ito Y; Imai N; Ikeda N; Mera Y; Morita O
[Ad] Endereço:R&D Safety Science Research, Kao Corporation, 2606 Akabane, Ichikai-machi, Haga-gun, Tochigi 321-3497, Japan. Electronic address: honda.hiroshi@kao.co.jp.
[Ti] Título:Alpha-linolenic acid-enriched diacylglycerol oil does not promote tumor development in tongue and gastrointestinal tract tissues in a medium-term multi-organ carcinogenesis bioassay using male F344 rat.
[So] Source:Food Chem Toxicol;106(Pt A):185-192, 2017 Aug.
[Is] ISSN:1873-6351
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Alpha-linolenic acid (ALA)-enriched diacylglycerol (DAG) oil is an edible oil enriched with DAG (>80%) and ALA (>50%). The present study investigated whether ALA-DAG oil promotes tumorigenesis in the tongue and gastrointestinal tract, using a rat medium-term multi-organ carcinogenesis bioassay model. Rats were treated with five genotoxic carcinogens to induce multi-organ tumorigenesis until week 4, and from 1 week after withdrawal, fed a semi-synthetic diet (AIN-93G) containing ALA-DAG oil at concentrations of 0, 13,750, 27,500, and 55,000 ppm. Rats fed AIN-93G containing 55,000 ppm ALA-triacylglycerol or a standard basal diet served as reference and negative control groups, respectively. Animals were euthanized at week 30. ALA-DAG oil was shown to have no effects on survival, general condition, body weight, food consumption, or organ weight. More discolored spots were observed in the stomachs of the 13,750- and 55,000-ppm ALA-DAG groups than in those of the control groups; however, there were no differences in the frequency of histopathological findings across groups. There were no meaningful increases in the incidence of pre-neoplastic and neoplastic lesions in the tongue and gastrointestinal tract among the groups. We therefore conclude that ALA-DAG oil does not promote tumor development in the digestive system.
[Mh] Termos MeSH primário: Diglicerídeos/farmacologia
Trato Gastrointestinal/efeitos dos fármacos
Língua/efeitos dos fármacos
Ácido alfa-Linolênico/farmacologia
[Mh] Termos MeSH secundário: Animais
Bioensaio
Testes de Carcinogenicidade
Diglicerídeos/análise
Trato Gastrointestinal/patologia
Masculino
Ratos
Ratos Endogâmicos F344
Língua/patologia
Ácido alfa-Linolênico/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Diglycerides); 0RBV727H71 (alpha-Linolenic Acid)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  4 / 7113 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28768703
[Au] Autor:Lundsgaard AM; Sjøberg KA; Høeg LD; Jeppesen J; Jordy AB; Serup AK; Fritzen AM; Pilegaard H; Myrmel LS; Madsen L; Wojtaszewski JFP; Richter EA; Kiens B
[Ad] Endereço:Section of Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.
[Ti] Título:Opposite Regulation of Insulin Sensitivity by Dietary Lipid Versus Carbohydrate Excess.
[So] Source:Diabetes;66(10):2583-2595, 2017 Oct.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To understand the mechanisms in lipid-induced insulin resistance, a more physiological approach is to enhance fatty acid (FA) availability through the diet. Nine healthy men ingested two hypercaloric diets (in 75% excess of habitual caloric intake) for 3 days, enriched in unsaturated FA (78 energy % [E%] fat) (UNSAT) or carbohydrates (80 E% carbohydrate) (CHO) as well as a eucaloric control diet (CON). Compared with CON, the UNSAT diet reduced whole-body and leg glucose disposal during a hyperinsulinemic-euglycemic clamp, while decreasing hepatic glucose production. In muscle, diacylglycerol (DAG) and intramyocellular triacylglycerol were increased. The accumulated DAG was -1,3 DAG, which is known not to activate PKC, and insulin signaling was intact. UNSAT decreased PDH-E1α protein content and increased inhibitory PDH-E1α Ser phosphorylation and FA oxidation. CHO increased whole-body and leg insulin sensitivity, while increasing hepatic glucose production. After CHO, muscle PDH-E1α Ser phosphorylation was decreased, and glucose oxidation increased. After UNSAT, but not CHO, muscle glucose-6-phosphate content was 103% higher compared with CON during the clamp. Thus, PDH-E1α expression and covalent regulation, and hence the tricarboxylic acid cycle influx of pyruvate-derived acetyl-CoA relative to ß-oxidation-derived acetyl-CoA, are suggested to impact on insulin-stimulated glucose uptake. Taken together, the oxidative metabolic fluxes of glucose and FA are powerful and opposite regulators of insulin action in muscle.
[Mh] Termos MeSH primário: Metabolismo dos Carboidratos/fisiologia
Gorduras na Dieta/efeitos adversos
Resistência à Insulina/fisiologia
[Mh] Termos MeSH secundário: Adulto
Ciclo do Ácido Cítrico/genética
Ciclo do Ácido Cítrico/fisiologia
Diglicerídeos/metabolismo
Ácidos Graxos/sangue
Ácidos Graxos/metabolismo
Seres Humanos
Fígado/metabolismo
Masculino
Músculo Esquelético/metabolismo
Oxirredução
Fosforilação/genética
Fosforilação/fisiologia
Piruvato Desidrogenase (Lipoamida)/genética
Piruvato Desidrogenase (Lipoamida)/metabolismo
Triglicerídeos/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dietary Fats); 0 (Diglycerides); 0 (Fatty Acids); 0 (Triglycerides); EC 1.2.4.1 (Pyruvate Dehydrogenase (Lipoamide)); EC 1.2.4.1 (pyruvate dehydrogenase E1alpha subunit)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.2337/db17-0046


  5 / 7113 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28716882
[Au] Autor:Zhang Z; Meszaros G; He WT; Xu Y; de Fatima Magliarelli H; Mailly L; Mihlan M; Liu Y; Puig Gámez M; Goginashvili A; Pasquier A; Bielska O; Neven B; Quartier P; Aebersold R; Baumert TF; Georgel P; Han J; Ricci R
[Ad] Endereço:Institut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, France.
[Ti] Título:Protein kinase D at the Golgi controls NLRP3 inflammasome activation.
[So] Source:J Exp Med;214(9):2671-2693, 2017 Sep 04.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The inflammasomes are multiprotein complexes sensing tissue damage and infectious agents to initiate innate immune responses. Different inflammasomes containing distinct sensor molecules exist. The NLRP3 inflammasome is unique as it detects a variety of danger signals. It has been reported that NLRP3 is recruited to mitochondria-associated endoplasmic reticulum membranes (MAMs) and is activated by MAM-derived effectors. Here, we show that in response to inflammasome activators, MAMs localize adjacent to Golgi membranes. Diacylglycerol (DAG) at the Golgi rapidly increases, recruiting protein kinase D (PKD), a key effector of DAG. Upon PKD inactivation, self-oligomerized NLRP3 is retained at MAMs adjacent to Golgi, blocking assembly of the active inflammasome. Importantly, phosphorylation of NLRP3 by PKD at the Golgi is sufficient to release NLRP3 from MAMs, resulting in assembly of the active inflammasome. Moreover, PKD inhibition prevents inflammasome autoactivation in peripheral blood mononuclear cells from patients carrying NLRP3 mutations. Hence, Golgi-mediated PKD signaling is required and sufficient for NLRP3 inflammasome activation.
[Mh] Termos MeSH primário: Complexo de Golgi/fisiologia
Inflamassomos/fisiologia
Proteína 3 que Contém Domínio de Pirina da Família NLR/fisiologia
Proteína Quinase C/fisiologia
[Mh] Termos MeSH secundário: Animais
Diglicerídeos/metabolismo
Retículo Endoplasmático/fisiologia
Seres Humanos
Leucócitos Mononucleares/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fosforilação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Diglycerides); 0 (Inflammasomes); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (Nlrp3 protein, mouse); EC 2.7.10.- (protein kinase D); EC 2.7.11.13 (Protein Kinase C)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20162040


  6 / 7113 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28671468
[Au] Autor:Ohashi N; Kobayashi R; Nomura W; Kobayakawa T; Czikora A; Herold BK; Lewin NE; Blumberg PM; Tamamura H
[Ad] Endereço:Department of Medicinal Chemistry, Institute of Biomaterials and Bioengineering, Tokyo Medical and Dental University , 2-3-10 Kandasurugadai, Chiyoda-ku, Tokyo 101-0062, Japan.
[Ti] Título:Synthesis and Evaluation of Dimeric Derivatives of Diacylglycerol-Lactones as Protein Kinase C Ligands.
[So] Source:Bioconjug Chem;28(8):2135-2144, 2017 Aug 16.
[Is] ISSN:1520-4812
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Protein kinase C (PKC) mediates a central cellular signal transduction pathway involved in disorders such as cancer and Alzheimer's disease. PKC is regulated by binding of the second messenger sn-1,2-diacylglycerol (DAG) to its tandem C1 domains, designated C1a and C1b, leading both to PKC activation and to its translocation to the plasma membrane and to internal organelles. Depending on the isoform, there may be differences in the ligand selectivity of the C1a and C1b domains, and there is different spacing between the C1 domains of the conventional and novel PKCs. Bivalent ligands have the potential to exploit these differences between isoforms, yielding isoform selectivity. In the present study, we describe the synthesis of a series of dimeric derivatives of conformationally constrained diacylglycerol (DAG) analogs (DAG-lactones). We characterize the derivatives in vitro for their binding affinities, both to a single C1 domain (the C1b domain of PKCδ) as well as to the conventional PKCα isoform and the novel PKCδ isoform, and we measure their abilities to cause translocation of PKCδ and PKCε in intact cells. The dimeric compound with the 10-carbon linker was modestly more effective for the isolated PKCδ C1b domain than was the monomeric compound. For the intact PKCα and PKCδ, the shortest DAG-lactone dimer had similar affinity to the monomer and affinity decreased progressively up to the 16-carbon linker. The dimeric derivatives did not cause the Golgi accumulation of PKCδ. The present results provide important insights into the development of new chemical tools for biological studies on PKC.
[Mh] Termos MeSH primário: Diglicerídeos/química
Dimerização
Lactonas/síntese química
Lactonas/metabolismo
Proteína Quinase C-delta/química
Proteína Quinase C-delta/metabolismo
[Mh] Termos MeSH secundário: Animais
Células CHO
Técnicas de Química Sintética
Cricetinae
Cricetulus
Lactonas/química
Ligantes
Modelos Moleculares
Domínios Proteicos
Transporte Proteico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (1,2-diacylglycerol); 0 (Diglycerides); 0 (Lactones); 0 (Ligands); EC 2.7.11.13 (Protein Kinase C-delta)
[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:170704
[St] Status:MEDLINE
[do] DOI:10.1021/acs.bioconjchem.7b00299


  7 / 7113 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28573851
[Au] Autor:Sánchez DA; Tonetto GM; Ferreira ML
[Ad] Endereço:Planta Piloto de Ingeniería Química (PLAPIQUI), Universidad Nacional del Sur (UNS)-CONICET , Camino La Carrindanga Km 7, CC 717, 8000 Bahía Blanca, Argentina.
[Ti] Título:Screening of Lipases with Unusual High Activity in the sn-2 Esterification of 1,3-Dicaprin under Mild Operating Conditions.
[So] Source:J Agric Food Chem;65(24):5010-5017, 2017 Jun 21.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this work, the synthesis of acylglycerides with high nutritional value was carried out by enzymatic esterification at sn-2 position of 1,3-dicaprin with palmitic acid. A comparative study of the performance of several biocatalysts according to the obtained products was carried out. The results obtained with several of the biocatalysts evaluated are very interesting, and it would be possible to use them to obtain a mixture of acylglycerides to act as a fat substitute. The final product was composed of about 90% of nutritionally attractive glycerides. These glycerides were medium-chain length triglycerides, medium-long chain triglycerides (mainly triglycerides with medium chain fatty acids at sn-1 and sn-3 positions and long chain fatty acid at sn-2 position), and 1,3-diglycerides. Pseudomonas fluorescens lipase and Burkholderia cepacia lipase immobilized on chitosan demonstrated unusual high activity in the sn-2 esterification of 1,3-dicaprin with palmitic acid at 45 °C and 12 h with 33% yield to 1,3-dicaproyl-2-palmitoyl glycerol. Burkholderia cepacia lipase has the advantage of being immobilized; however, BCL/chitosan has the advantages of being immobilized and therefore its easy recovery from the reaction media.
[Mh] Termos MeSH primário: Proteínas de Bactérias/química
Burkholderia cepacia/enzimologia
Diglicerídeos/química
Proteínas Fúngicas/química
Lipase/química
Pseudomonas fluorescens/enzimologia
Rhizomucor/enzimologia
[Mh] Termos MeSH secundário: Biocatálise
Enzimas Imobilizadas/química
Esterificação
Estrutura Molecular
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Diglycerides); 0 (Enzymes, Immobilized); 0 (Fungal Proteins); 17598-93-5 (1,3-didecanoylglycerol); EC 3.1.1.3 (Lipase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170703
[Lr] Data última revisão:
170703
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b01327


  8 / 7113 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28551355
[Au] Autor:Petersen MC; Shulman GI
[Ad] Endereço:Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06520, USA.
[Ti] Título:Roles of Diacylglycerols and Ceramides in Hepatic Insulin Resistance.
[So] Source:Trends Pharmacol Sci;38(7):649-665, 2017 Jul.
[Is] ISSN:1873-3735
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Although ample evidence links hepatic lipid accumulation with hepatic insulin resistance, the mechanistic basis of this association is incompletely understood and controversial. Diacylglycerols (DAGs) and ceramides have emerged as the two best-studied putative mediators of lipid-induced hepatic insulin resistance. Both lipids were first associated with insulin resistance in skeletal muscle and were subsequently hypothesized to mediate insulin resistance in the liver. However, the putative roles for DAGs and ceramides in hepatic insulin resistance have proved more complex than originally imagined, with various genetic and pharmacologic manipulations yielding a vast and occasionally contradictory trove of data to sort. In this review we examine the state of this field, turning a critical eye toward both DAGs and ceramides as putative mediators of lipid-induced hepatic insulin resistance.
[Mh] Termos MeSH primário: Ceramidas/metabolismo
Diglicerídeos/metabolismo
Resistência à Insulina
Hepatopatia Gordurosa não Alcoólica/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Ceramides); 0 (Diglycerides)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170529
[St] Status:MEDLINE


  9 / 7113 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28515375
[Au] Autor:Satou C; Goto H; Yamazaki Y; Saitou K; Matsumoto S; Takahashi O; Miyazaki Y; Ikuta K; Yajima Y
[Ad] Endereço:The Nisshin OilliO Group.
[Ti] Título:Modified Gas Chromatographic Method to Determine Monoacylglycerol and Diacylglycerol Contents in Edible Fats and Oils.
[So] Source:J Oleo Sci;66(6):601-606, 2017 Jun 01.
[Is] ISSN:1347-3352
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Monoacylglycerol (MAG) and diacylglycerol (DAG) are minor components of edible fats and oils, and they relate to the quality of these foods. The AOCS official method Cd 11b-91 has been used to determine MAG and DAG contents in fats and oils. There are, however, difficulties in the determination of MAG and DAG using this analytical procedure. Therefore, we improved this method by modifying the trimethylsilyl derivatization procedure and replacing the internal standard (IS) material. In our modified method, TMS-HT (mixture of hexamethyldisilazane and trimethylchlorosilane) was used for derivatization of MAG and DAG, which was followed by liquid-liquid extraction with water and n-hexane solution containing the IS, tricaprin. Using the modified method, we demonstrated superior repeatability in comparison with that of the AOCS method by reducing procedural difficulties. The relative standard deviation of distearin peak areas was 1.8% or 2.9% in the modified method, while it was 5.6% in the AOCS method. In addition, capillary columns, such as DB-1ht and DB-5ht could be used in this method.
[Mh] Termos MeSH primário: Cromatografia Gasosa/métodos
Gorduras Insaturadas na Dieta/análise
Gorduras na Dieta/análise
Diglicerídeos/análise
Monoglicerídeos/análise
[Mh] Termos MeSH secundário: Qualidade dos Alimentos
Hexanos
Extração Líquido-Líquido/métodos
Compostos de Organossilício
Reprodutibilidade dos Testes
Soluções
Triglicerídeos
Compostos de Trimetilsilil
Água
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dietary Fats); 0 (Dietary Fats, Unsaturated); 0 (Diglycerides); 0 (Hexanes); 0 (Monoglycerides); 0 (Organosilicon Compounds); 0 (Solutions); 0 (Triglycerides); 0 (Trimethylsilyl Compounds); 059QF0KO0R (Water); 2DDG612ED8 (n-hexane); 62UO4690X6 (trimethylchlorosilane); H36C68P1BH (hexamethylsilazane); O1PB8EU98M (tricaprin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.5650/jos.ess16143


  10 / 7113 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28505428
[Au] Autor:Stewart MD; Igumenova TI
[Ad] Endereço:Department of Biochemistry and Biophysics, Texas A&M University , College Station, Texas 77843, United States.
[Ti] Título:Toggling of Diacylglycerol Affinity Correlates with Conformational Plasticity in C1 Domains.
[So] Source:Biochemistry;56(21):2637-2640, 2017 May 30.
[Is] ISSN:1520-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Conserved homology-1 (C1) domains are peripheral membrane domains that target their host proteins to diacylglycerol (DAG)-containing membranes. It has been previously shown that a conservative aromatic mutation of a single residue in the C1 domain has a profound effect on DAG affinity. We report that the "DAG-toggling" mutation changes the conformational dynamics of the loop region that forms the binding site for the C1 activators. Moreover, there is a correlation among the residue identity at the mutation site, DAG affinity, and loop dynamics in four C1 variants. We propose that "toggling" of DAG affinity may occur through modulation of both protein-membrane interactions and the geometry of the activator-binding cleft, with the loop dynamics being responsible for the latter.
[Mh] Termos MeSH primário: Diglicerídeos/química
Proteína Quinase C/química
[Mh] Termos MeSH secundário: Diglicerídeos/metabolismo
Modelos Moleculares
Conformação Proteica
Proteína Quinase C/metabolismo
Termodinâmica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Diglycerides); EC 2.7.11.13 (Protein Kinase C)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170917
[Lr] Data última revisão:
170917
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170516
[St] Status:MEDLINE
[do] DOI:10.1021/acs.biochem.7b00228



página 1 de 712 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