Literatura académica sobre el tema "ABCA1/ABCG1"
Crea una cita precisa en los estilos APA, MLA, Chicago, Harvard y otros
Consulte las listas temáticas de artículos, libros, tesis, actas de conferencias y otras fuentes académicas sobre el tema "ABCA1/ABCG1".
Junto a cada fuente en la lista de referencias hay un botón "Agregar a la bibliografía". Pulsa este botón, y generaremos automáticamente la referencia bibliográfica para la obra elegida en el estilo de cita que necesites: APA, MLA, Harvard, Vancouver, Chicago, etc.
También puede descargar el texto completo de la publicación académica en formato pdf y leer en línea su resumen siempre que esté disponible en los metadatos.
Artículos de revistas sobre el tema "ABCA1/ABCG1"
Esobi, Ikechukwu, Oladosu Olanrewaju, Jing Echesabal-Chen y Alexis Stamatikos. "Utilizing the LoxP-Stop-LoxP System to Control Transgenic ABC-Transporter Expression In Vitro". Biomolecules 12, n.º 5 (8 de mayo de 2022): 679. http://dx.doi.org/10.3390/biom12050679.
Texto completoTavoosi, Zahra, Hemen Moradi-Sardareh, Massoud Saidijam, Reza Yadegarazari, Shiva Borzuei, Alireza Soltanian y Mohammad Taghi Goodarzi. "Cholesterol Transporters ABCA1 and ABCG1 Gene Expression in Peripheral Blood Mononuclear Cells in Patients with Metabolic Syndrome". Cholesterol 2015 (15 de diciembre de 2015): 1–6. http://dx.doi.org/10.1155/2015/682904.
Texto completoMiroshnikova, V. V., A. A. Panteleeva, E. A. Bazhenova, E. P. Demina, T. S. Usenko, M. A. Nikolaev, I. A. Semenova et al. "Regulation of ABCA1 and ABCG1 gene expression in the intraabdominal adipose tissue". Biomeditsinskaya Khimiya 62, n.º 3 (2016): 283–89. http://dx.doi.org/10.18097/pbmc20166203283.
Texto completoPorsch-Özcürümez, Mustafa, Thomas Langmann, Susanne Heimerl, Hana Borsukova, Wolfgang E. Kaminski, Wolfgang Drobnik, Christian Honer, Chistoph Schumacher y Gerd Schmitz. "The Zinc Finger Protein 202 (ZNF202) Is a Transcriptional Repressor of ATP Binding Cassette Transporter A1 (ABCA1) and ABCG1 Gene Expression and a Modulator of Cellular Lipid Efflux". Journal of Biological Chemistry 276, n.º 15 (22 de enero de 2001): 12427–33. http://dx.doi.org/10.1074/jbc.m100218200.
Texto completoCheng-Mao, Xie, Long Yan, Lin Li, Jin Hua, Wang Xiao-Ju y Zhang Jie-Wen. "Placental ABCA1 Expression Is Increased in Spontaneous Preterm Deliveries Compared with Iatrogenic Preterm Deliveries and Term Deliveries". BioMed Research International 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/8248094.
Texto completoOladosu, Olanrewaju, Ikechukwu C. Esobi, Rhonda R. Powell, Terri Bruce y Alexis Stamatikos. "Dissecting the Impact of Vascular Smooth Muscle Cell ABCA1 versus ABCG1 Expression on Cholesterol Efflux and Macrophage-like Cell Transdifferentiation: The Role of SR-BI". Journal of Cardiovascular Development and Disease 10, n.º 10 (2 de octubre de 2023): 416. http://dx.doi.org/10.3390/jcdd10100416.
Texto completoMani, Orlando, Meike Körner, Martin T. Sorensen, Kristen Sejrsen, Carlos Wotzkow, Corneille E. Ontsouka, Robert R. Friis, Rupert M. Bruckmaier y Christiane Albrecht. "Expression, localization, and functional model of cholesterol transporters in lactating and nonlactating mammary tissues of murine, bovine, and human origin". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, n.º 2 (agosto de 2010): R642—R654. http://dx.doi.org/10.1152/ajpregu.00723.2009.
Texto completoLin, Hung-Chih, Chong-Kuei Lii, Hui-Chun Chen, Ai-Hsuan Lin, Ya-Chen Yang y Haw-Wen Chen. "Andrographolide Inhibits Oxidized LDL-Induced Cholesterol Accumulation and Foam Cell Formation in Macrophages". American Journal of Chinese Medicine 46, n.º 01 (enero de 2018): 87–106. http://dx.doi.org/10.1142/s0192415x18500052.
Texto completoМирошникова, В. В., А. А. Пантелеева, И. А. Побожева, Н. Д. Разгильдина, К. В. Драчева, Е. А. Полякова, А. В. Марков et al. "Аdipose tissue expression of ABCA1 and ABCG1 transporters genes in obesity, metabolic syndrome and ischemic heart disease". Nauchno-prakticheskii zhurnal «Medicinskaia genetika», n.º 5(214) (29 de mayo de 2020): 56–57. http://dx.doi.org/10.25557/2073-7998.2020.05.56-57.
Texto completoDelvecchio, Christopher J., Patricia Bilan, Parameswaran Nair y John P. Capone. "LXR-induced reverse cholesterol transport in human airway smooth muscle is mediated exclusively by ABCA1". American Journal of Physiology-Lung Cellular and Molecular Physiology 295, n.º 5 (noviembre de 2008): L949—L957. http://dx.doi.org/10.1152/ajplung.90394.2008.
Texto completoTesis sobre el tema "ABCA1/ABCG1"
Matsuda, Akihiro. "(24S)-Hydroxycholesterol efflux from neuronal cells by ABC proteins". Kyoto University, 2014. http://hdl.handle.net/2433/185211.
Texto completo0048
新制・課程博士
博士(農学)
甲第17986号
農博第2033号
新制||農||1019(附属図書館)
学位論文||H26||N4811(農学部図書室)
80830
京都大学大学院農学研究科応用生命科学専攻
(主査)教授 植田 和光, 教授 植田 充美, 教授 三芳 秀人
学位規則第4条第1項該当
Brüggmann, Nina [Verfasser]. "Untersuchungen zum ABCA1-/ABCG1-vermittelten Cholesterin-Efflux in humanen Kontroll- und Tangierfibroblasten / Nina Brüggmann". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2021. http://d-nb.info/1228861153/34.
Texto completoZago, Vanessa Helena de Souza 1984. "Estudo molecular dos genes ABCA1, ABCG1, ABCG5, ABCG8 e SCARB1 em amostra populacional brasileira assintomática". [s.n.], 2015. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312594.
Texto completoTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-26T20:49:38Z (GMT). No. of bitstreams: 1 Zago_VanessaHelenadeSouza_D.pdf: 5059555 bytes, checksum: 854d9d1d1674a14d2ebcf5798acc31b3 (MD5) Previous issue date: 2015
Resumo: Dado o importante papel desempenhado pelos transportadores ATP binding cassete A1 (ABCA1), G1 (ABCG1), G5 (ABCG5), G8 (ABCG8) e pelo scavenger receptor class B type I (SR-BI) para a homeostase corpórea de colesterol e desenvolvimento da aterosclerose, este trabalho se propôs a: (i) investigar a relação dos polimorfismos rs2275543 (ABCA1), rs1893590 (ABCG1), rs6720173 (ABCG5), rs6544718 (ABCG8) e rs5888 (SCARB1) com gênero, idade e índice de massa corpórea (IMC) e suas interações sobre variáveis clínicas e bioquímicas (n=654); (ii) determinar a repercussão destes polimorfismos sobre os parâmetros estudados na população total e de forma gênero-específica (n=590) e (iii) avaliar se os miRNAs hsa-miR-33a e hsa-miR-128a são diferencialmente expressos em um subgrupo da população (n=51) e averiguar sua associação com as concentrações plasmáticas do colesterol da lipoproteína de alta densidade (HDL-C), aterosclerose subclínica e expressão de ABCA1, ABCG1 e SCARB1. Para tanto, foram selecionados voluntários normolipidêmicos e assintomáticos, de ambos os gêneros, com idade entre 20 e 75 anos. Dados clínicos e antropométricos foram obtidos, assim como sangue venoso periférico para as determinações bioquímicas e extração de DNA e RNA. O subgrupo de 51 voluntários foi classificado de acordo com HDL-C (mg/dL) em hipoalfalipoproteinêmicos (hipo, HDL-C?39), hiperalfalipoproteinêmicos (hiper, HDL-C?68) e controles (CTL, HDL-C?40<68) e determinadas a espessura íntimo-medial das artérias carótidas e proteínas relacionadas ao metabolismo de HDL. Determinamos que o rs1893590 interage com a idade e o IMC, modulando as concentrações de HDL-C, bem como o tamanho e volume da partícula, sugerindo que este pode modificar seu metabolismo e composição. Nas análises comparativas o rs2275543 apresentou efeitos diferentes, porém benéficos para ambos os gêneros; adicionalmente, o rs6720173 determinou um fenótipo lipoproteico proaterogênico no gênero masculino, enquanto as variantes rs5888 e rs6544718 repercutiram sobre marcadores de adiposidade no gênero feminino. A análise dos cinco polimorfismos nesta população fornece evidências de que estes atuam em diferentes vias do metabolismo lipoproteico, e tem na maioria dos casos características gênero-específicas. Adicionalmente, a avaliação da expressão de hsa-miR-33a, hsa-miR-128a, ABCA1, ABCG1 e SCARB1 revelou que os indivíduos hiper apresentam um aumento da expressão de ABCA1 e ABCG1 em relação ao grupo CTL, somado a uma redução de 72% na expressão do hsa-miR-33a; em conjunto, estes resultados indicam um potencial papel regulatório deste miRNA em indivíduos assintomáticos, possivelmente contribuindo para o aumento do efluxo e do transporte reverso de colesterol
Abstract: Given the important role played by ATP binding cassete transporters A1 (ABCA1), G1 (ABCG1), G5 (ABCG5), G8 (ABCG8) and by scavenger receptor class B type I (SR-BI) on body cholesterol homeostasis and atherosclerosis development, this study proposes to: (i) investigate the relationship of polymorphisms rs2275543 (ABCA1), rs1893590 (ABCG1), rs6720173 (ABCG5), rs6544718 (ABCG8) e rs5888 (SCARB1) with gender, age and body mass index (BMI) and its interactions with clinical and biochemical variables (n=654); (ii) determine the effects of these polymorphisms on the studied parameters in the total population and in a gender-specific manner (n=590) and (iii) evaluate if miRNAs hsa-miR-33a e hsa-miR-128a are differentially expressed in a subgroup of the population (n=51) and verify its association with plasma levels of high-density lipoprotein cholesterol (HDL-C), subclinical atherosclerosis plus ABCA1, ABCG1 and SCARB1 expression. Thus, normolipidemic and asymptomatic volunteers from both genders, with ages ranging from 20 to 75 years were selected. Clinical and anthropometric data were obtained, as well as peripheral venous blood for biochemical determinations plus DNA and RNA extraction. The subgroup of 51 individuals was classified according HDL-C (mg/dL) in hypoalphalipoproteinemics (hypo, HDL-C?39), hyperalphalipoproteinemics (hyper, HDL-C?68) and controls (CTL, HDL-C?40<68); then, were determinated the carotid intima-media thickness and proteins related to HDL metabolism. The polymorphism rs1893590 interacts with age and BMI, modulating HDL-C levels as well as the particle size and volume, suggesting its role on HDL metabolism and composition. Comparative analysis demonstrated that rs2275543 has different, but beneficial repercussions in both genders; furthermore, rs6720173 determines a pro-atherogenic lipoprotein profile in males, while the variants rs5888 and rs6544718 affect positively adiposity markers in females. The analyses of the five studied polymorphism in this population provide evidences of its role in several pathways of lipoproteins metabolism, in most cases in a gender-specific manner. Moreover, the ABCA1, ABCG1, SCARB1, hsa-miR-33a and hsa-miR-128a expression analysis revealed that hyper group presents a significant increase of ABCA1 and ABCG1 expression in relation to the control group; additionally, hsa-miR-33a decreased by 72%. Together, these results indicate a potential regulatory role of this miRNA in asymptomatic individuals, probably contributing to increased cholesterol efflux and reverse cholesterol transport
Doutorado
Ciencias Biomedicas
Doutora em Ciências Médicas
Monzel, Judith Verena [Verfasser]. "Regulation der Cholesteroltransporter ABCA1 und ABCG1 im Kontext der Doxorubicin-induzierten Kardiotoxizität / Judith Verena Monzel". Greifswald : Universitätsbibliothek Greifswald, 2017. http://d-nb.info/1143131673/34.
Texto completoAleidi, Shereen Mohammad Suleimann. "Characterization of the Post-Translational Regulation of the ABCA1 and ABCG1 Lipid Transporters by E3 Ligases". Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/15477.
Texto completoGuilbaud, Emma. "Nouvelles altérations métaboliques des cancers bronchiques non à petites cellules : rôle de l’efflux du cholestérol et de la mitophagie". Electronic Thesis or Diss., Université Côte d'Azur, 2021. http://theses.univ-cotedazur.fr/2021COAZ6021.
Texto completoLung cancer is the leading cause of cancer death worldwide, with non-small cell lung cancer (NSCLC) accounting for up to 85% of all cases. Most of patients are diagnosed with late-stage lung cancer and despite recent advances in effective therapies such as targeted therapies and immunotherapies, the average 5-year survival rate is around 20%. Therefore, a better biological insights of cancer cells to exploit their vulnerabilities are essential to improve potential therapeutic targets and patient outcome. In this context, I got interested in metabolic alterations in NSCLC.First, I focused on the role of cholesterol efflux pathways during NSCLC development. High density lipoproteins (HDLs), mainly consisting of apolipoprotein A-I (ApoA-I), are involved in the process of cellular cholesterol efflux. HDLs remove cholesterol excess from peripheral tissue cells by active cholesterol transport, mediated by ABC transporters ABCA1 and ABCG1. Using a mouse model of lung-tumor bearing KRASG12D mutation (CCSPCRE-ERTM/+;KrasG12D/+), we identified that disruption of cholesterol efflux pathways by specific inactivation of Abca1 and Abcg1 in cancer cells promoted a pro-tolerogenic tumor microenvironment and tumor growth. Overexpression of the apolipoprotein A-I, to raise HDL levels, limited the cholesterol lung retention and protected these mice from tumor development and dire pathologic consequences. Cholesterol removal therapy with methyl-β-cyclodextrin inhalation also reduced tumor burden in progressing tumor by suppressing the proliferation and expansion of epithelial progenitor cells of tumor-origin. Local and systemic perturbations of cholesterol efflux pathways was confirmed in human lung adenocarcinoma. Our results position cholesterol removal therapy as a putative metabolic target in lung cancer progenitor cells.Next, I studied the role of mitophagy during NSCLC development. The selective elimination of damaged mitochondria by the machinery of autophagy is crucial to regulate mitochondrial activity, a process called mitophagy. The most-characterized mitophagy pathway relies on the PTEN-induced kinase 1 (PINK1) and the ubiquitin E3 ligase PARKIN. Hence, we explored the role of PINK1-mediated mitophagy in two murine lung cancer cell lines, LLC-1 and tumor-derived cell line from KrasG12D/+;p53-/- mouse (KP), in vitro and in vivo. First, we demonstrated in vitro the ability of two murine lung cancer cell lines, LLC-1 and KP cells, to remove damaged mitochondria by mitophagy following mitochondrial damages. This process requires the formation of autophagosomes by the ATG7 (autophagy related 7) protein. We also demonstrated that mitochondrial damages in LLC-1 and KP cells stabilize and activate PINK1, but not PARKIN, which is not expressed in those cells. Finally, using immunocompetent mice, we identified that disruption of PINK1-dependent mitophagy, similar to ATG7 loss as a complete autophagy/mitophagy inhibition, significantly increased LLC-1 tumor growth in vivo. PINK1-deficient tumors accumulated aberrant mitochondria and reduced inflammatory cytokines production, correlating with reduction of neutrophil infiltration. Those preliminary data suggest that PINK1-dependent PARKIN-independent mitophagy in lung cancer cells contributes to the control of lung tumor growth. We hypothesize that it may be based, at least in part, on the induction of an effective anti-cancer immune surveillance
Teixeira, Mayza Dalcin. "Estudo da associação de polimorfismos dos genes FTO, ABCA1, ABCA7 e ABCG1 com marcadores de obesidade e perfil lipídico em mulheres obesas". reponame:Repositório Institucional da UFPR, 2017. http://hdl.handle.net/1884/47563.
Texto completoCoorientadora : Drª Luciane Viater Tureck
Dissertação (mestrado) - Universidade Federal do Paraná, Setor de Ciências Biológicas, Programa de Pós-Graduação em Genética. Defesa: Curitiba, 31/03/2017
Inclui referências : f. 85-88
Resumo: A maioria dos casos de obesidade e de dislipidemias possui origem complexa, pois é resultante da interação entre fatores genéticos e ambientais. Diversos genes têm sido relacionados com a susceptibilidade a estas doenças, incluindo variantes alélicas dos genes FTO, ABCA1, ABCA7 e ABCG1. Desse modo, o objetivo deste trabalho foi verificar se há influência de polimorfismos de nucleotídeo único (SNPs) destes genes em variáveis relacionadas à obesidade e ao perfil lipídico em mulheres obesas e avaliar o efeito destes SNPs na mudança destas variáveis em resposta a uma dieta de restrição calórica. Para isso, foi coletado sangue de 211 mulheres obesas para análises bioquímicas (níveis de triglicerídeos - TG, colesterol total - CT, HDL-c, LDL-c e VLDL) e genotípicas, além de medidas antropométricas (índice de massa corporal - IMC, circunferência da cintura - CC, e circunferência abdominal - CA), antes e depois de uma dieta com redução de 600Kcal por dia. As amostras foram genotipadas por ensaio de discriminação alélica TaqMan® e posteriormente foram feitas análises estatísticas. Como resultado, as mulheres portadoras do alelo A do SNP rs9939609 (FTO) apresentaram uma menor redução de CA e maior redução dos níveis de HDL-c em resposta à dieta. As portadoras do alelo A do SNP rs1800977 (ABCA1) perderam menos IMC após a intervenção do que as não portadoras. As portadoras do genótipo TT do SNP rs2230806 (ABCA1) reduziram mais seus níveis de CT em resposta a dieta do que as portadoras do genótipo GG. Além disso, o alelo T foi mais frequente que o alelo C no grupo de mulheres com níveis de HDL-c maiores e níveis de LDL-c menores. As portadoras do genótipo GG do SNP rs2279796 (ABCA7) apresentaram níveis de CT e LDL-c maiores. Além disso, o alelo G foi mais frequente no grupo de mulheres com nível de CT e LDL-c maiores. Na resposta a intervenção dietética, as portadoras do genótipo GG aumentaram os níveis de TG e VLDL. As portadoras do alelo G do SNP rs692383 (ABCG1) apresentaram IMC maior, menor redução da CA em resposta a dieta e, em contrapartida, níveis de TG e VLDL menores e uma redução menor nos níveis de HDL-c. As portadoras do alelo A do SNP rs3827225 (ABCG1) tiveram uma maior redução de CA que as não portadoras, porém apresentaram um aumento maior nos níveis de LDL-c após a intervenção dietética. Esses resultados são indicativos de que possivelmente o alelo T do SNP rs2230806 (ABCA1) está associado com o efeito de proteção contra doenças cardiovasculares, pelos seus efeitos nos níveis de lipídeos séricos. Outrossim, o alelo G do SNP rs2279796 (ABCA7) pode estar conferindo um risco para doenças cardiovasculares, assim como o alelo A do SNP rs9939609 (FTO) sobre uma maior dificuldade em reduzir a CA e pela maior perda de HDL-c. Palavras-chave: Obesidade. Mulheres obesas. Intervenção dietética. Perfil lipídico. Gene FTO. Transportadores ABC. Estudo de associação.
Abstract: Obesity and dyslipidemias, in the majority of cases, have complex origin, as they result from the interaction between genetic and environmental factors. Many genes have been related to the susceptibility for these diseases, including FTO, ABCA1, ABCA7 and ABCG1 gene variants. Thus, the aim of this study was to verify if single nucleotide polymorphisms (SNPs) of these genes influence variables related to obesity and lipid profile in obese women and evaluate the effect of these SNPs in the variation of the variables in response to a calorie restriction diet. Thereunto, blood of 211 obese women was collected for biochemical (triglycerides - TG, total cholesterol - TC, HDL-c, LDL-c and VLDL levels) and genotypic analyses, besides anthropometric measures (body mass index - BMI, waist circumference - WC and abdominal circumference - AC), before and after a dietetic intervention with reduction of 600kcal per day. The samples were genotyped by allelic discrimination assay TaqMan® and analyzed statistically. As result, women carrying rs9939609 SNP (FTO) allele A had a lower AC reduction and a greater reduction of HDL-c levels in response to diet. A allele carriers of rs1800977 SNP (ABCA1) lost less BMI after intervention than non-carriers. TT genotype carriers of rs2230806 SNP (ABCA1) reduced more their TC levels than GG genotype carriers in response to diet. In addition, the T allele was more frequent than C allele in the group of women with higher HDL-c levels and lower LDL-c levels. GG genotype carriers of rs2279796 SNP (ABCA7) had higher TC and LDL-c levels. In addition, the G allele was more frequent in the group of women with higher TC and LDL-c levels. In response to dietary intervention, GG genotype carriers increased TG and VLDL levels. G allele carriers of rs692383 SNP (ABCG1) had higher BMI and lower AC reduction in response to diet but, on the other hand, lower TG and VLDL levels and a lower reduction in HDL-c levels. A allele carriers of SNP rs3827225 SNP (ABCG1) had a greater reduction in AC than non-carriers, but they had a higher increase in LDL-c levels after dietary intervention. These results are indicative that possibly T allele of rs2230806 SNP (ABCA1) is associated with the protective effect against cardiovascular diseases by their effects on serum lipid levels. In addition, the G allele of rs2279796 SNP (ABCA7) possibly is conferring a risk for cardiovascular diseases, as well as the A allele of rs9939609 SNP (FTO) on a greater difficulty in reducing AC and the greater loss of HDL-c. Keywords: Obesity. Obese women. Dietetic intervention. Lipid profile. FTO gene. ABC transporters. Association study.
Nascimento, Gabrielle Araújo do. "Avaliação do efeito de polimorfismos nos genes FTO, ABCA1, ABCA7 e ABCG1 sobre indicadores de obesidade e dislipidemias em crianças e adolescentes submetidos a treinamentos físico". reponame:Repositório Institucional da UFPR, 2017. http://hdl.handle.net/1884/47393.
Texto completoCoorientadora : Profª Drª Lupe Furtado Alle
Dissertação (mestrado) - Universidade Federal do Paraná, Setor de Ciências Biológicas, Programa de Pós-Graduação em Genética. Defesa: Curitiba, 27/03/2017
Inclui referências
Resumo: A obesidade e as dislipidemias geralmente estão associadas, e na maior parte dos casos possuem origem complexa, sendo decorrentes da interação entre os fatores ambientais e fatores genéticos. Dentre os fatores genéticos já conhecidos encontram-se genes relacionados ao metabolismo, como o gene FTO (Fat Mass and Obesity Associated) e os genes dos transportadores ABC. Polimorfismos de nucleotídeo único (SNPs) no gene FTO foram associados com o ganho de peso, enquanto os transportadores ABC estão relacionados com o efluxo de colesterol, e, nesse trabalho, foram analisados SNPs dos genes ABCA1, ABCA7 e ABCG1. Visto isso, o objetivo desse estudo é avaliar se há influência de polimorfismos nesses genes sobre variáveis antropométricas (índice de massa corporal ajustado para idade e sexo (IMC escore-Z), circunferência abdominal (CA), circunferência da cintura (CC), gordura corporal (GC) e massa magra (MM)) e bioquímicas (glicose em jejum, glicose 120, insulina em jejum, insulina 120, HOMA-IR (do inglês homeostasis model assessment of insulin resistance), QUICKI (do inglês quantitative insulin sensitivity check index) e perfil lipídico) de 557 crianças e adolescentes (eutróficos, sobrepeso e obesos) estudantes de escolas de Curitiba (PR), além de verificar o efeito de tais polimorfismos nas mudanças desses marcadores em resposta a um programa de exercícios físicos. A genotipagem foi realizada por ensaio de discriminação alélica. As análises estatísticas realizadas foram contagem direta dos genótipos, cálculo de frequência alélica, comparação de médias (teste T e teste Mann Whitney), análise de regressão múltipla e predição de risco. Todos os SNPs analisados promoveram variação significativa em alguma das variáveis analisadas. Com relação ao gene FTO, o alelo A do SNP rs9939609 foi associado a um aumento da insulina e HOMA-IR, e diminuição de QUICKI. Em relação aos genes dos transportadores ABC, o alelo C do SNP rs1800977 (ABCA1) foi associado a aumento no IMC escore-Z, CA, GC, insulina 120 e redução em QUICKI; o alelo A do SNP rs2230806 (ABCA1) foi associado a aumento no IMC escore-Z, CA e redução em %MM; o alelo C do SNP rs2279796 (ABCA7) foi associado à maior IMC escore-Z; o SNP rs692383 (ABCG1) foi associado à maior IMC escore-Z, CA, HDL-C, glicose, insulina e HOMA-IR e o alelo G do SNP rs3827225 (ABCG1) foi associado à maior VLDL-C e glicose. Com relação ao efeito na resposta aos exercícios físicos, os genes FTO, ABCA7 e ABCG1 não apresentaram interação, enquanto o alelo C do SNP rs1800977 (ABCA1) foi associado à maior redução de IMC escore-Z e maior aumento de QUICKI em resposta ao exercício e o alelo A do SNP rs2230806 (ABCA1) foi associado à maior ganho de MM. Nesse trabalho nós verificamos os efeitos dos polimorfismos analisados em variáveis relacionadas ao metabolismo (adiposidade, metabolismo da glicose e de lipídeos), sendo que alguns desses polimorfismos também interagiram com os programas de exercícios físicos aplicados. Os resultados obtidos corroboram e abrem novas perspectivas de estudo quanto ao papel da interação entre fatores ambientais e genéticos na prevenção e tratamento de patologias complexas, como a obesidade e as dislipidemias, no sentido de tornar tais medidas cada vez mais individualizadas. Palavras chave: Obesidade, dislipidemias, exercício físico, FTO, ABCA1, ABCA7, ABCG1, rs9939609, rs1800977, rs2230806, rs2279796, rs692383, rs3827225.
Abstract: Obesity and dyslipidemias are usually associated, and in most cases have complex origin, resulting from interaction between environmental and genetic factors. Among these already know genetic factors there are genes related to metabolism, such as FTO (Fat Mass and Obesity Associated) and the ABC transporters genes. Single nucleotide polymorphisms (SNPs) in FTO gene are associated to weight gain, while ABC transporters are related to cholesterol efflux, and SNPs in ABCA1, ABCA7 and ABCG1 genes were analyzed in this work. The objective of this study is to evaluate the influence of polymorphisms in these genes on anthropometric (body mass index adjusted for age and sex (BMI Z-score), abdominal circumference (AC), waist circumference (WC), fat mass (FM) and lean body mass (LBM)) and biochemical variables (fasting glucose, glucose 120, fasting insulin, insulin 120, HOMA-IR (homeostasis model assessment of insulin resistance), QUICKI (quantitative insulin sensitivity check index) and lipid profile) of 557 children and adolescents (normal weight, overweight and obese) in Curitiba (PR), and verify these polymorphisms effects in the changes of these markers in response to a physical exercise program. Genotyping was carried out by allelic discrimination assay. The statistical analyzes made were direct counting of genotypes, allelic frequency calculation, comparison of means (T test and Mann-Whitney test), multiple regression analysis and risk prediction. All the analyzed SNPs promoted significant variation in some of the variables. Regarding FTO gene, the rs9939609 SNP A-allele was associated to higher insulin and HOMA-IR, and reduced QUICKI. In relation to the ABC transporter genes, SNP rs1800977 C-allele (ABCA1) was associated to higher BMI-Z score, AC, FM and insulin 120 increase and QUICKI reduction; SNP rs2230806 (ABCA1) A-allele was associated to higher BMI-Z score and AC and %LBM reduction; SNP rs2279796 (ABCA7) C-allele was associated to higher BMI Z-score; SNP rs692383 (ABCG1) was associated to higher BMI Z-score, AC, HDL-C, glucose, insulin and HOMA-IR, and SNP rs3827225 (ABCG1) G-allele was associated to higher VLDL-C and glucose. Regarding the effect on physical exercise response, FTO, ABCA7 and ABCG1 genes did not shown interaction, whereas rs1800977 (ABCAI) C-allele was associated to higher reduction of BMI Z-score and increase in QUICKI in response to physical exercise and rs2230806 SNP (ABCA1) A-allele was associated to higher gain of LBM. In this study, we verified the effects of the polymorphisms analyzed on variables related to metabolism (adiposity, glucose metabolism and lipid metabolism), and some of these polymorphisms also interacted with the applied physical exercise programs. The results obtained corroborate and open new perspectives on the role of the interaction between environmental and genetic factors in the prevention and treatment of complex pathologies, such as obesity and dyslipidemias, in order to make these measures more individualized. Key-words: Obesity, dyslipidemia, physical exercise, FTO, ABCA1, ABCA7, ABCG1, rs9939609, rs1800977, rs2230806, rs2279796, rs692383, rs3827225.
Capítulos de libros sobre el tema "ABCA1/ABCG1"
Yu, Xiao-Hua y Chao-Ke Tang. "ABCA1, ABCG1, and Cholesterol Homeostasis". En HDL Metabolism and Diseases, 95–107. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-1592-5_7.
Texto completoTerasaka, Naoki. "Sterol Efflux by ABCA1 and ABCG1". En The HDL Handbook, 199–214. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-382171-3.10010-5.
Texto completoYuan, Z., X. Tan, X. Xu, J. Zhang, X. Nan, Y. Li y L. Yang. "Arsenic impaired cholesterol efflux by inhibiting ABCA1 and ABCG1". En Arsenic in the Environment - Proceedings, 436–38. CRC Press, 2016. http://dx.doi.org/10.1201/b20466-203.
Texto completo