Base de dados : MEDLINE
Pesquisa : D08.811.277.352.100.430 [Categoria DeCS]
Referências encontradas : 7599 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 760 ir para página                         

  1 / 7599 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29304082
[Au] Autor:Gadek KE; Wang H; Hall MN; Sungello M; Libby A; MacLaskey D; Eckel RH; Olwin BB
[Ad] Endereço:Department of Molecular, Cellular and Developmental Biology, University of Colorado Boulder, Boulder, Colorado United States of America.
[Ti] Título:Striated muscle gene therapy for the treatment of lipoprotein lipase deficiency.
[So] Source:PLoS One;13(1):e0190963, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Excessive circulating triglycerides due to reduction or loss of lipoprotein lipase activity contribute to hypertriglyceridemia and increased risk for pancreatitis. The only gene therapy treatment for lipoprotein lipase deficiency decreases pancreatitis but minimally reduces hypertriglyceridemia. Synthesized in multiple tissues including striated muscle and adipose tissue, lipoprotein lipase is trafficked to blood vessel endothelial cells where it is anchored at the plasma membrane and hydrolyzes triglycerides into free fatty acids. We conditionally knocked out lipoprotein lipase in differentiated striated muscle tissue lowering striated muscle lipoprotein lipase activity causing hypertriglyceridemia. We then crossed lipoprotein lipase striated muscle knockout mice with mice possessing a conditional avian retroviral receptor gene and injected mice with either a human lipoprotein lipase retrovirus or an mCherry control retrovirus. Post-heparin plasma lipoprotein lipase activity increased for three weeks following human lipoprotein lipase retroviral infection compared to mCherry infected mice. Human lipoprotein lipase infected mice had significantly lower blood triglycerides compared to mCherry controls and were comparable to wild-type blood triglyceride levels. Thus, targeted delivery of human lipoprotein lipase into striated muscle tissue identifies a potential therapeutic target for lipoprotein lipase deficiency.
[Mh] Termos MeSH primário: Terapia Genética
Lipase Lipoproteica/genética
Músculo Estriado/patologia
[Mh] Termos MeSH secundário: Animais
Vetores Genéticos
Seres Humanos
Hipertrigliceridemia/etiologia
Camundongos
Camundongos Knockout
Músculo Estriado/enzimologia
Retroviridae/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 3.1.1.34 (Lipoprotein Lipase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190963


  2 / 7599 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27771332
[Au] Autor:Geldenhuys WJ; Lin L; Darvesh AS; Sadana P
[Ad] Endereço:Department of Pharmaceutical Sciences, School of Pharmacy, West Virginia University, Morgantown, WV 26505, USA.
[Ti] Título:Emerging strategies of targeting lipoprotein lipase for metabolic and cardiovascular diseases.
[So] Source:Drug Discov Today;22(2):352-365, 2017 Feb.
[Is] ISSN:1878-5832
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Although statins and other pharmacological approaches have improved the management of lipid abnormalities, there exists a need for newer treatment modalities especially for the management of hypertriglyceridemia. Lipoprotein lipase (LPL), by promoting hydrolytic cleavage of the triglyceride core of lipoproteins, is a crucial node in the management of plasma lipid levels. Although LPL expression and activity modulation is observed as a pleiotropic action of some the commonly used lipid lowering drugs, the deliberate development of drugs targeting LPL has not occurred yet. In this review, we present the biology of LPL, highlight the LPL modulation property of currently used drugs and review the novel emerging approaches to target LPL.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/enzimologia
Lipase Lipoproteica/metabolismo
Doenças Metabólicas/enzimologia
[Mh] Termos MeSH secundário: Animais
Doenças Cardiovasculares/tratamento farmacológico
Seres Humanos
Lipase Lipoproteica/química
Doenças Metabólicas/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
EC 3.1.1.34 (Lipoprotein Lipase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161030
[St] Status:MEDLINE


  3 / 7599 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29179206
[Au] Autor:Stellavato A; La Noce M; Corsuto L; Pirozzi AVA; De Rosa M; Papaccio G; Schiraldi C; Tirino V
[Ti] Título:Hybrid Complexes of High and Low Molecular Weight Hyaluronans Highly Enhance HASCs Differentiation: Implication for Facial Bioremodelling.
[So] Source:Cell Physiol Biochem;44(3):1078-1092, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Adipose-derived Stem Cells (ASCs) are used in Regenerative Medicine, including fat grafting, recovery from local tissue ischemia and scar remodeling. The aim of this study was to evaluate hyaluronan based gel effects on ASCs differentiation and proliferation. METHODS: Comparative analyses using high (H) and low (L) molecular weight hyaluronans (HA), hyaluronan hybrid cooperative complexes (HCCs), and high and medium cross-linked hyaluronan based dermal fillers were performed. Human ASCs were characterized by flow cytometry using CD90, CD34, CD105, CD29, CD31, CD45 and CD14 markers. Then, cells were treated for 7, 14 and 21 days with hyaluronans. Adipogenic differentiation was evaluated using Oil red-O staining and expression of leptin, PPAR-γ, LPL and adiponectin using qRT-PCR. Adiponectin was analyzed by immunofluorescence, PPAR-γ and adiponectin were analyzed using western blotting. ELISA assays for adiponectin and leptin were performed. RESULTS: HCCs highly affected ASCs differentiation by up-regulating adipogenic genes and related proteins, that were also secreted in the culture medium. H-HA and L-HA induced a lower level of ASCs differentiation. CONCLUSION: HCCs-based formulations clearly enhance adipogenic differentiation and proliferation, when compared with linear HA and cross-linked hyaluronans. Injection of HCCs in subdermal fat compartment may recruit and differentiate stem cells in adipocytes, and considerably improving fat tissue renewal.
[Mh] Termos MeSH primário: Diferenciação Celular/efeitos dos fármacos
Ácido Hialurônico/farmacologia
[Mh] Termos MeSH secundário: Adipogenia/efeitos dos fármacos
Adiponectina/análise
Adiponectina/metabolismo
Tecido Adiposo/citologia
Adulto
Antígenos CD/metabolismo
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Ácido Hialurônico/química
Leptina/análise
Leptina/metabolismo
Lipase Lipoproteica/metabolismo
Microscopia de Fluorescência
Meia-Idade
Peso Molecular
PPAR gama/metabolismo
Fenótipo
Células-Tronco/citologia
Células-Tronco/metabolismo
Cirurgia Plástica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adiponectin); 0 (Antigens, CD); 0 (Leptin); 0 (PPAR gamma); 9004-61-9 (Hyaluronic Acid); EC 3.1.1.34 (Lipoprotein Lipase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485414


  4 / 7599 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29176657
[Au] Autor:Agrawal S; Zaritsky JJ; Fornoni A; Smoyer WE
[Ad] Endereço:Center for Clinical and Translational Research, The Research Institute at Nationwide Children's Hospital, and Department of Pediatrics, The Ohio State University, 700 Children's Drive, W303, Columbus, Ohio 43205, USA.
[Ti] Título:Dyslipidaemia in nephrotic syndrome: mechanisms and treatment.
[So] Source:Nat Rev Nephrol;14(1):57-70, 2018 Jan.
[Is] ISSN:1759-507X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Nephrotic syndrome is a highly prevalent disease that is associated with high morbidity despite notable advances in its treatment. Many of the complications of nephrotic syndrome, including the increased risk of atherosclerosis and thromboembolism, can be linked to dysregulated lipid metabolism and dyslipidaemia. These abnormalities include elevated plasma levels of cholesterol, triglycerides and the apolipoprotein B-containing lipoproteins VLDL and IDL; decreased lipoprotein lipase activity in the endothelium, muscle and adipose tissues; decreased hepatic lipase activity; and increased levels of the enzyme PCSK9. In addition, there is an increase in the plasma levels of immature HDL particles and reduced cholesterol efflux. Studies from the past few years have markedly improved our understanding of the molecular pathogenesis of nephrotic syndrome-associated dyslipidaemia, and also heightened our awareness of the associated exacerbated risks of cardiovascular complications, progressive kidney disease and thromboembolism. Despite the absence of clear guidelines regarding treatment, various strategies are being increasingly utilized, including statins, bile acid sequestrants, fibrates, nicotinic acid and ezetimibe, as well as lipid apheresis, which seem to also induce partial or complete clinical remission of nephrotic syndrome in a substantial percentage of patients. Future potential treatments will likely also include inhibition of PCSK9 using recently-developed anti-PCSK9 monoclonal antibodies and small inhibitory RNAs, as well as targeting newly identified molecular regulators of lipid metabolism that are dysregulated in nephrotic syndrome.
[Mh] Termos MeSH primário: Anticolesterolemiantes/uso terapêutico
Dislipidemias/tratamento farmacológico
Ácidos Fíbricos/uso terapêutico
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
Síndrome Nefrótica/metabolismo
[Mh] Termos MeSH secundário: Colesterol/metabolismo
HDL-Colesterol/metabolismo
VLDL-Colesterol/metabolismo
Dislipidemias/complicações
Dislipidemias/metabolismo
Ezetimiba/uso terapêutico
Seres Humanos
Hipolipemiantes/uso terapêutico
Lipase/metabolismo
Lipase Lipoproteica/metabolismo
Lipoproteínas/metabolismo
Síndrome Nefrótica/complicações
Niacina/uso terapêutico
Pró-Proteína Convertase 9/metabolismo
Triglicerídeos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anticholesteremic Agents); 0 (Cholesterol, HDL); 0 (Cholesterol, VLDL); 0 (Fibric Acids); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Hypolipidemic Agents); 0 (Lipoproteins); 0 (Triglycerides); 0 (lipoprotein cholesterol); 2679MF687A (Niacin); 97C5T2UQ7J (Cholesterol); EC 3.1.1.3 (Lipase); EC 3.1.1.3 (hepatic lipase, human); EC 3.1.1.34 (Lipoprotein Lipase); EC 3.4.21.- (PCSK9 protein, human); EC 3.4.21.- (Proprotein Convertase 9); EOR26LQQ24 (Ezetimibe)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180117
[Lr] Data última revisão:
180117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1038/nrneph.2017.155


  5 / 7599 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27778288
[Au] Autor:Baggelaar MP; Van der Stelt M
[Ad] Endereço:Department of Bio-organic Synthesis, Leiden University, 9500, Einsteinweg 55, 2333 CC, Leiden, The Netherlands. m.p.baggelaar@chem.leidenuniv.nl.
[Ti] Título:Competitive ABPP of Serine Hydrolases: A Case Study on DAGL-Alpha.
[So] Source:Methods Mol Biol;1491:161-169, 2017.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Competitive activity-based protein profiling is a highly efficient chemical biology technique to determine target engagement and selectivity profiles of enzyme inhibitors in complex proteomes. Fluorophosphonate-based fluorescent inhibitors are widely used as broad-spectrum probes for serine hydrolases. However, diacylglycerol lipase-α is not labeled by fluorophosphonate-based probes. To overcome this problem, we have developed a tailor-made activity-based probe that reacts with diacylglycerol lipase-α. Here we describe a case study in which we apply competitive activity-based protein profiling using a broad-spectrum and a tailor-made activity-based probe to establish selectivity and activity profiles of inhibitors targeting diacylglycerol lipase-α in the mouse brain proteome.
[Mh] Termos MeSH primário: Hidrolases/metabolismo
Lipase Lipoproteica/metabolismo
Serina/química
[Mh] Termos MeSH secundário: Animais
Encéfalo/enzimologia
Encéfalo/metabolismo
Hidrolases/química
Camundongos
Proteoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Proteome); 452VLY9402 (Serine); EC 3.- (Hydrolases); EC 3.1.1.34 (Lipoprotein Lipase); EC 3.1.1.34 (diacylglycerol lipase alpha, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


  6 / 7599 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29198193
[Au] Autor:Cai Z; Mai K; Ai Q
[Ad] Endereço:Key Laboratory of Aquaculture Nutrition and Feed (Ministry of Agriculture) & Key Laboratory of Mariculture (Ministry of Education),Ocean University of China,5 Yushan Road,Qingdao,Shandong 266003,People's Republic of China.
[Ti] Título:Regulation of hepatic lipid deposition by phospholipid in large yellow croaker.
[So] Source:Br J Nutr;118(12):999-1009, 2017 Dec.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Dietary phospholipid (PL) supplementation has been shown to reduce lipid accumulation in the tissues of farmed fish; however, the mechanisms underlying this effect are largely unknown. Thus, the present study was conducted to evaluate the potential impacts of PL on hepatic lipid metabolism both in vivo and in vitro. For in vivo study, four experimental diets - low lipid and low PL diet, as control diet (LL-LP diet, containing 12 % lipid and 1·5 % PL), low-lipid and high-PL diet (containing 12 % lipid and 8 % PL), high-lipid and low-PL diet (HL-LP diet, containing 20 % lipid and 1·5 % PL) and high-lipid and high-PL diet (HL-HP diet, containing 20 % lipid and 8 % PL) - were randomly allocated to four groups of large yellow croaker (Larimichthys crocea) (three cages per group) with similar initial body weight (approximately 8 g). For in vitro study, primary hepatocytes isolated from large yellow croaker were incubated either with graded levels of phosphatidylcholine (PC) (0-250 µm) or small interfering RNA (siRNA) for CTP: choline phosphate cytidylyltranferase α (CCTα) (siRNA-CCTα). Results showed that survival was independent of dietary treatments (P>0·05). Weight gain and feed efficiency in the HL-HP group were significantly higher than in the LL-LP and HL-LP groups (P<0·05). High level of dietary PL could markedly reduce abnormal hepatic lipid accumulation induced by the HL-LP diet (P<0·05). Similarly, compared with the corresponding controls, a significant decrease/increase in lipid content was observed in primary hepatocytes incubated with PC/siRNA-CCTα (P<0·05). High level of dietary PL reversed the HL-LP diet-induced increased levels of mRNA of fatty acid uptake and lipid synthesis related genes (P<0·05). In addition, High level of dietary PL markedly down-regulated the transcript levels of fatty acid oxidation-related genes and enhanced the transcript levels of VLDL assembly-related genes regardless of dietary lipid levels (P<0·05). Compared with corresponding controls, primary hepatocytes treated with PC showed significantly higher mRNA expression of lipid synthesis and VLDL assembly-related genes and lower mRNA expression of fatty acid oxidation-related genes, with hepatocytes treated with siRNA-CCTα exhibiting the opposite trend (P<0·05). In summary, these results demonstrated that high level of dietary PL might reverse the HL-LP diet-induced abnormal lipid accumulation in the liver through inhibiting fatty acid uptake and lipid synthesis, together with promoting the lipid export at the transcriptional level. Lipid export-promoting effect of PC was confirmed by in vitro studies. The present study showed for the first time that PL or PC could influence various metabolic pathways to regulate hepatic lipid deposition in fish at least at the transcriptional level.
[Mh] Termos MeSH primário: Dieta/veterinária
Metabolismo dos Lipídeos
Fígado/metabolismo
Perciformes/metabolismo
Fosfolipídeos/administração & dosagem
[Mh] Termos MeSH secundário: Ração Animal
Animais
Antígenos CD36/genética
Antígenos CD36/metabolismo
Células Cultivadas
Diacilglicerol O-Aciltransferase/genética
Diacilglicerol O-Aciltransferase/metabolismo
Ácido Graxo Sintases/genética
Ácido Graxo Sintases/metabolismo
Proteínas de Transporte de Ácido Graxo/genética
Proteínas de Transporte de Ácido Graxo/metabolismo
Proteínas de Ligação a Ácido Graxo/genética
Proteínas de Ligação a Ácido Graxo/metabolismo
Ácidos Graxos/metabolismo
Proteínas de Peixes/genética
Proteínas de Peixes/metabolismo
Hepatócitos/metabolismo
Lipase/genética
Lipase/metabolismo
Lipase Lipoproteica/genética
Lipase Lipoproteica/metabolismo
Fosfatidilcolinas/administração & dosagem
Proteína de Ligação a Elemento Regulador de Esterol 1/genética
Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD36 Antigens); 0 (Fatty Acid Transport Proteins); 0 (Fatty Acid-Binding Proteins); 0 (Fatty Acids); 0 (Fish Proteins); 0 (Phosphatidylcholines); 0 (Phospholipids); 0 (Sterol Regulatory Element Binding Protein 1); EC 2.3.1.20 (Diacylglycerol O-Acyltransferase); EC 2.3.1.85 (Fatty Acid Synthases); EC 3.1.1.3 (Lipase); EC 3.1.1.34 (Lipoprotein Lipase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171227
[Lr] Data última revisão:
171227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.1017/S000711451700294X


  7 / 7599 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28980889
[Au] Autor:Tian JJ; Lei CX; Ji H; Kaneko G; Zhou JS; Yu HB; Li Y; Yu EM; Xie J
[Ad] Endereço:1College of Animal Science and Technology,Northwest A&F University,Yangling 712100,People's Republic of China.
[Ti] Título:Comparative analysis of effects of dietary arachidonic acid and EPA on growth, tissue fatty acid composition, antioxidant response and lipid metabolism in juvenile grass carp, Ctenopharyngodon idellus.
[So] Source:Br J Nutr;118(6):411-422, 2017 Sep.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Four isonitrogenous and isoenergetic purified diets containing free arachidonic acid (ARA) or EPA (control group), 0·30 % ARA, 0·30 % EPA and 0·30 % ARA+EPA (equivalent) were designed to feed juvenile grass carp (10·21 (sd 0·10) g) for 10 weeks. Only the EPA group presented better growth performance compared with the control group (P<0·05). Dietary ARA and EPA were incorporated into polar lipids more than non-polar lipids in hepatopancreas but not intraperitoneal fat (IPF) tissue. Fish fed ARA and EPA showed an increase of serum superoxide dismutase and catalase activities, and decrease of glutathione peroxidase activity and malondialdehyde contents (P<0·05). The hepatopancreatic TAG levels decreased both in ARA and EPA groups (P<0·05), accompanied by the decrease of lipoprotein lipase (LPL) activity in the ARA group (P<0·05). Fatty acid synthase (FAS), diacylglycerol O-acyltransferase and apoE gene expression in the hepatopancreas decreased in fish fed ARA and EPA, but only the ARA group exhibited increased mRNA level of adipose TAG lipase (ATGL) (P<0·05). Decreased IPF index and adipocyte sizes were found in the ARA group (P<0·05). Meanwhile, the ARA group showed decreased expression levels of adipogenic genes CCAAT enhancer-binding protein α, LPL and FAS, and increased levels of the lipid catabolic genes PPAR α, ATGL, hormone-sensitive lipase and carnitine palmitoyltransferase 1 (CPT-1) in IPF, whereas the EPA group only increased PPAR α and CPT-1 mRNA expression and showed less levels than the ARA group. Overall, dietary EPA is beneficial to the growth performance, whereas ARA is more potent in inducing lipolysis and inhibiting adipogenesis, especially in IPF. Meanwhile, dietary ARA and EPA showed the similar preference in esterification and the improvement in antioxidant response.
[Mh] Termos MeSH primário: Antioxidantes/metabolismo
Ácido Araquidônico/administração & dosagem
Composição Corporal
Carpas/fisiologia
Ácido Eicosapentaenoico/administração & dosagem
Metabolismo dos Lipídeos
[Mh] Termos MeSH secundário: Adipócitos/efeitos dos fármacos
Adipócitos/metabolismo
Adipogenia/efeitos dos fármacos
Adipogenia/genética
Ração Animal/análise
Animais
Proteína alfa Estimuladora de Ligação a CCAAT/genética
Proteína alfa Estimuladora de Ligação a CCAAT/metabolismo
Carnitina O-Palmitoiltransferase/genética
Carnitina O-Palmitoiltransferase/metabolismo
Dieta/veterinária
Glutationa Peroxidase/sangue
Hepatopâncreas/efeitos dos fármacos
Hepatopâncreas/metabolismo
Lipase Lipoproteica/sangue
Malondialdeído/sangue
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Superóxido Dismutase/sangue
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (CCAAT-Enhancer-Binding Protein-alpha); 0 (RNA, Messenger); 27YG812J1I (Arachidonic Acid); 4Y8F71G49Q (Malondialdehyde); AAN7QOV9EA (Eicosapentaenoic Acid); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase); EC 2.3.1.21 (Carnitine O-Palmitoyltransferase); EC 3.1.1.34 (Lipoprotein Lipase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171006
[St] Status:MEDLINE
[do] DOI:10.1017/S000711451700215X


  8 / 7599 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28965514
[Au] Autor:Turkmen S; Zamorano MJ; Fernández-Palacios H; Hernández-Cruz CM; Montero D; Robaina L; Izquierdo M
[Ad] Endereço:Aquaculture Research Group (GIA),Research Institute in Sustainable Aquaculture and Marine Conservation (IU-ECOAQUA),Universidad de Las Palmas de Gran Canaria,Crta. Taliarte s/n,35214 Telde,Spain.
[Ti] Título:Parental nutritional programming and a reminder during juvenile stage affect growth, lipid metabolism and utilisation in later developmental stages of a marine teleost, the gilthead sea bream (Sparus aurata).
[So] Source:Br J Nutr;118(7):500-512, 2017 Oct.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Nutrition during periconception and early development can modulate metabolic routes to prepare the offspring for adverse conditions through a process known as nutritional programming. In gilthead sea bream, replacement of fish oil (FO) with linseed oil (LO) in broodstock diets improves growth in the 4-month-old offspring challenged with low-FO and low-fishmeal (FM) diets for 1 month. The present study further investigated the effects of broodstock feeding on the same offspring when they were 16 months old and were challenged for a second time with the low-FM and low-FO diet for 2 months. The results showed that replacement of parental moderate-FO feeding with LO, combined with juvenile feeding at 4 months old with low-FM and low-FO diets, significantly (P<0·05) improved offspring growth and feed utilisation of low-FM/FO diets even when they were 16 months old: that is, when they were on the verge of their first reproductive season. Liver fatty acid composition was significantly affected by broodstock or reminder diets as well as by their interaction. Moreover, the reduction of long-chain PUFA and increase in α-linolenic acid and linoleic acid in broodstock diets lead to a significant down-regulation of hepatic lipoprotein lipase (P<0·001) and elongation of very long-chain fatty acids protein 6 (P<0·01). Besides, fatty acid desaturase 2 values were positively correlated to hepatic levels of 18 : 4n-3, 18 : 3n-6, 20 : 5n-3, 22 : 6n-3 and 22 : 5n-6. Thus, this study demonstrated the long-term nutritional programming of gilthead sea bream through broodstock feeding, the effect of feeding a 'reminder' diet during juvenile stages to improve utilisation of low-FM/FO diets and fish growth as well as the regulation of gene expression along the fish's life-cycle.
[Mh] Termos MeSH primário: Ração Animal/análise
Dieta/veterinária
Metabolismo dos Lipídeos
Dourada/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Animais
Regulação para Baixo
Ácidos Graxos Dessaturases/genética
Ácidos Graxos Dessaturases/metabolismo
Ácidos Graxos/administração & dosagem
Ácidos Graxos Insaturados/administração & dosagem
Óleos de Peixe/administração & dosagem
Ácido Linoleico/administração & dosagem
Óleo de Semente do Linho/administração & dosagem
Lipase Lipoproteica/genética
Lipase Lipoproteica/metabolismo
Fígado/metabolismo
Ácido alfa-Linolênico/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids); 0 (Fatty Acids, Unsaturated); 0 (Fish Oils); 0RBV727H71 (alpha-Linolenic Acid); 8001-26-1 (Linseed Oil); 9KJL21T0QJ (Linoleic Acid); EC 1.14.19.- (Fatty Acid Desaturases); EC 3.1.1.34 (Lipoprotein Lipase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171003
[St] Status:MEDLINE
[do] DOI:10.1017/S0007114517002434


  9 / 7599 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28938452
[Au] Autor:Forner-Piquer I; Maradonna F; Gioacchini G; Santangeli S; Allarà M; Piscitelli F; Habibi HR; Di Marzo V; Carnevali O
[Ad] Endereço:Dipartimento Scienze della Vita e dell'Ambiente, Università Politecnica delle Marche, 60131 Ancona, Italy.
[Ti] Título:Dose-Specific Effects of Di-Isononyl Phthalate on the Endocannabinoid System and on Liver of Female Zebrafish.
[So] Source:Endocrinology;158(10):3462-3476, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Phthalates, used as plasticizers, have become a ubiquitous contaminant and have been reported for their potential to induce toxicity in living organisms. Among them, di-isononyl phthalate (DiNP) has been recently used to replace di(2-ethylhexyl) phthalate (DEHP). Nowadays, there is evidence that DiNP is an endocrine-disrupting chemical; however, little is known about its effects on the endocannabinoid system (ECS) and lipid metabolism. Hence, the aim of our study was to investigate the effects of DiNP on the ECS in zebrafish liver and brain and on hepatic lipid storage. To do so, adult female zebrafish were exposed to three concentrations (0.42 µg/L, 4.2 µg/L, and 42 µg/L) of DiNP via water for 3 weeks. Afterwards, we investigated transcript levels for genes involved in the ECS of the brain and liver as well as liver histology and image analysis, Fourier-transform infrared spectroscopy imaging, and measurement of endocannabinoid levels. Our results demonstrate that DiNP upregulates orexigenic signals and causes hepatosteatosis together with deregulation of the peripheral ECS and lipid metabolism. A decrease in the levels of ECS components at the central level was observed after exposure to the highest DiNP concentration tested. These findings suggest that replacement of DEHP with DiNP should be considered with caution because of observed adverse DiNP effects on aquatic organisms.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Endocanabinoides/metabolismo
Metabolismo dos Lipídeos/efeitos dos fármacos
Fígado/efeitos dos fármacos
Ácidos Ftálicos/farmacologia
Plastificantes/farmacologia
[Mh] Termos MeSH secundário: Animais
Ácidos Araquidônicos/metabolismo
Encéfalo/metabolismo
Relação Dose-Resposta a Droga
Disruptores Endócrinos/farmacologia
Fígado Gorduroso/metabolismo
Feminino
Expressão Gênica/efeitos dos fármacos
Glicerídeos/metabolismo
Lipase Lipoproteica/efeitos dos fármacos
Lipase Lipoproteica/genética
Lipase Lipoproteica/metabolismo
Fosfolipase D/efeitos dos fármacos
Fosfolipase D/genética
Fosfolipase D/metabolismo
Alcamidas Poli-Insaturadas/metabolismo
Receptor CB1 de Canabinoide/efeitos dos fármacos
Receptor CB1 de Canabinoide/genética
Receptor CB1 de Canabinoide/metabolismo
Receptor CB2 de Canabinoide/efeitos dos fármacos
Receptor CB2 de Canabinoide/genética
Receptor CB2 de Canabinoide/metabolismo
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arachidonic Acids); 0 (Endocannabinoids); 0 (Endocrine Disruptors); 0 (Glycerides); 0 (Phthalic Acids); 0 (Plasticizers); 0 (Polyunsaturated Alkamides); 0 (Receptor, Cannabinoid, CB1); 0 (Receptor, Cannabinoid, CB2); 4010KIX4CK (diisononyl phthalate); 8D239QDW64 (glyceryl 2-arachidonate); EC 3.1.1.34 (Lipoprotein Lipase); EC 3.1.4.4 (N-acylphosphatidylethanolamine phospholipase D, mouse); EC 3.1.4.4 (Phospholipase D); UR5G69TJKH (anandamide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00458


  10 / 7599 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28795592
[Au] Autor:Zaher NH; Rashed ER; El-Ghazaly MA
[Ad] Endereço:Department of Drug Radiation Research, National Center for Radiation Research & Technology, Technology (NCRRT), Egyptian Atomic Energy Authority (EAEA), PO box 29, Nasr City, Cairo, Egypt.
[Ti] Título:Semi-synthetic thymoquinone analogs: new prototypes as potential antihyperlipidemics in irradiated rats.
[So] Source:Future Med Chem;9(13):1483-1493, 2017 Sep.
[Is] ISSN:1756-8927
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIM: Thymoquinone (TQ), has been reported to possess strong antihyperlipidemic properties. However, a variety of serious side effects has been reported for TQ. The present study aimed to evaluate the potential antihyperlipidemic activity of newly synthesized TQ analogs. METHODS & RESULTS: first, novel TQ derivatives were studied against radiation-induced dyslipidemia in male rats. Second, the most promising sulfur derivatives (4-7), were further tested to elucidate their possible mechanism(s) of actions. Results showed that they possess Hydroxymethyl Glutaryl-Co A reductase inhibitory activity, as well as stimulatory effects on the activities of each of plasma Lecithin-Cholesterol Acyltransferase and lipoprotein lipase enzymes. CONCLUSION: TQ derivatives (4-7), could be considered as promising agents in pathologies implicating impaired lipid metabolism, preclinical evaluation is warranted. [Formula: see text].
[Mh] Termos MeSH primário: Benzoquinonas/química
Hidroximetilglutaril-CoA Redutases/metabolismo
Hipolipemiantes/síntese química
[Mh] Termos MeSH secundário: Animais
Benzoquinonas/metabolismo
Benzoquinonas/uso terapêutico
Dislipidemias/tratamento farmacológico
Dislipidemias/etiologia
Dislipidemias/veterinária
Raios gama
Hidroximetilglutaril-CoA Redutases/sangue
Hidroximetilglutaril-CoA Redutases/química
Hipolipemiantes/farmacologia
Hipolipemiantes/uso terapêutico
Metabolismo dos Lipídeos/efeitos dos fármacos
Lipídeos/sangue
Lipase Lipoproteica/antagonistas & inibidores
Lipase Lipoproteica/metabolismo
Fígado/efeitos dos fármacos
Fígado/enzimologia
Fígado/efeitos da radiação
Masculino
Fosfatidilcolina-Esterol O-Aciltransferase/antagonistas & inibidores
Fosfatidilcolina-Esterol O-Aciltransferase/metabolismo
Ratos
Ratos Wistar
Irradiação Corporal Total/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzoquinones); 0 (Hypolipidemic Agents); 0 (Lipids); 490-91-5 (thymoquinone); EC 1.1.1.- (Hydroxymethylglutaryl CoA Reductases); EC 2.3.1.43 (Phosphatidylcholine-Sterol O-Acyltransferase); EC 3.1.1.34 (Lipoprotein Lipase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.4155/fmc-2017-0054



página 1 de 760 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