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  1 / 2106 MEDLINE  
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[PMID]:28460556
[Au] Autor:Perani CV; Langgartner D; Uschold-Schmidt N; Füchsl AM; Neumann ID; Reber SO; Slattery DA
[Ad] Endereço:a Department of Behavioural and Molecular Neurobiology , University of Regensburg , Regensburg , Germany.
[Ti] Título:Adrenal gland plasticity in lactating rats and mice is sufficient to maintain basal hypersecretion of corticosterone.
[So] Source:Stress;20(3):303-311, 2017 May.
[Is] ISSN:1607-8888
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Increased basal glucocorticoid secretion and a reduced glucocorticoid response during acute stress, despite only minor changes in the secretion of the major secretagogue adrenocorticotropic hormone (ACTH), have been documented in the peripartum period in several species. We recently showed that the adrenal gland, the site of glucocorticoid synthesis, undergoes substantial postpartum-associated plasticity in the rat at mid-lactation. Here, we asked the question whether adrenal changes already take place around parturition in the rat and in another species, namely the mouse. After demonstrating that several components of the adrenal machinery mediating cholesterol supply for steroidogenesis, including protein levels of hormone-sensitive lipase, low-density lipoprotein receptor (LDLR) and scavenger receptor class-B type-1 (SRB1), are upregulated, while hydroxymethylglutaryl coenzyme A reductase (HMGCR) is downregulated in the lactating rat one day after delivery, as previously observed at mid-lactation, we demonstrated profound changes in the mouse. In detail, protein expression of LDLR, SRB1, HMGCR and adrenal lipid store density were increased in the mouse adrenal one day after parturition as tested via western blot analysis and oil-red lipid staining, respectively. Moreover, using in vitro culture techniques, we observed that isolated adrenal explants from lactating mice secreted higher levels of corticosterone under basal conditions, but showed impaired responsiveness to ACTH, mimicking the in vivo scenario. These results suggest that mechanisms of adaptation in the maternal adrenal after delivery, namely increased cholesterol availability and decreased ACTH sensitivity, are crucial for the basal increase in circulating glucocorticoids and maternal stress hyporesponsiveness that are typical of this period.
[Mh] Termos MeSH primário: Glândulas Suprarrenais/secreção
Corticosterona/secreção
Lactação/metabolismo
[Mh] Termos MeSH secundário: Hormônio Adrenocorticotrópico/metabolismo
Animais
Colesterol/metabolismo
Feminino
Hidroximetilglutaril-CoA Redutases/metabolismo
Camundongos
Fosfoproteínas/metabolismo
Período Pós-Parto/metabolismo
Ratos
Receptores da Corticotropina/metabolismo
Receptores de LDL/metabolismo
Receptores Depuradores Classe B/metabolismo
Esterol Esterase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phosphoproteins); 0 (Receptors, Corticotropin); 0 (Receptors, LDL); 0 (Scavenger Receptors, Class B); 0 (steroidogenic acute regulatory protein); 9002-60-2 (Adrenocorticotropic Hormone); 97C5T2UQ7J (Cholesterol); EC 1.1.1.- (Hydroxymethylglutaryl CoA Reductases); EC 3.1.1.13 (Sterol Esterase); W980KJ009P (Corticosterone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1080/10253890.2017.1325462


  2 / 2106 MEDLINE  
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[PMID]:29254319
[Au] Autor:Musolino V; Gliozzi M; Carresi C; Maiuolo J; Mollace R; Bosco F; Scarano F; Scicchitano M; Maretta A; Palma E; Iannone M; Morittu VM; Gratteri S; Muscoli C; Fini M; Mollace V
[Ad] Endereço:Institute of Research for Food Safety and Health (IRC-FSH), Department of Health Science, Magna Græcia University of Catanzaro, Catanzaro, Italy.
[Ti] Título:Lipid-lowering effect of bergamot polyphenolic fraction: role of pancreatic cholesterol ester hydrolase.
[So] Source:J Biol Regul Homeost Agents;31(4):1087-1093, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Bergamot polyphenolic fraction (BPF) has been shown to positively modulate several mechanisms involved in metabolic syndrome, suggesting its use in therapy. In particular, it is able to induce a significant amelioration of serum lipid profile in hyperlipemic patients at different levels. The purpose of our study was to investigate the effect of BPF on cholesterol absorption physiologically mediated by pancreatic cholesterol ester hydrolase (pCEH). An in vitro activity assay was performed to study the effect of BPF on pCEH, whereas the rate of cholesterol absorption was evaluated through in vivo studies. In particular, male, Sprague-Dawley rats (200–225 g) were fed either normal chow or chow supplemented with 0.5% cholic acid, 5.5% peanut oil, and varying amounts of cholesterol (0 to 1.5%). BPF (10 mg/Kg) was daily administrated by means of a gastric gavage to animals fed with lipid supplemented diet for 4 weeks and, at the end of the study, plasma lipids and liver cholesteryl esters were measured in all experimental groups. Our results show that BPF was able to inhibit pCEH activity and this effect was confirmed, in vivo, via detection of lymphatic cholesteryl ester in rats fed with a cholesterol-rich diet. This evidence clarifies a further mechanism responsible for the hypolipemic properties of BPF previously observed in humans, confirming its beneficial effect in the therapy of hypercholesterolemia and in the treatment of metabolic syndrome.
[Mh] Termos MeSH primário: Suplementos Nutricionais
Hiperlipidemias/tratamento farmacológico
Hipolipemiantes/farmacologia
Óleos Vegetais/farmacologia
Esterol Esterase/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Colesterol/administração & dosagem
Colesterol/sangue
Ésteres do Colesterol/sangue
Ácido Cólico/administração & dosagem
Ácido Cólico/sangue
Absorção Gastrointestinal/fisiologia
Seres Humanos
Hiperlipidemias/metabolismo
Hiperlipidemias/patologia
Hipolipemiantes/metabolismo
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Síndrome Metabólica/tratamento farmacológico
Síndrome Metabólica/metabolismo
Síndrome Metabólica/patologia
Óleos Vegetais/metabolismo
Ratos
Ratos Sprague-Dawley
Esterol Esterase/metabolismo
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholesterol Esters); 0 (Hypolipidemic Agents); 0 (Plant Oils); 0 (Triglycerides); 39W1PKE3JI (bergamot oil); 97C5T2UQ7J (Cholesterol); EC 3.1.1.- (bile salt-stimulated lipase); EC 3.1.1.13 (Sterol Esterase); G1JO7801AE (Cholic Acid)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE


  3 / 2106 MEDLINE  
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[PMID]:29232702
[Au] Autor:Xia B; Cai GH; Yang H; Wang SP; Mitchell GA; Wu JW
[Ad] Endereço:College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, China.
[Ti] Título:Adipose tissue deficiency of hormone-sensitive lipase causes fatty liver in mice.
[So] Source:PLoS Genet;13(12):e1007110, 2017 12.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fatty liver is a major health problem worldwide. People with hereditary deficiency of hormone-sensitive lipase (HSL) are reported to develop fatty liver. In this study, systemic and tissue-specific HSL-deficient mice were used as models to explore the underlying mechanism of this association. We found that systemic HSL deficient mice developed fatty liver in an age-dependent fashion between 3 and 8 months of age. To further explore the mechanism of fatty liver in HSL deficiency, liver-specific HSL knockout mice were created. Surprisingly, liver HSL deficiency did not influence liver fat content, suggesting that fatty liver in HSL deficiency is not liver autonomous. Given the importance of adipose tissue in systemic triglyceride metabolism, we created adipose-specific HSL knockout mice and found that adipose HSL deficiency, to a similar extent as systemic HSL deficiency, causes age-dependent fatty liver in mice. Mechanistic study revealed that deficiency of HSL in adipose tissue caused inflammatory macrophage infiltrates, progressive lipodystrophy, abnormal adipokine secretion and systemic insulin resistance. These changes in adipose tissue were associated with a constellation of changes in liver: low levels of fatty acid oxidation, of very low density lipoprotein secretion and of triglyceride hydrolase activity, each favoring the development of hepatic steatosis. In conclusion, HSL-deficient mice revealed a complex interorgan interaction between adipose tissue and liver: the role of HSL in the liver is minimal but adipose tissue deficiency of HSL can cause age-dependent hepatic steatosis. Adipose tissue is a potential target for treating the hepatic steatosis of HSL deficiency.
[Mh] Termos MeSH primário: Tecido Adiposo/metabolismo
Fígado Gorduroso/genética
Fígado/metabolismo
Obesidade/genética
Esterol Esterase/genética
[Mh] Termos MeSH secundário: Tecido Adiposo/patologia
Animais
Modelos Animais de Doenças
Fígado Gorduroso/metabolismo
Fígado Gorduroso/patologia
Seres Humanos
Resistência à Insulina/genética
Metabolismo dos Lipídeos/genética
Fígado/patologia
Camundongos
Camundongos Knockout
Obesidade/metabolismo
Obesidade/patologia
Esterol Esterase/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 3.1.1.13 (Sterol Esterase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180111
[Lr] Data última revisão:
180111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007110


  4 / 2106 MEDLINE  
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[PMID]:28958330
[Au] Autor:Amor-Salamanca A; Castillo S; Gonzalez-Vioque E; Dominguez F; Quintana L; Lluís-Ganella C; Escudier JM; Ortega J; Lara-Pezzi E; Alonso-Pulpon L; Garcia-Pavia P
[Ad] Endereço:Inherited Cardiac Diseases Unit, Department of Cardiology, Hospital Universitario Puerta de Hierro, Madrid, Spain.
[Ti] Título:Genetically Confirmed Familial Hypercholesterolemia in Patients With Acute Coronary Syndrome.
[So] Source:J Am Coll Cardiol;70(14):1732-1740, 2017 Oct 03.
[Is] ISSN:1558-3597
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Genetic screening programs in unselected individuals with increased levels of low-density lipoprotein cholesterol (LDL-C) have shown modest results in identifying individuals with familial hypercholesterolemia (FH). OBJECTIVES: This study assessed the prevalence of genetically confirmed FH in patients with acute coronary syndrome (ACS) and compared the diagnostic performance of FH clinical criteria versus FH genetic testing. METHODS: Genetic study of 7 genes (LDLR, APOB, PCSK9, APOE, STAP1, LDLRAP1, and LIPA) associated with FH and 12 common alleles associated with polygenic hypercholesterolemia was performed in 103 patients with ACS, age ≤65 years, and LDL-C levels ≥160 mg/dl. Dutch Lipid Clinic (DLC) and Simon Broome (SB) FH clinical criteria were also applied. RESULTS: The prevalence of genetically confirmed FH was 8.7% (95% confidence interval [CI]: 4.3% to 16.4%; n = 9); 29% (95% CI: 18.5% to 42.1%; n = 18) of patients without FH variants had a score highly suggestive of polygenic hypercholesterolemia. The prevalence of probable to definite FH according to DLC criteria was 27.2% (95% CI: 19.1% to 37.0%; n = 28), whereas SB criteria identified 27.2% of patients (95% CI: 19.1% to 37.0%; n = 28) with possible to definite FH. DLC and SB algorithms failed to diagnose 4 (44%) and 3 (33%) patients with genetically confirmed FH, respectively. Cascade genetic testing in first-degree relatives identified 6 additional individuals with FH. CONCLUSIONS: The prevalence of genetically confirmed FH in patients with ACS age ≤65 years and with LDL-C levels ≥160 mg/dl is high (approximately 9%). FH clinical algorithms do not accurately classify patients with FH. Genetic testing should be advocated in young patients with ACS and high LDL-C levels to allow prompt identification of patients with FH and relatives at risk.
[Mh] Termos MeSH primário: Síndrome Coronariana Aguda
LDL-Colesterol/sangue
Hiperlipoproteinemia Tipo II
Hipolipemiantes/uso terapêutico
Herança Multifatorial/genética
[Mh] Termos MeSH secundário: Síndrome Coronariana Aguda/diagnóstico
Síndrome Coronariana Aguda/epidemiologia
Síndrome Coronariana Aguda/prevenção & controle
Proteínas Adaptadoras de Transdução de Sinal/genética
Apolipoproteína B-100/genética
Apolipoproteínas E/genética
Comorbidade
Feminino
Testes Genéticos/métodos
Seres Humanos
Hiperlipoproteinemia Tipo II/diagnóstico
Hiperlipoproteinemia Tipo II/tratamento farmacológico
Hiperlipoproteinemia Tipo II/epidemiologia
Hiperlipoproteinemia Tipo II/genética
Masculino
Meia-Idade
Seleção de Pacientes
Prevalência
Prognóstico
Pró-Proteína Convertase 9/genética
Receptores de LDL/genética
Reprodutibilidade dos Testes
Medição de Risco/métodos
Fatores de Risco
Espanha/epidemiologia
Esterol Esterase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APOB protein, human); 0 (Adaptor Proteins, Signal Transducing); 0 (ApoE protein, human); 0 (Apolipoprotein B-100); 0 (Apolipoproteins E); 0 (Cholesterol, LDL); 0 (Hypolipidemic Agents); 0 (LDLR protein, human); 0 (LDLRAP1 protein, human); 0 (Receptors, LDL); 0 (STAP1 protein, human); EC 3.1.1.13 (LIPA protein, human); EC 3.1.1.13 (Sterol Esterase); EC 3.4.21.- (PCSK9 protein, human); EC 3.4.21.- (Proprotein Convertase 9)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170930
[St] Status:MEDLINE


  5 / 2106 MEDLINE  
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[PMID]:28946929
[Au] Autor:Chen GH; Hogstrand C; Luo Z; Zhang DG; Ling SC; Wu K
[Ad] Endereço:1Key Laboratory of Freshwater Animal Breeding,Ministry of Agriculture of P.R.C.,Fishery College,Huazhong Agricultural University,Wuhan 430070,People's Republic of China.
[Ti] Título:Dietary zinc addition influenced zinc and lipid deposition in the fore- and mid-intestine of juvenile yellow catfish Pelteobagrus fulvidraco.
[So] Source:Br J Nutr;118(8):570-579, 2017 Oct.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The present study explored the mechanisms of dietary Zn influencing Zn and lipid deposition in the fore- and mid- intestine in yellow catfish Pelteobagrus fulvidraco, and investigated whether the mechanism was intestinal-region dependent. For this purpose, yellow catfish were fed three diets containing Zn levels of 8·83, 19·20 and 146·65 mg Zn/kg, respectively. Growth performance, intestinal TAG and Zn contents as well as activities and mRNA expression of enzymes and genes involved in Zn transport and lipid metabolism in the fore- and mid-intestine were analysed. Dietary Zn increased Zn accumulation as well as activities of Cu-, Zn-superoxide dismutase and ATPase in the fore- and mid-intestine. In the fore-intestine, dietary Zn up-regulated mRNA levels of ZnT1, ZnT5, ZnT7, metallothionein (MT) and metal response element-binding transcription factor-1 (MTF-1), but down-regulated mRNA levels of ZIP4 and ZIP5. In the mid-intestine, dietary Zn up-regulated mRNA levels of ZnT1, ZnT5, ZnT7, MT and MTF-1, but down-regulated mRNA levels of ZIP4 and ZIP5. Dietary Zn reduced TAG content, down-regulated activities of 6-phosphogluconate dehydrogenase (6PGD), glucose-6-phosphate dehydrogenase (G6PD), malic enzyme (ME) and fatty acid synthase (FAS) activities, and reduced mRNA levels of 6PGD, G6PD, FAS, PPARγ and sterol-regulator element-binding protein (SREBP-1), but up-regulated mRNA levels of carnitine palmitoyltransferase IA, hormone-sensitive lipase (HSLa), adipose TAG lipase (ATGL) and PPARα in the fore-intestine. In the mid-intestine, dietary Zn reduced TAG content, activities of G6PD, ME, isocitrate dehydrogenase and FAS, down-regulated mRNA levels of 6PGD, G6PD, FAS, acetyl-CoA carboxylase a, PPARγ and SREBP-1, but up-regulated mRNA expression of HSLa, ATGL and PPARγ. The reduction in TAG content following Zn addition was attributable to reduced lipogenesis and increased lipolysis, and similar regulatory mechanisms were observed between the fore- and mid-intestine.
[Mh] Termos MeSH primário: Peixes-Gato/metabolismo
Intestinos/efeitos dos fármacos
Metabolismo dos Lipídeos/efeitos dos fármacos
Zinco/administração & dosagem
[Mh] Termos MeSH secundário: Acetil-CoA Carboxilase/genética
Acetil-CoA Carboxilase/metabolismo
Ração Animal/análise
Animais
Carnitina O-Palmitoiltransferase/genética
Carnitina O-Palmitoiltransferase/metabolismo
Dieta/veterinária
Regulação para Baixo
Regulação da Expressão Gênica
Glucosefosfato Desidrogenase/genética
Glucosefosfato Desidrogenase/metabolismo
Intestinos/metabolismo
Malato Desidrogenase/genética
Malato Desidrogenase/metabolismo
PPAR alfa/genética
PPAR alfa/metabolismo
PPAR gama/genética
PPAR gama/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Esterol Esterase/genética
Esterol Esterase/metabolismo
Proteína de Ligação a Elemento Regulador de Esterol 1/genética
Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo
Superóxido Dismutase/genética
Superóxido Dismutase/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PPAR alpha); 0 (PPAR gamma); 0 (RNA, Messenger); 0 (Sterol Regulatory Element Binding Protein 1); EC 1.1.1.37 (Malate Dehydrogenase); EC 1.1.1.39 (malate dehydrogenase (decarboxylating)); EC 1.1.1.49 (Glucosephosphate Dehydrogenase); EC 1.15.1.1 (Superoxide Dismutase); EC 2.3.1.21 (Carnitine O-Palmitoyltransferase); EC 3.1.1.13 (Sterol Esterase); EC 6.4.1.2 (Acetyl-CoA Carboxylase); J41CSQ7QDS (Zinc)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170927
[St] Status:MEDLINE
[do] DOI:10.1017/S0007114517002446


  6 / 2106 MEDLINE  
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[PMID]:28882870
[Au] Autor:Zhang H; Shi J; Hachet MA; Xue C; Bauer RC; Jiang H; Li W; Tohyama J; Millar J; Billheimer J; Phillips MC; Razani B; Rader DJ; Reilly MP
[Ad] Endereço:From the Division of Cardiology, Department of Medicine, Columbia University Medical Center, New York (H.Z., J.S., M.A.H., C.X., R.C.B., M.P.R.); Irving Institute for Clinical and Translational Research, Columbia University, New York (H.J., M.P.R.); Cardiovascular Institute, Perelman School of Medic
[Ti] Título:CRISPR/Cas9-Mediated Gene Editing in Human iPSC-Derived Macrophage Reveals Lysosomal Acid Lipase Function in Human Macrophages-Brief Report.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2156-2160, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To gain mechanistic insights into the role of (lipase A), the gene encoding LAL (lysosomal acid lipase) protein, in human macrophages. APPROACH AND RESULTS: We used CRISPR (clustered regularly interspaced short palindromic repeats)/Cas9 (CRISPR-associated protein 9) technology to knock out in human induced pluripotent stem cells and then differentiate to macrophage (human-induced pluripotent stem cells-derived macrophage [IPSDM]) to explore the human macrophage loss-of-function phenotypes. was abundantly expressed in monocyte-derived macrophages and was markedly induced on IPSDM differentiation to comparable levels as in human monocyte-derived macrophage. IPSDM with knockout of ( ) had barely detectable LAL enzymatic activity. Control and IPSDM were loaded with [ H]-cholesteryl oleate-labeled AcLDL (acetylated low-density lipoprotein) followed by efflux to apolipoprotein A-I. Efflux of liberated [ H]-cholesterol to apolipoprotein A-I was abolished in IPSDM, indicating deficiency in LAL-mediated lysosomal cholesteryl ester hydrolysis. In cells loaded with [ H]-cholesterol-labeled AcLDL, [ H]-cholesterol efflux was, however, not different between control and IPSDM. (ATP-binding cassette, subfamily A, member 1) expression was upregulated by AcLDL loading but to a similar extent between control and IPSDM. In nonlipid loaded state, IPSDM had high levels of cholesteryl ester mass compared with minute amounts in control IPSDM. Yet, with AcLDL loading, overall cholesteryl ester mass was increased to similar levels in both control and IPSDM. did not impact lysosomal apolipoprotein-B degradation or expression of , , and CONCLUSIONS: IPSDM reveals macrophage-specific hallmarks of deficiency. CRISPR/Cas9 and IPSDM provide important tools to study human macrophage biology and more broadly for future studies of disease-associated genetic variation in human macrophages.
[Mh] Termos MeSH primário: Sistemas CRISPR-Cas
Edição de Genes/métodos
Células-Tronco Pluripotentes Induzidas/enzimologia
Lisossomos/enzimologia
Macrófagos/enzimologia
Esterol Esterase/metabolismo
[Mh] Termos MeSH secundário: Transportador 1 de Cassete de Ligação de ATP/genética
Transportador 1 de Cassete de Ligação de ATP/metabolismo
Apolipoproteína A-I/metabolismo
Apolipoproteína B-100/metabolismo
Diferenciação Celular
Quimiocina CCL5/genética
Quimiocina CCL5/metabolismo
Ésteres do Colesterol/metabolismo
Regulação Enzimológica da Expressão Gênica
Técnicas de Silenciamento de Genes
Genótipo
Células HEK293
Células Hep G2
Seres Humanos
Hidrólise
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Interleucina-6/genética
Interleucina-6/metabolismo
Lipoproteínas LDL/metabolismo
Fenótipo
Proteólise
Esterol Esterase/genética
Fatores de Tempo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABCA1 protein, human); 0 (APOA1 protein, human); 0 (APOB protein, human); 0 (ATP Binding Cassette Transporter 1); 0 (Apolipoprotein A-I); 0 (Apolipoprotein B-100); 0 (CCL5 protein, human); 0 (Chemokine CCL5); 0 (Cholesterol Esters); 0 (IL1B protein, human); 0 (IL6 protein, human); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Lipoproteins, LDL); 0 (acetyl-LDL); 3DPK9KFN2M (cholesteryl oleate); EC 3.1.1.13 (LIPA protein, human); EC 3.1.1.13 (Sterol Esterase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.310023


  7 / 2106 MEDLINE  
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[PMID]:28756012
[Au] Autor:Ogiyama T; Yamaguchi M; Kurikawa N; Honzumi S; Terayama K; Nagaoka N; Yamamoto Y; Kimura T; Sugiyama D; Inoue SI
[Ad] Endereço:Modality Research Laboratories, Daiichi Sankyo Co., Ltd., 1-2-58, Hiromachi, Shinagawa-ku, Tokyo 140-8710, Japan. Electronic address: yamamoto.tomoko.me@daiichisankyo.co.jp.
[Ti] Título:Design, synthesis, and pharmacological evaluation of a novel series of hormone sensitive lipase inhibitor.
[So] Source:Bioorg Med Chem;25(17):4817-4828, 2017 Sep 01.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:HSL inhibition is a promising approach to the treatment of dyslipidemia. As a result of re-optimization of lead compound 2, we identified novel compound 25a exhibiting potent inhibitory activity against HSL enzyme and cell with high selectivity for cholinesterases (AChE and BuChE). Reflecting its potent in vitro activity, compound 25a exhibited antilipolytic effect in rats at 1mg/kg p.o., which indicated that this novel compound is the most potent orally active HSL inhibitor. Moreover, compound 25a did not show bioactivation liability.
[Mh] Termos MeSH primário: Desenho de Drogas
Hipolipemiantes/síntese química
Hipolipemiantes/farmacologia
Esterol Esterase/antagonistas & inibidores
[Mh] Termos MeSH secundário: Acetilcolinesterase/química
Acetilcolinesterase/metabolismo
Administração Oral
Animais
Butirilcolinesterase/química
Butirilcolinesterase/metabolismo
Ativação Enzimática/efeitos dos fármacos
Inibidores Enzimáticos/síntese química
Inibidores Enzimáticos/química
Inibidores Enzimáticos/farmacocinética
Inibidores Enzimáticos/farmacologia
Glutationa/química
Glutationa/metabolismo
Glicerol/sangue
Meia-Vida
Seres Humanos
Hipolipemiantes/química
Hipolipemiantes/farmacocinética
Concentração Inibidora 50
Masculino
Ratos
Ratos Wistar
Proteínas Recombinantes/biossíntese
Proteínas Recombinantes/química
Proteínas Recombinantes/isolamento & purificação
Esterol Esterase/genética
Esterol Esterase/metabolismo
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Hypolipidemic Agents); 0 (Recombinant Proteins); EC 3.1.1.13 (Sterol Esterase); EC 3.1.1.7 (Acetylcholinesterase); EC 3.1.1.8 (Butyrylcholinesterase); GAN16C9B8O (Glutathione); PDC6A3C0OX (Glycerol)
[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:170731
[St] Status:MEDLINE


  8 / 2106 MEDLINE  
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[PMID]:28615446
[Au] Autor:Tuohetahuntila M; Molenaar MR; Spee B; Brouwers JF; Wubbolts R; Houweling M; Yan C; Du H; VanderVen BC; Vaandrager AB; Helms JB
[Ad] Endereço:From the Department of Biochemistry and Cell Biology, Faculty of Veterinary Medicine, Utrecht University, 3584 CM, Utrecht, The Netherlands.
[Ti] Título:Lysosome-mediated degradation of a distinct pool of lipid droplets during hepatic stellate cell activation.
[So] Source:J Biol Chem;292(30):12436-12448, 2017 Jul 28.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Activation of hepatic stellate cells (HSCs) is a critical step in the development of liver fibrosis. During activation, HSCs lose their lipid droplets (LDs) containing triacylglycerols (TAGs), cholesteryl esters, and retinyl esters (REs). We previously provided evidence for the presence of two distinct LD pools, a preexisting and a dynamic LD pool. Here we investigate the mechanisms of neutral lipid metabolism in the preexisting LD pool. To investigate the involvement of lysosomal degradation of neutral lipids, we studied the effect of lalistat, a specific lysosomal acid lipase (LAL/Lipa) inhibitor on LD degradation in HSCs during activation The LAL inhibitor increased the levels of TAG, cholesteryl ester, and RE in both rat and mouse HSCs. Lalistat was less potent in inhibiting the degradation of newly synthesized TAG species as compared with a more general lipase inhibitor orlistat. Lalistat also induced the presence of RE-containing LDs in an acidic compartment. However, targeted deletion of the Lipa gene in mice decreased the liver levels of RE, most likely as the result of a gradual disappearance of HSCs in livers of Lipa mice. Lalistat partially inhibited the induction of activation marker α-smooth muscle actin (α-SMA) in rat and mouse HSCs. Our data suggest that LAL/Lipa is involved in the degradation of a specific preexisting pool of LDs and that inhibition of this pathway attenuates HSC activation.
[Mh] Termos MeSH primário: Células Estreladas do Fígado/metabolismo
Gotículas Lipídicas/metabolismo
Lisossomos/metabolismo
Esterol Esterase/metabolismo
[Mh] Termos MeSH secundário: Animais
Inibidores Enzimáticos/farmacologia
Feminino
Células Estreladas do Fígado/efeitos dos fármacos
Gotículas Lipídicas/efeitos dos fármacos
Lisossomos/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Ratos
Ratos Wistar
Esterol Esterase/antagonistas & inibidores
Esterol Esterase/deficiência
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enzyme Inhibitors); EC 3.1.1.13 (Sterol Esterase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.778472


  9 / 2106 MEDLINE  
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[PMID]:28538091
[Au] Autor:Gopakumar KG; Thankamony P; Nampoothiri S; Bali D; Raj J; A Vasudevan J; K Nair R
[Ad] Endereço:Departments of *Pediatric Oncology §Imageology ∥Pathology, Regional Cancer Centre, Trivandrum †Department of Pediatric Genetics, Amrita Institute of Medical Sciences, Kochi, Kerala, India ‡Department of Pediatrics Medical Genetics, Duke Health, Durham, NC.
[Ti] Título:Wolman Disease: A Mimic of Infant Leukemia.
[So] Source:J Pediatr Hematol Oncol;39(8):e489-e492, 2017 Nov.
[Is] ISSN:1536-3678
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Infant leukemia most commonly present with pallor and hepatosplenomegaly. The possibility of other differential diagnosis also has to be kept in mind during evaluation, as identifying the precise etiology for this clinical presentation is crucial for management. OBSERVATION: An infant, was referred to us with suspected infant leukemia and was subsequently diagnosed to have lysosomal acid lipase deficiency/Wolman disease with a novel 5 bp deletion "c.1180_1184del" in the last exon (exon 10) of the lipase A (LIPA) gene. CONCLUSIONS: Hepatosplenomegaly and pallor resulting from nutritional deficiency or bone marrow involvement in Wolman disease can mimic infant leukemia.
[Mh] Termos MeSH primário: Doença de Wolman/diagnóstico
[Mh] Termos MeSH secundário: Biópsia
Medula Óssea/patologia
Diagnóstico Diferencial
Hepatomegalia
Homozigoto
Seres Humanos
Lactente
Leucemia/diagnóstico
Masculino
Radiografia Abdominal
Deleção de Sequência
Esterol Esterase/genética
Doença de Wolman/genética
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.1.1.13 (LIPA protein, human); EC 3.1.1.13 (Sterol Esterase)
[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:170525
[St] Status:MEDLINE
[do] DOI:10.1097/MPH.0000000000000861


  10 / 2106 MEDLINE  
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[PMID]:28515323
[Au] Autor:Schott MB; Rasineni K; Weller SG; Schulze RJ; Sletten AC; Casey CA; McNiven MA
[Ad] Endereço:From the Department of Biochemistry and Molecular Biology and.
[Ti] Título:ß-Adrenergic induction of lipolysis in hepatocytes is inhibited by ethanol exposure.
[So] Source:J Biol Chem;292(28):11815-11828, 2017 Jul 14.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In liver steatosis ( fatty liver), hepatocytes accumulate many large neutral lipid storage organelles known as lipid droplets (LDs). LDs are important in the maintenance of energy homeostasis, but the signaling mechanisms that stimulate LD metabolism in hepatocytes are poorly defined. In adipocytes, catecholamines target the ß-adrenergic (ß-AR)/cAMP pathway to activate cytosolic lipases and induce their recruitment to the LD surface. Therefore, the goal of this study was to determine whether hepatocytes, like adipocytes, also undergo cAMP-mediated lipolysis in response to ß-AR stimulation. Using primary rat hepatocytes and human hepatoma cells, we found that treatment with the ß-AR agent isoproterenol caused substantial LD loss via activation of cytosolic lipases adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL). ß-Adrenergic stimulation rapidly activated PKA, which led to the phosphorylation of ATGL and HSL and their recruitment to the LD surface. To test whether this ß-AR-dependent lipolysis pathway was altered in a model of alcoholic fatty liver, primary hepatocytes from rats fed a 6-week EtOH-containing Lieber-DeCarli diet were treated with cAMP agonists. Compared with controls, EtOH-exposed hepatocytes showed a drastic inhibition in ß-AR/cAMP-induced LD breakdown and the phosphorylation of PKA substrates, including HSL. This observation was supported in VA-13 cells, an EtOH-metabolizing human hepatoma cell line, which displayed marked defects in both PKA activation and isoproterenol-induced ATGL translocation to the LD periphery. In summary, these findings suggest that ß-AR stimulation mobilizes cytosolic lipases for LD breakdown in hepatocytes, and perturbation of this pathway could be a major consequence of chronic EtOH insult leading to fatty liver.
[Mh] Termos MeSH primário: Agonistas Adrenérgicos beta/farmacologia
AMP Cíclico/agonistas
Fígado Gorduroso Alcoólico/metabolismo
Hepatócitos/efeitos dos fármacos
Lipólise/efeitos dos fármacos
Receptores Adrenérgicos beta/metabolismo
Sistemas do Segundo Mensageiro/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Células Cultivadas
AMP Cíclico/metabolismo
Proteínas Quinases Dependentes de AMP Cíclico/química
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Ativação Enzimática/efeitos dos fármacos
Fígado Gorduroso Alcoólico/patologia
Feminino
Hepatócitos/citologia
Hepatócitos/metabolismo
Hepatócitos/patologia
Seres Humanos
Lipase/química
Lipase/metabolismo
Gotículas Lipídicas/efeitos dos fármacos
Gotículas Lipídicas/metabolismo
Gotículas Lipídicas/patologia
Masculino
Fosforilação/efeitos dos fármacos
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
Transporte Proteico/efeitos dos fármacos
Ratos
Receptores Adrenérgicos beta/química
Esterol Esterase/química
Esterol Esterase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-Agonists); 0 (Receptors, Adrenergic, beta); E0399OZS9N (Cyclic AMP); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 3.1.1.13 (Sterol Esterase); EC 3.1.1.3 (Lipase); EC 3.1.1.3 (PNPLA2 protein, rat)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170803
[Lr] Data última revisão:
170803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.777748



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