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La ingesta alta de grasa mantiene la intolerancia al sorbitol después del agotamiento de Clostridia mediado por
Jee-Yon Lee1, Connor R Tiffany1, Scott P Mahan1
1Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, One Shields Ave, Davis, CA 95616, USA.
Cell
|February 17, 2024
Resumen
La exposición a los antibióticos y las dietas altas en grasas pueden causar intolerancia al sorbitol de larga duración al interrumpir las bacterias intestinales. La restauración de la degradación microbiana del sorbitol, en particular con los productores de butirato, ofrece una estrategia terapéutica potencial.
Área de la Ciencia:
- Microbiología
- Gastroenterología
- Inmunología
Sus antecedentes:
- La intolerancia a los carbohidratos, incluida la intolerancia al sorbitol, afecta a una parte significativa de la población.
- Los mecanismos precisos que subyacen a la intolerancia al sorbitol, a menudo vinculados a la malabsorción, no se comprenden completamente.
Objetivo del estudio:
- Para aclarar los mecanismos detrás de la intolerancia al sorbitol.
- Identificar posibles objetivos terapéuticos para la intolerancia al sorbitol.
Principales métodos:
- Inducción de la intolerancia al sorbitol en ratones a través de la exposición a antibióticos y una dieta alta en grasas.
- Evaluación de la abundancia microbiana de Clostridia y el catabolismo del sorbitol.
- Intervención con los probióticos Escherichia coli y los anaerostipos caccae productores de butirato.
- Investigación del papel de la señalización del receptor gamma activado por el proliferador peroxisómico (PPAR-γ) y la hipoxia epitelial.
Principales resultados:
- La exposición a antibióticos y la dieta alta en grasas redujeron la abundancia de Clostridia, deteriorando el catabolismo microbiano del sorbitol y causando intolerancia al sorbitol en ratones.
- La inoculación de Escherichia coli restauró parcialmente el catabolismo del sorbitol, pero no la abundancia de Clostridia.
- La inoculación de caccae de Anaerostipes restauró la abundancia de Clostridia y protegió contra la diarrea inducida por sorbitol, incluso después del aclaramiento probiótico.
- El butirato, producido por A. caccae, restauró la abundancia de Clostridia al estimular la señalización de PPAR-γ y la hipoxia epitelial.
Conclusiones:
- El catabolismo microbiano del sorbitol es un factor clave en la intolerancia al sorbitol.
- El restablecimiento de la abundancia y la función de Clostridia, potencialmente a través del butirato, es un enfoque terapéutico prometedor.
- Dirigirse al catabolismo microbiano del sorbitol ofrece el potencial para diagnosticar, tratar y prevenir la intolerancia al sorbitol.
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