Estudo do envolvimento da atividade mitocondrial na super-resposta à restrição calórica em Caenorhabditis elegans mutantes para lipl-5
Objective: To evaluate the involvement of mitochondrial activity on the slower consumption of lipid storages on C. elegans mutants for lipl-5 under calorie restriction. Methods: Wild-type animais N2 Bristol and lipl-5 mutants were submitted to 24 hours bacterial deprivation (BO). Metabolic rate were...
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| Tipo de recurso: | tesis de maestría |
| Estado: | Versión publicada |
| Fecha de publicación: | 2017 |
| País: | Brasil |
| Institución: | Universidade Federal de São Paulo (UNIFESP) |
| Repositorio: | Repositório Institucional da UNIFESP |
| Idioma: | portugués |
| OAI Identifier: | oai:repositorio.unifesp.br:11600/50555 |
| Acceso en línea: | https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=5064452 http://repositorio.unifesp.br/handle/11600/50555 |
| Access Level: | acceso abierto |
| Palabra clave: | Caenorhabditis elegans Restrição calórica Mitocôndrias Metabolismo energético Metabolismo dos lipídeos |
| Sumario: | Objective: To evaluate the involvement of mitochondrial activity on the slower consumption of lipid storages on C. elegans mutants for lipl-5 under calorie restriction. Methods: Wild-type animais N2 Bristol and lipl-5 mutants were submitted to 24 hours bacterial deprivation (BO). Metabolic rate were evaluated by in vivo O2 consumption and heat dissipation. Mitochondrial mass was analyzed by citrate synthase activity. Mitochondrial activity was evaluated by isolating these organelles from the worms and measuring O2 consumption supported by complex I, 11 and 13- oxidation substrates, separately. Results: Bacterial deprivation modulated the animais' metabolism, as indicated by decreased O2 consumption and heat generation in vivo on both strains, but to a lesser extent in lipl-5 mutants, since lipl-5 knockout, per se, modulated the worm's metabolism. The decreased in vivo O2 consumption was due to reduced mitochondrial mass, as assessed by citrate synthase activity. Oxidative capacity of mitochondria was modulated by BO, with enhanced phosphorylation capacity in complex I and l3-oxidation in wild-type mitochondria. In lipl-5 mutants, complex 11- but not complex 1- or l3-oxidation-driven. respiration was enhanced by BO. Indeed, it was observed that the mutation itself was capable of increasing complex I and l3-oxidation-driven respiration to similar levels of that measured in wild-type mitochondria from animais submitted to BO. Conclusion: lipl- 5 mutation probably triggers a yet unidentified stress signal, which leads to enhanced mitochondrial respiratory capacity. The fact that mitochondria form lipl-5 animal submitted to BO presented enhanced phosphorylation capacity towards complex I and II substrates may explain, at least in part, the lipid sparing observed in these animais upon BO. Besides that, the smaller extent of metabolic remodeling in lipl-5 mutants when submitted to BO might reduce energy resources consumption, that would diminish fat storages utilization for energy production. |
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