Esteatosis de origen dietético: ¿la inflamación y la oxidación actúan de forma coordinada?
Diet-induced hepatic steatosis: Do inflammation and oxidation act coordinately?The metabolic response to high-fat, high-cholesterol diet may differ in mice with different genetic and metabolic background (ApoE-/- and LDLr-/-). Some develop steatohepatitis and increased expression of genes related to...
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| Tipo de recurso: | tesis doctoral |
| Estado: | Versión publicada |
| Fecha de publicación: | 2010 |
| País: | España |
| Institución: | Universitat Rovira i virgili (URV) |
| Repositorio: | Repositori Institucional de la Universitat Rovira i Virgili |
| OAI Identifier: | oai:urv.cat:TDX:670 |
| Acceso en línea: | https://hdl.handle.net/20.500.11797/TDX670 http://hdl.handle.net/10803/8892 |
| Access Level: | acceso abierto |
| Palabra clave: | 61 - Medicina |
| Sumario: | Diet-induced hepatic steatosis: Do inflammation and oxidation act coordinately?The metabolic response to high-fat, high-cholesterol diet may differ in mice with different genetic and metabolic background (ApoE-/- and LDLr-/-). Some develop steatohepatitis and increased expression of genes related to both inflammation and oxidation; in others, the expression of genes protective for the development of obesity and steatosis is decreased. Similar differences have been found in humans and consequently obtained data should be considered in translational research. We tested the hypothesis that molecules preventing oxidation (mainly paraoxonases) may coordinately act with responsible effectors for macrophage recruitment (especially monocyte chemoattractant proteins). We present here data indicating that both molecules are constitutively expressed in most tissues from C57BL/6J mice. Surprisingly this ubiquity and the apparent co-expression suggest, at least in liver, that antioxidand and pro-inflammatory responses may jointly determine the course of lesions induced by nutrient excess. |
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