Papel de PAS quinasa en la adaptación a diferentes estados nutricionales y en la resistencia a la obesidad
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2019
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17/06/2018
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Universidad Complutense de Madrid
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El hígado es un órgano vital para el mantenimiento de la homeostasis de glucosa y lípidos durante los periodos de ayuno/alimentación. La adaptación a esta situación está sujeta a las respuestas hormonales de insulina y glucagón. Estos cambios conducen a la estimulación de genes metabólicos que a su vez son regulados por factores de transcripción y coactivadores. Durante el ayuno, tiene lugar la gluconeogenesis en la cual intervienen las enzimas Fosfoenolpiruvato carboxiquinasa (PEPCK) y Glucosa 6-fosfatasa (G6Pasa) y cuya regulación está controlada por el Coactivador 1α del receptor activado por el proliferador de peroxisomas γ (PGC1α) y el “Forkhead O box 1” (FOXO1), que forman un complejo que es desactivado mediante fosforilación por Akt/PKB (Proteína quinasa B). A su vez, también tiene lugar la β-oxidación de ácidos grasos, que depende del transporte por la Carnitinapalmitoil transferasa (CPT) y las Acil-CoA deshidrogenasas (CAD) que son reguladas por el receptor activado por los proliferadores peroxisomales α (PPARα). En situación postprandial, ocurren las rutas de la glucolisis, donde participan la Glucoquinasa (GCK), la Fosfofructoquinasa 1 (PFK-1) y la Piruvato quinasa hepática (L-PK),y la síntesis de ácidos grasos llevada a cabo por las enzimas Acetil-CoA carboxilasa (ACC), la Ácido graso sintasa (FAS) y la Estearoil-CoA desaturasa (SCD). Las enzimas del metabolismo lipídico son reguladas por el receptor X hepático (LXR), la proteína de unión a elementos de respuesta a esteroles (SREBP1) y la proteína de unión a elementos de respuesta a carbohidratos (ChREBP). Estos procesos son activados por la acción de la insulina, en cuya señalización es clave la enzima Akt...
The liver is a vital organ for maintaining glucose and lipid homeostasis in response to fasting and refeeding periods. The adaptation to this situation depends on the hormonal response of insulin and glucagon. These changes stimulate metabolic genes which are regulated by transcription factors and coactivators. During fasting, gluconeogenesis occurs and it is done by Phosphoenolpyruvate carboxykinase (PEPCK) and Glucose 6-phosphatase (G6Pase) and whose regulation iscontrolled by Transcriptional coactivator peroxisome proliferator-activated receptor γ coactivator-1α (PGC1α) and Forkhead O box 1 (FOXO1), both form a complex that is deactivated by phosphorylation by Akt/PKB (Protein kinase B). Likewise, β-oxidation of fattyacids also occurs and it depends on the transport by Carnitine Palmitoyltransferase 1 (CPT1) and Acyl-CoA Dehydrogenase (CAD), which are regulated by Peroxisome proliferator activated receptor alpha (PPARα).During postprandial periods, glycolysis occurs, involving Glucokinase (GCK),Phosphofructokinase-1 (PFK-1) and Hepatic pyruvate kinase (L-PK), and fatty acid synthesis also carried out by Acetyl CoA carboxylase (ACC), Fatty acid synthase (FAS) and Stearoyl-CoA desaturase (SCD). Enzymes of lipid metabolism are regulated by Liver X receptor (LXR),Sterol regulatory element-binding protein 1c (SREBP1c) and Carbohydrate-responsive element-binding protein (ChREBP). These processes are activated by insulin, whosesignalling is mediated by the key Akt enzyme...
The liver is a vital organ for maintaining glucose and lipid homeostasis in response to fasting and refeeding periods. The adaptation to this situation depends on the hormonal response of insulin and glucagon. These changes stimulate metabolic genes which are regulated by transcription factors and coactivators. During fasting, gluconeogenesis occurs and it is done by Phosphoenolpyruvate carboxykinase (PEPCK) and Glucose 6-phosphatase (G6Pase) and whose regulation iscontrolled by Transcriptional coactivator peroxisome proliferator-activated receptor γ coactivator-1α (PGC1α) and Forkhead O box 1 (FOXO1), both form a complex that is deactivated by phosphorylation by Akt/PKB (Protein kinase B). Likewise, β-oxidation of fattyacids also occurs and it depends on the transport by Carnitine Palmitoyltransferase 1 (CPT1) and Acyl-CoA Dehydrogenase (CAD), which are regulated by Peroxisome proliferator activated receptor alpha (PPARα).During postprandial periods, glycolysis occurs, involving Glucokinase (GCK),Phosphofructokinase-1 (PFK-1) and Hepatic pyruvate kinase (L-PK), and fatty acid synthesis also carried out by Acetyl CoA carboxylase (ACC), Fatty acid synthase (FAS) and Stearoyl-CoA desaturase (SCD). Enzymes of lipid metabolism are regulated by Liver X receptor (LXR),Sterol regulatory element-binding protein 1c (SREBP1c) and Carbohydrate-responsive element-binding protein (ChREBP). These processes are activated by insulin, whosesignalling is mediated by the key Akt enzyme...
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Tesis de la Universidad Complutense de Madrid, Facultad de Medicina, Departamento de Bioquímica y Biología Molecular, leída el 07/06/2018