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El receptor de vitamina D como un sensor de ácido biliar intestinal
Makoto Makishima1, Timothy T Lu, Wen Xie
1Howard Hughes Medical Institute, Department of Pharmacology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9050, USA.
Science (New York, N.Y.)
|May 23, 2002
Resumen
El receptor de vitamina D (VDR) se une al ácido litocólico del ácido biliar (LCA), un compuesto relacionado con la toxicidad hepática y el cáncer. Esta interacción puede explicar cómo la vitamina D protege contra el cáncer de colon.
Área de la Ciencia:
- Endocrinología Endocrinología.
- Hepatología Hepatología.
- Gastroenterología y Gastroenterología.
Sus antecedentes:
- Se sabe que el receptor de vitamina D (VDR, por sus siglas en inglés) media los efectos de la 1alfa,25-dihidroxivitamina D3 [1,25(OH) 2D3].
- Los ácidos biliares secundarios, como el ácido litólico (ACL), están implicados en la toxicidad hepática y el cáncer colorrectal.
- Las interacciones específicas entre el VDR y los ácidos biliares no se comprenden completamente.
Objetivo del estudio:
- Investigar si el receptor de vitamina D (VDR) funciona como un receptor para el ácido litólico (LCA).
- Para determinar la sensibilidad de VDR a LCA y sus metabolitos en comparación con otros receptores nucleares.
- Para aclarar los mecanismos moleculares subyacentes a los efectos protectores potenciales de la vitamina D y VDR contra el cáncer de colon.
Principales métodos:
- Se realizaron ensayos para evaluar la afinidad de unión y la activación de VDR por LCA y sus metabolitos.
- El análisis de expresión génica se realizó in vivo para medir la inducción de enzimas de desintoxicación como el CYP3A.
- Se realizaron estudios comparativos utilizando otros receptores nucleares para determinar la sensibilidad relativa del VDR al LCA.
Principales resultados:
- VDR fue identificado como un receptor funcional para el ácido biliar secundario LCA.
- VDR demostró un orden de magnitud mayor sensibilidad a LCA y sus metabolitos en comparación con otros receptores nucleares.
- La activación de VDR por LCA o vitamina D condujo a la inducción in vivo de CYP3A, una enzima clave en la desintoxicación de LCA en el hígado y el intestino.
Conclusiones:
- El VDR se une y responde al ácido biliar hepatotóxico LCA.
- La interacción VDR-LCA, que conduce a la inducción de CYP3A, proporciona un mecanismo potencial para el papel protector de la vitamina D en la prevención del cáncer de colon.
- Estos hallazgos ponen de relieve una función novedosa de VDR en el metabolismo de los ácidos biliares y la quimioprevención del cáncer.
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