{"id":68077,"date":"2018-03-09T22:56:33","date_gmt":"2018-03-09T22:56:33","guid":{"rendered":"https:\/\/www.deberes.net\/tesis\/sin-categoria\/paperl-i-regulacio-de-la-dina-mica-mitocondrial-en-muscul-esquela%c2%a8tic-papel-y-regulacion-de-la-dinamica-mitocondrial-en-musculo-esqueletico\/"},"modified":"2018-03-09T22:56:33","modified_gmt":"2018-03-09T22:56:33","slug":"paperl-i-regulacio-de-la-dina-mica-mitocondrial-en-muscul-esquela%c2%a8tic-papel-y-regulacion-de-la-dinamica-mitocondrial-en-musculo-esqueletico","status":"publish","type":"post","link":"https:\/\/www.deberes.net\/tesis\/procesos-metabolicos\/paperl-i-regulacio-de-la-dina-mica-mitocondrial-en-muscul-esquela%c2%a8tic-papel-y-regulacion-de-la-dinamica-mitocondrial-en-musculo-esqueletico\/","title":{"rendered":"Paperl i regulaci\u00f3 de la din\u00c1\u00a0mica mitocondrial en m\u00fascul esquel\u00e9tic (papel y regulaci\u00f3n de la din\u00e1mica mitocondrial en m\u00fasculo esquel\u00e9tico)"},"content":{"rendered":"<h2>Tesis doctoral de <strong> Marc Liesa I Roig <\/strong><\/h2>\n<p>Hasta el momento, diferentes estudios demuestran que deficiencias en la actividad mitocondrial pueden contribuir a la resistencia a la insulina en m\u00fasculo esquel\u00e9tico, y, en consecuencia, al desarrollo de un cuadro de diabetes de tipo 2. Existen diferentes tipos de fibra muscular seg\u00fan su capacidad oxidativa y\/o actividad mitocondrial, las cuales generalmente se pueden clasificar seg\u00fan la siguiente correlaci\u00f3n: contracci\u00f3n lenta y oxidativa; contracci\u00f3n r\u00e1pida y glicol\u00edtica. Diferentes evidencias han demostrado que las fibras de contracci\u00f3n lenta y oxidativas (mayor actividad mitocondrial) son m\u00e1s sensibles a la acci\u00f3n de la insulina. Puesto que mfn2 es una prote\u00edna que regula la actividad mitocondrial y que su expresi\u00f3n se encuentra reducida en m\u00fasculo esquel\u00e9tico de pacientes diab\u00e9ticos de tipo 2, decidimos estudiar si la represi\u00f3n de mfn2 induc\u00eda cambios en el tipo de fibra muscular en un modelo in vitro de diferenciaci\u00f3n muscular (l\u00ednia de mioblastos c2c12 que diferencian a c\u00e9lulas musculares o miotubos). Hemos observado que la represi\u00f3n espec\u00edfica de mfn2 promueve la diferenciaci\u00f3n de los mioblastos c2c12 a miotubos con una mayor expresi\u00f3n de genes de fibras de contracci\u00f3n r\u00e1pida y glicol\u00edticas (ya que aumenta la expresi\u00f3n de la prote\u00edna mhc llb espec\u00edfica de este tipo de fibras, entre otras prote\u00ednas). Este fenotipo es espec\u00edfico de la inhibici\u00f3n de la fusi\u00f3n mitocondrial mediante la disminuci\u00f3n de mfn2, ya la activaci\u00f3n o la inhibici\u00f3n de la fisi\u00f3n mitocondrial mediante sobreexpresi\u00f3n de drp1, o un mutante dominante negativo de la misma, no afecta la expresi\u00f3n de estos genes musculares. En paralelo, tambi\u00e9n se han identificado que el coactivador de receptores nucleares pgc-10 (que tambi\u00e9n presenta una disminuci\u00f3n de su expresi\u00f3n en m\u00fasculo esquel\u00e9tico de pacientes diab\u00e9ticos de tipo 2) regula la transcripci\u00f3n de mfn2 en c\u00e9lulas musculares. Esta regulaci\u00f3n es suficiente para modular el balance de fusi\u00f3n mitocondrial. As\u00ed pues, un incremento en la expresi\u00f3n de pgc-1p activa la tasa de fusi\u00f3n mitocondrial en mioblastos c2c12. En conclusi\u00f3n, en esta tesis se han identificado reguladores de la expresi\u00f3n de mfn2 y la relevancia de su actividad en la diferenciaci\u00f3n muscular.<\/p>\n<p>&nbsp;<\/p>\n<h3>Datos acad\u00e9micos de la tesis doctoral \u00ab<strong>Paperl i regulaci\u00f3 de la din\u00c1\u00a0mica mitocondrial en m\u00fascul esquel\u00e9tic (papel y regulaci\u00f3n de la din\u00e1mica mitocondrial en m\u00fasculo esquel\u00e9tico)<\/strong>\u00ab<\/h3>\n<ul>\n<li><strong>T\u00edtulo de la tesis:<\/strong>\u00a0 Paperl i regulaci\u00f3 de la din\u00c1\u00a0mica mitocondrial en m\u00fascul esquel\u00e9tic (papel y regulaci\u00f3n de la din\u00e1mica mitocondrial en m\u00fasculo esquel\u00e9tico) <\/li>\n<li><strong>Autor:<\/strong>\u00a0 Marc Liesa I Roig <\/li>\n<li><strong>Universidad:<\/strong>\u00a0 Barcelona<\/li>\n<li><strong>Fecha de lectura de la tesis:<\/strong>\u00a0 19\/11\/2008<\/li>\n<\/ul>\n<p>&nbsp;<\/p>\n<h3>Direcci\u00f3n y tribunal<\/h3>\n<ul>\n<li><strong>Director de la tesis<\/strong>\n<ul>\n<li>Antonio Zorzano Olarte<\/li>\n<\/ul>\n<\/li>\n<li><strong>Tribunal<\/strong>\n<ul>\n<li>Presidente del tribunal: diego Haro bautista <\/li>\n<li>Manuel Rojo ort\u00edz de lanzagorta (vocal)<\/li>\n<li>Antonio Vidal puig (vocal)<\/li>\n<li>Marta Camps camprubi (vocal)<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<p>&nbsp;<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Tesis doctoral de Marc Liesa I Roig Hasta el momento, diferentes estudios demuestran que deficiencias en la actividad mitocondrial pueden 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