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Activación de MC4R mediada por setmelanotida mejora la obesidad hipotalámica a través de las vías CaMKK2/AMPK
Junjie Peng1, Yichao Ou1, Mingfeng Zhou1
1Department of Neurosurgery, Institute of Brain Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Frontiers in pharmacology
|January 28, 2026
Resumen
Setmelanotida, un agonista del receptor de melanocortina 4 (MC4R), revirtió la obesidad en un modelo de rata de obesidad hipotalámica (OH). Este tratamiento reactivó las neuronas MC4R restaurando la señalización CaMKK2/AMPK, ofreciendo una terapia potencial para la obesidad inducida por lesiones del SNC.
Área de la Ciencia:
- Neurociencia
- Endocrinología
- Farmacología
Conclusiones:
- La disfunción de MC4R es crítica en la obesidad inducida por lesión hipotalámica.
- La activación farmacológica de MC4R a través de la señalización CaMKK2/AMPK es una estrategia viable para restaurar la homeostasis metabólica.
- Setmelanotida representa un agente terapéutico potencial para el manejo de la obesidad causada por lesiones del sistema nervioso central.
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