Study of genetic, epigenetic and gut microbiota signatures involved in food addiction vulnerability
The easy access to hypercaloric and palatable foods is a major contributing factor for compulsive eating and food addiction development. The prevalence of food addiction measured with the validated Yale Food Addiction Scale (YFAS 2.0) increased in recent years. However, the precise neurobiological b...
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| Tipo de recurso: | tesis doctoral |
| Estado: | Versión publicada |
| Fecha de publicación: | 2023 |
| País: | España |
| Institución: | CBUC, CESCA |
| Repositorio: | TDR. Tesis Doctorales en Red |
| OAI Identifier: | oai:www.tdx.cat:10803/688637 |
| Acceso en línea: | http://hdl.handle.net/10803/688637 |
| Access Level: | acceso abierto |
| Palabra clave: | Food addiction miRNAs gut microbiota prebiotics CB2R Adicción a la comida microbiota intestinal prebióticos 616.8 |
| Sumario: | The easy access to hypercaloric and palatable foods is a major contributing factor for compulsive eating and food addiction development. The prevalence of food addiction measured with the validated Yale Food Addiction Scale (YFAS 2.0) increased in recent years. However, the precise neurobiological basis of food addiction is still unknown, obstructing the design of effective treatments. This thesis aims to investigate and characterize the signatures of food addiction vulnerability to discover diagnosis biomarkers and possible therapeutic interventions for this disease. As food addiction is a multifactorial disorder, we implemented a multidisciplinary approach and interrogated genetic, epigenetic and gut microbiota signatures. In order to accomplish this aim, we used a mouse operant model of food addiction, followed by small RNA sequencing, RNA-sequencing, and metagenomics sequencing. Once several signatures were identified, we further confirm their relationships with food addiction establishment and predisposition. We performed a functional validation by viral-mediated intervention, prebiotic treatment, or generation of genetically modified mice. The results of this thesis will provide new insights into mechanistic neurobiological correlates, epigenetic findings, and metagenomic signatures that will contribute to building novel preventive approaches and therapeutic interventions to battle food addiction disorder. |
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