23 de abril de 2010

Control neural del hambre

A nivel del sistema nervioso central (SNC), las sustancias que regulan el hambre y el metabolismo actúan en el tronco del encéfalo, el hipotálamo y otros centros cerebrales superiores.

En el tronco del encéfalo, el núcleo del tracto solitario (NTS) recibe información (tanto química como mecánica) de los órganos internos mediante el tracto gastrointestinal (línea verde), y también de los niveles de glucosa en sangre. Este sistema es a corto plazo.


La información que proviene de la lengua, los órganos internos, los mecanoreceptores y los niveles de glucosa se procesa en el tronco del encéfalo, concretamente en el área postrema (AP) y el núcleo del tracto solitario (NTS). Además, el tronco del encéfalo tiene receptores de glucosa que le permiten recibir información sobre los niveles de esta sustancia. Desde aquí, la información se dirige al hipotálamo.


El núcleo arqueado tiene receptores para la leptina y la insulina, que producen las señales periféricas a largo plazo que modulan la conducta de ingesta. El hipotálamo lateral controla la conducta de ingesta, mientras que el núcleo paraventricular controla los procesos vegetativos y endocrinos relacionados con el metabolismo.


Cuando el núcleo arqueado genera el neuropéptido Y (NPY) y la proteína relacionada con el péptido Agouti (AgRP), activan el hipotálamo lateral, que produce hipocretinas y hormonas concentradoras de melanina (MCH). Ambas sustancias favorecen la conducta de ingesta, a la vez que disminuyen el metabolismo mediante conexiones con el núcleo paraventricular. Por otro lado, cuando el núcleo arqueado produce pro-opiomelanocortina (POMC) y el péptido de transcripción regulada por anfetamina y cocaína (CART), inhibe el hipotálamo lateral. De esta manera, reduce la conducta de ingesta y aumenta el metabolismo, de manera inversa al proceso anterior.
Diferentes anomalías relacionadas con la leptina ocasionan trastornos de la conducta de ingesta y el metabolismo. Por ejemplo, la mutación del gen Ob, productor de leptina (proteína OB), y los defectos en el gen que codifica los receptores de leptina (ObR), que producen insensibilidad a la leptina. Sin embargo, por sí solas, son insuficientes para explicar y tratar la obesidad en humanos.


Las ratas de Zucker tienen deficiencias en los receptores de leptina. Puesto que son insensibles a la leptina, tienen más NPY hipotalámico que las ratas normales. Esto explicaría su hambre sin control, que las lleva a una obesidad importante.


A la izquerda, un niño con una mutación en el gen de la leptina, y a la derecha, el niño tratado con leptina. En humanos, la obesidad raramente se debe a una mutación del gen de la leptina o de su receptor. El papel principal de la leptina podría ser proteger al organismo contra la pérdida de peso en periodos de privación, y no contra el aumento de peso en periodos de abundancia.

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