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Pesquisa : A11.284.430.214.190.875.393 [Categoria DeCS]
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[PMID]:29328968
[Au] Autor:Gruber JV; Holtz R; In Yang S
[Ad] Endereço:Botaneco, 201 S. Main Street, Lambertville, NJ 08530, USA. Electronic address: vgruber@botaneco.com.
[Ti] Título:In vitro examination of an oleosome-based sun protection product on the influence of UVB-induced inflammation markers in human epidermal skin equivalent tissue model.
[So] Source:J Photochem Photobiol B;179:39-45, 2018 Feb.
[Is] ISSN:1873-2682
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:In vitro human epidermal skin equivalent tissues (MatTek EpiDerm™) were employed to examine the influence of UVB radiation on various established inflammation markers in the presence of topically applied sunscreens. MatTek EpiDerm™ tissues were treated with 2.0mg/cm of an Experimental oleosome-based SPF 30 product or a commercial SPF 30 beach product. Tissues were irradiated with 300mJ/cm of UVB radiation. Inflammatory cytokines IL-1α, IL-6 and IL-8 as well as arachidonic acid cascade marker PGE were examined via ELISA-based antibody detection. Untreated tissues irradiated with 300mJ/cm of UVB radiation showed statistically significant upregulation of IL-1α, IL-6 and IL-8 as well as PGE . Application of both the experimental oleosome-based SPF 30 formulation and the commercial SPF 30 formulation demonstrated an ability to prevent the upregulation of all four markers when applied prior to irradiation. The experimental oleosome-based SPF 30 product contained approximately 80% less sunscreen actives than the commercial formulation. This study demonstrates that in vitro reconstructed human tissues can be used to study the influences of sun screen actives in the presence of UVB radiation. The results support previously reported clinical results that demonstrated that oleosome-based sun care formulations can function with high protection effects with significantly less sun care actives.
[Mh] Termos MeSH primário: Biomarcadores/metabolismo
Gotículas Lipídicas/química
Modelos Biológicos
Protetores Solares/farmacologia
Tecidos Suporte/química
Raios Ultravioleta
[Mh] Termos MeSH secundário: Linhagem Celular
Dinoprostona/metabolismo
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Inflamação/metabolismo
Inflamação/patologia
Interleucina-1alfa/análise
Interleucina-1alfa/metabolismo
Interleucina-6/análise
Interleucina-6/metabolismo
Interleucina-8/análise
Interleucina-8/metabolismo
Queratinócitos/efeitos dos fármacos
Queratinócitos/efeitos da radiação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Interleukin-1alpha); 0 (Interleukin-6); 0 (Interleukin-8); 0 (Sunscreening Agents); K7Q1JQR04M (Dinoprostone)
[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:180113
[St] Status:MEDLINE


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[PMID]:28743757
[Au] Autor:Nielsen J; Christensen AE; Nellemann B; Christensen B
[Ad] Endereço:Department of Sports Science and Clinical Biomechanics, SDU Muscle Research Cluster (SMRC), University of Southern Denmark, Odense M, Denmark; jnielsen@health.sdu.dk.
[Ti] Título:Lipid droplet size and location in human skeletal muscle fibers are associated with insulin sensitivity.
[So] Source:Am J Physiol Endocrinol Metab;313(6):E721-E730, 2017 12 01.
[Is] ISSN:1522-1555
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In skeletal muscle, an accumulation of lipid droplets (LDs) in the subsarcolemmal space is associated with insulin resistance, but the underlying mechanism is not clear. We aimed to investigate how the size, number, and location of LDs are associated with insulin sensitivity and muscle fiber types and are regulated by aerobic training and treatment with an erythropoiesis-stimulating agent (ESA) in healthy young untrained men. LD analyses were performed by quantitative transmission electron microscopy, and insulin sensitivity was assessed by a hyperinsulinemic-euglycemic clamp. At baseline, we found that only the diameter (and not the number) of individual subsarcolemmal LDs was negatively associated with insulin sensitivity ( = 0.20, = 0.03, = 29). Despite 34% ( = 0.004) fewer LDs, the diameter of individual subsarcolemmal LDs was 20% ( = 0.0004) larger in type 2 fibers than in type 1 fibers. Furthermore, aerobic training decreased the size of subsarcolemmal LDs in the type 2 fibers, and ESA treatment lowered the number of both intermyofibrillar and subsarcolemmal LDs in the type 1 fibers. In conclusion, the size of individual subsarcolemmal LDs may be involved in the mechanism by which LDs are associated with insulin resistance in skeletal muscle.
[Mh] Termos MeSH primário: Resistência à Insulina
Gotículas Lipídicas/metabolismo
Metabolismo dos Lipídeos/fisiologia
Fibras Musculares Esqueléticas/metabolismo
Músculo Esquelético/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Adulto
Exercício/fisiologia
Técnica Clamp de Glucose
Seres Humanos
Gotículas Lipídicas/patologia
Masculino
Tamanho da Partícula
Resistência Física
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1152/ajpendo.00062.2017


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[PMID]:29293661
[Au] Autor:Monson EA; Crosse KM; Das M; Helbig KJ
[Ad] Endereço:Department of Physiology, Anatomy and Microbiology, La Trobe University, Melbourne, Victoria.
[Ti] Título:Lipid droplet density alters the early innate immune response to viral infection.
[So] Source:PLoS One;13(1):e0190597, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cellular localisation of many innate signalling events following viral infection has yet to be elucidated, however there has been a few cases in which membranes of certain cellular organelles have acted as platforms to these events. Of these, lipid droplets (LDs) have recently been identified as signalling platforms for innate TLR7 and 9 signalling. Despite their wide range of similar roles in various metabolic pathways, LDs have been overlooked as potential platforms for antiviral innate signalling events. This study established an in vitro model to evaluate the efficiency of the early innate immune response in cells with reduced LD content to the viral mimics, dsDNA and dsRNA, and Sendai viral infection. Using RT-qPCR, the expression of IFN-ß and IFN-λ was quantified following stimulation along with the expression of specific ISGs. Luciferase based assays evaluated the combined expression of ISRE-promoter driven ISGs under IFN-ß stimulation. Cellular LD content did not alter the entry of fluorescently labelled viral mimics into cells, but significantly decreased the ability of both Huh-7 and HeLa cells to produce type I and III IFN, as well as downstream ISG expression, indicative of an impeded innate immune response. This observation was also seen during Sendai virus infection of HeLa cells, where both control and LD reduced cells replicated the virus to the same level, but a significantly impaired type I and III IFN response was observed in the LD reduced cells. In addition to altered IFN production, cells with reduced LD content exhibited decreased expression of specific antiviral ISGs: Viperin, IFIT-1 and OAS-1 under IFN-ß stimulation; However the overall induction of the ISRE-promoter was not effected. This study implicates a role for LDs in an efficient early innate host response to viral infection and future work will endeavour to determine the precise role these important organelles play in induction of an antiviral response.
[Mh] Termos MeSH primário: Imunidade Inata
Gotículas Lipídicas/metabolismo
Viroses/imunologia
[Mh] Termos MeSH secundário: Western Blotting
Linhagem Celular
Meios de Cultura
Seres Humanos
Interferon Tipo I/imunologia
Ácidos Nucleicos/metabolismo
RNA de Cadeia Dupla/imunologia
Reação em Cadeia da Polimerase em Tempo Real
Vírus Sendai/patogenicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Culture Media); 0 (Interferon Type I); 0 (Nucleic Acids); 0 (RNA, Double-Stranded)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190597


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[PMID]:28454542
[Au] Autor:Itabe H; Yamaguchi T; Nimura S; Sasabe N
[Ad] Endereço:Division of Biological Chemistry, Department of Molecular Biology, Showa University School of Pharmacy, 1-5-8 Hatanodai, Shinagawa, Tokyo, 142-8555, Japan. h-itabe@pharm.showa-u.ac.jp.
[Ti] Título:Perilipins: a diversity of intracellular lipid droplet proteins.
[So] Source:Lipids Health Dis;16(1):83, 2017 Apr 28.
[Is] ISSN:1476-511X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Intracellular lipid droplets (LDs) are found in a wide variety of cell types and have been recognized as organelles with unique spherical structures. Although LDs are not stable lipid-depots, they are active sites of neutral lipid metabolism, and comprise neutral lipid or cholesterol cores surrounded by phospholipid monolayers containing specialized proteins. However, sizes and protein compositions vary between cell and tissue types. Proteins of the perilipin family have been associated with surfaces of LDs and all carry a conserved 11-mer repeat motif. Accumulating evidence indicates that all perilipins are involved in LD formation and that all play roles in LD function under differing conditions. In this brief review, we summarize current knowledge of the roles of perilipins and lipid metabolizing enzymes in a variety of mammalian cell types.
[Mh] Termos MeSH primário: Adipócitos/metabolismo
Hidroxiesteroide Desidrogenases/genética
Gotículas Lipídicas/metabolismo
Metabolismo dos Lipídeos/genética
Perilipinas/genética
[Mh] Termos MeSH secundário: Animais
Colesterol/metabolismo
Retículo Endoplasmático/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Hidroxiesteroide Desidrogenases/metabolismo
Mitocôndrias/metabolismo
Perilipinas/química
Perilipinas/classificação
Perilipinas/metabolismo
Domínios Proteicos
Transdução de Sinais
Triglicerídeos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Perilipins); 0 (Triglycerides); 97C5T2UQ7J (Cholesterol); EC 1.1.- (Hydroxysteroid Dehydrogenases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.1186/s12944-017-0473-y


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[PMID]:29304246
[Au] Autor:Ma Y; Zhou Y; Zhu YC; Wang SQ; Ping P; Chen XF
[Ad] Endereço:Center for Reproductive Medicine, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200135, China.
[Ti] Título:Lipophagy Contributes to Testosterone Biosynthesis in Male Rat Leydig Cells.
[So] Source:Endocrinology;159(2):1119-1129, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In recent years, autophagy was found to regulate lipid metabolism through a process termed lipophagy. Lipophagy modulates the degradation of cholesteryl esters to free cholesterol (FC), which is the substrate of testosterone biosynthesis. However, the role of lipophagy in testosterone production is unknown. To investigate this, primary rat Leydig cells and varicocele rat models were administered to inhibit or promote autophagy, and testosterone, lipid droplets (LDs), total cholesterol (TC), and FC were evaluated. The results demonstrated that inhibiting autophagy in primary rat Leydig cells reduced testosterone production. Further studies demonstrated that inhibiting autophagy increased the number and size of LDs and the level of TC, but decreased the level of FC. Furthermore, hypoxia promoted autophagy in Leydig cells. We found that short-term hypoxia stimulated testosterone secretion; however, the inhibition of autophagy abolished stimulated testosterone release. Hypoxia decreased the number and size of LDs in Leydig cells, but the changes could be largely rescued by blocking autophagy. In experimental varicocele rat models, the administration of autophagy inhibitors substantially reduced serum testosterone. These data demonstrate that autophagy contributes to testosterone biosynthesis at least partially through degrading intracellular LDs/TC. Our observations might reveal an autophagic regulatory mode regarding testosterone biosynthesis.
[Mh] Termos MeSH primário: Autofagia/fisiologia
Células Intersticiais do Testículo/metabolismo
Lipólise/fisiologia
Testosterona/biossíntese
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Colesterol/metabolismo
Gotículas Lipídicas/metabolismo
Metabolismo dos Lipídeos/fisiologia
Masculino
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
3XMK78S47O (Testosterone); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-03020


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[PMID]:29227097
[Au] Autor:McClements DJ; Decker E
[Ad] Endereço:Department of Food Science, University of Massachusetts Amherst , Amherst, Massachusetts 01003, United States.
[Ti] Título:Interfacial Antioxidants: A Review of Natural and Synthetic Emulsifiers and Coemulsifiers That Can Inhibit Lipid Oxidation.
[So] Source:J Agric Food Chem;66(1):20-35, 2018 Jan 10.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There has been strong interest in developing effective strategies to inhibit lipid oxidation in emulsified food products due to the need to incorporate oxidatively labile bioactive lipids, such as ω-3 fatty acids, conjugated linoleic acids, or carotenoids. Emulsifiers or coemulsifiers can be utilized to inhibit lipid oxidation in emulsions. Both of these molecular types can adsorb to droplet surfaces and inhibit lipid oxidation, but emulsifiers can also stabilize droplets against aggregation whereas coemulsifiers cannot. There are a host of existing emulsifiers, covalent conjugates, or physical complexes that have the potential to inhibit lipid oxidation by a variety of mechanisms. Existing emulsifiers with antioxidant potential consist of surfactants, phospholipids, proteins, polysaccharides, and colloidal particles. Conjugates and complexes are typically formed by covalently or physically linking together a surface-active molecule with an antioxidant molecule. This article reviews the molecular and physicochemical basis for the surface and antioxidant activities of emulsifiers and coemulsifiers, highlights the important properties of interfacial layers that can be engineered to control lipid oxidation, and outlines different kinds of existing emulsifiers, conjugates, and complexes that can be used to inhibit oxidation.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Emulsificantes/química
Emulsificantes/farmacologia
Lipídeos/química
[Mh] Termos MeSH secundário: Adsorção
Antioxidantes/química
Depuradores de Radicais Livres/química
Depuradores de Radicais Livres/farmacologia
Interações Hidrofóbicas e Hidrofílicas
Gotículas Lipídicas/química
Metabolismo dos Lipídeos
Oxirredução
Fosfolipídeos/química
Polissacarídeos/química
Proteínas/química
Eletricidade Estática
Tensoativos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antioxidants); 0 (Emulsifying Agents); 0 (Free Radical Scavengers); 0 (Lipids); 0 (Phospholipids); 0 (Polysaccharides); 0 (Proteins); 0 (Surface-Active Agents)
[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:171212
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b05066


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[PMID]:29247649
[Au] Autor:Park KY; Kim WT; Kim EY
[Ad] Endereço:Department of Systems Biology, College of Life Sciences and Biotechnology, Yonsei University, Seoul 03722, South Korea.
[Ti] Título:The proper localization of RESPONSIVE TO DESICCATION 20 in lipid droplets depends on their biogenesis induced by STRESS-RELATED PROTEINS in vegetative tissues.
[So] Source:Biochem Biophys Res Commun;495(2):1885-1889, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Arabidopsis LD surface proteins, SRPs are found only in higher plants and are important for LD biogenesis and abiotic stress signaling. However, the cellular mechanism of SRPs is still unclear. To investigate molecular functions of SRPs, we used tobacco transient expression system. Transient expression of SRPs was sufficient and synergistic for LD biogenesis, and SRPs participated in the formation step of LD in tobacco leaves. RESPONSIVE TO DESICCATION 20 (RD20), a known LD-localizing peroxygenase, localized to LD in the presence of an SRP, and its peroxygenase activity correlated with proper localization of RD20 to LD. Our data suggest that Arabidopsis SRPs play roles as positive factors for LD biogenesis to provide a proper localization of LD-localizing proteins in vegetative tissues.
[Mh] Termos MeSH primário: Proteínas de Arabidopsis/biossíntese
Arabidopsis/metabolismo
Proteínas de Ligação ao Cálcio/biossíntese
Regulação da Expressão Gênica de Plantas/fisiologia
Proteínas de Choque Térmico/metabolismo
Gotículas Lipídicas/metabolismo
Frações Subcelulares/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Arabidopsis Proteins); 0 (Calcium-Binding Proteins); 0 (Heat-Shock Proteins); 0 (RD20 protein, Arabidopsis)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE


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[PMID]:29216638
[Au] Autor:Wu GY; Rui C; Chen JQ; Sho E; Zhan SS; Yuan XW; Ding YT
[Ad] Endereço:Department of Hepatobiliary Surgery, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China.
[Ti] Título:MicroRNA-122 Inhibits Lipid Droplet Formation and Hepatic Triglyceride Accumulation via Yin Yang 1.
[So] Source:Cell Physiol Biochem;44(4):1651-1664, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: An increase in intracellular lipid droplet formation and hepatic triglyceride (TG) content usually results in nonalcoholic fatty liver disease. However, the mechanisms underlying the regulation of hepatic TG homeostasis remain unclear. METHODS: Oil red O staining and TG measurement were performed to determine the lipid content. miRNA expression was evaluated by quantitative PCR. A luciferase assay was performed to validate the regulation of Yin Yang 1 (YY1) by microRNA (miR)-122. The effects of miR-122 expression on YY1 and its mechanisms involving the farnesoid X receptor and small heterodimer partner (FXR-SHP) pathway were evaluated by quantitative PCR and Western blot analyses. RESULTS: miR-122 was downregulated in free fatty acid (FFA)-induced steatotic hepatocytes, and streptozotocin and high-fat diet (STZ-HFD) induced nonalcoholic steatohepatitis (NASH) in mice. Transfection of hepatocytes with miR-122 mimics before FFA induction inhibited lipid droplet formation and TG accumulation in vitro. These results were verified by overexpressing miR-122 in the livers of STZ-HFD-induced NASH mice. The 3'-untranslated region (3'UTR) of YY1 mRNA is predicted to contain an evolutionarily conserved miR-122 binding site. In silico searches, a luciferase reporter assay and quantitative PCR analysis confirmed that miR-122 directly bound to the YY1 3'UTR to negatively regulate YY1 mRNA in HepG2 and Huh7 cells. The (FXR-SHP) signaling axis, which is downstream of YY1, may play a key role in the mechanism of miR-122-regulated lipid homeostasis. YY1-FXR-SHP signaling, which is negatively regulated by FFA, was enhanced by miR-122 overexpression. This finding was also confirmed by overexpression of miR-122 in the livers of NASH mice. CONCLUSIONS: The present results indicate that miR-122 plays an important role in lipid (particularly TG) accumulation in the liver by reducing YY1 mRNA stability to upregulate FXR-SHP signaling.
[Mh] Termos MeSH primário: Gotículas Lipídicas/metabolismo
MicroRNAs/metabolismo
Triglicerídeos/metabolismo
Fator de Transcrição YY1/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Antagomirs/metabolismo
Sequência de Bases
Linhagem Celular Tumoral
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Experimental/patologia
Dieta Hiperlipídica
Modelos Animais de Doenças
Regulação para Baixo/efeitos dos fármacos
Ácidos Graxos não Esterificados/farmacologia
Proteína do X Frágil de Retardo Mental/genética
Proteína do X Frágil de Retardo Mental/metabolismo
Células Hep G2
Seres Humanos
Gotículas Lipídicas/efeitos dos fármacos
Fígado/metabolismo
Fígado/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
MicroRNAs/antagonistas & inibidores
MicroRNAs/genética
Hepatopatia Gordurosa não Alcoólica/metabolismo
Hepatopatia Gordurosa não Alcoólica/patologia
Receptores Citoplasmáticos e Nucleares/genética
Receptores Citoplasmáticos e Nucleares/metabolismo
Alinhamento de Sequência
Fator de Transcrição YY1/química
Fator de Transcrição YY1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Antagomirs); 0 (Fatty Acids, Nonesterified); 0 (MIRN122 microRNA, human); 0 (MicroRNAs); 0 (Receptors, Cytoplasmic and Nuclear); 0 (Triglycerides); 0 (YY1 Transcription Factor); 0 (nuclear receptor subfamily 0, group B, member 2); 139135-51-6 (Fragile X Mental Retardation Protein)
[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:171208
[St] Status:MEDLINE
[do] DOI:10.1159/000485765


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[PMID]:28465089
[Au] Autor:Zahradka P; Neumann S; Aukema HM; Taylor CG
[Ad] Endereço:Department of Physiology and Pathophysiology, University of Manitoba, Canada; Department of Human Nutritional Sciences, University of Manitoba, Canada; Canadian Centre for Agri-Food Research in Health and Medicine, St. Boniface Albrechtsen Research Centre, Winnipeg, Canada. Electronic address: pzahr
[Ti] Título:Adipocyte lipid storage and adipokine production are modulated by lipoxygenase-derived oxylipins generated from 18-carbon fatty acids.
[So] Source:Int J Biochem Cell Biol;88:23-30, 2017 07.
[Is] ISSN:1878-5875
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Generation of oxylipins (oxygenated metabolites of fatty acids) by lipoxygenases may be responsible for the beneficial effects of 20- and 22-carbon n-3 fatty acids on adipose tissue dysfunction in obesity, but the potential actions of oxylipins derived from 18-carbon fatty acids, which are generally at higher levels in the diet, are unknown. We therefore compared the effects of select lipoxygenase-derived oxylipins produced from α-linolenic acid (ALA, C18:3 n-3), linoleic acid (LA, C18:2 n-6), and arachidonic acid (AA, C20:4 n-6) on key adipocyte functions that are altered in obesity. Individual oxylipins were added to the culture medium of differentiating 3T3-L1 preadipocytes for 6days. Lipid accumulation was subsequently determined by Oil Red O staining, while Western blotting was used to measure levels of proteins associated with lipid metabolism and characteristics of adipocyte functionality. Addition of all oxylipins at 30nM was sufficient to significantly decrease triglyceride accumulation in lipid droplets, and higher levels completely blocked lipid production. Our results establish that lipoxygenase-derived oxylipins produced from 18-carbon PUFA differentially affect multiple adipocyte processes associated with lipid storage and adipokine production. However, these effects are not due to the oxylipins blocking adipocyte maturation and thus globally suppressing all adipocyte characteristics. Furthermore, these oxylipin species decrease the lipid content of adipocytes regardless from which precursor fatty acid or lipoxygenase they were derived. Consequently, adipocyte characteristics can be altered through the ability of oxylipins to selectively modulate levels of proteins involved in both lipid metabolism and adipokine production.
[Mh] Termos MeSH primário: Adipócitos/efeitos dos fármacos
Adipócitos/metabolismo
Adipocinas/biossíntese
Gotículas Lipídicas/efeitos dos fármacos
Lipoxigenase/metabolismo
Oxilipinas/metabolismo
Oxilipinas/farmacologia
[Mh] Termos MeSH secundário: Células 3T3-L1
Adipócitos/citologia
Animais
Diferenciação Celular/efeitos dos fármacos
Gotículas Lipídicas/metabolismo
Camundongos
Oxilipinas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adipokines); 0 (Oxylipins); EC 1.13.11.12 (Lipoxygenase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:29203241
[Au] Autor:Mikoluk C; Nagengast AA; DiAngelo JR
[Ad] Endereço:Division of Science, Penn State Berks, Reading, PA, United States.
[Ti] Título:The splicing factor transformer2 (tra2) functions in the Drosophila fat body to regulate lipid storage.
[So] Source:Biochem Biophys Res Commun;495(1):1528-1533, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Excess nutrients are stored as triglycerides mainly in the adipose tissue of an animal and these triglycerides are located in structures called lipid droplets. Previous genome-wide RNAi screens in Drosophila cells identified splicing factors as playing a role in lipid droplet formation. Our lab has recently identified the SR protein, 9G8, as an important factor in fat storage as decreasing its levels results in augmented triglyceride storage in the fat body. Previous in vitro studies have implicated 9G8 in the regulation of splicing of the sex determination gene doublesex (dsx) by binding to transformer (tra) and transformer2 (tra2); however, any function of these sex determination proteins in regulating metabolism is unknown. In this study, we have uncovered a role of tra2 to regulate fat storage in vivo. Inducing tra2 in the adult fat body resulted in an increase in triglyceride levels but had no effect on glycogen storage. Consistent with the triglyceride phenotype, tra2 knockdown flies lived longer under starvation conditions. In addition, this increase in triglycerides is due to more fat storage per cell and not an increase in the number of fat cells. Interestingly, the splicing of CPT1, an enzyme involved in the breakdown of lipids, was altered in flies with decreased tra2. The less-catalytically active isoform of CPT1 accumulated in tra2 flies suggesting a decrease in lipid breakdown, which is consistent with the increased triglyceride levels observed in these flies. Together, these results suggest a link between mRNA splicing, sex determination and lipid metabolism and may provide insight into the mechanisms underlying tissue-specific splicing and nutrient storage.
[Mh] Termos MeSH primário: Proteínas de Drosophila/metabolismo
Drosophila melanogaster/fisiologia
Regulação da Expressão Gênica/fisiologia
Gotículas Lipídicas/fisiologia
Metabolismo dos Lipídeos/fisiologia
Fatores de Processamento de RNA/metabolismo
Ribonucleoproteínas/metabolismo
[Mh] Termos MeSH secundário: Animais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Drosophila Proteins); 0 (RNA Splicing Factors); 0 (Ribonucleoproteins); 0 (tra2 protein, Drosophila)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE



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