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La luz modula el metabolismo de la glucosa por el eje retina-hipotálamo-tejido adiposo marrón

Jian-Jun Meng¹, Jia-Wei Shen¹, Guang Li¹

¹Hefei National Research Center for Physical Sciences at the Microscale, CAS Key Laboratory of Brain Function and Disease, Biomedical Sciences and Health Laboratory of Anhui Province, School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230026, China.

|January 20, 2023

Resumen

La exposición a la luz artificial reduce agudamente la tolerancia a la glucosa mediante la activación de una vía neuronal desde la retina hasta el hipotálamo y el tejido adiposo marrón (TAB). Este eje retina-SON-BAT bloquea la termogénesis, afectando la salud metabólica.

Área de la Ciencia:

La neurociencia
Investigación metabólica
Cronología

Sus antecedentes:

Los estudios de salud pública relacionan la exposición a la luz artificial con un mayor riesgo de trastornos metabólicos.
Los mecanismos neuronales precisos por los cuales la luz influye en la regulación metabólica no se comprenden bien.

Objetivo del estudio:

Para aclarar el circuito neuronal que media los efectos agudos de la luz en la tolerancia a la glucosa.
Identificar las vías específicas involucradas en la modulación metabólica inducida por la luz.

Principales métodos:

Investigó el impacto de la luz en la tolerancia a la glucosa en ratones.
Utilizó técnicas optogenéticas y de trazado neural para mapear el eje retina-hipotalamo-adiposo.
Examen de la tolerancia humana a la glucosa bajo condiciones de luz controladas.

Principales resultados:

La exposición a la luz disminuyó agudamente la tolerancia a la glucosa en ratones.
La activación de las células ganglionares de la retina intrínsecamente fotosensibles (ipRGC) que innervan el núcleo supraóptico (SON) fue identificada como un mediador clave.
Se aclaró un circuito neuronal que involucra neuronas de vasopresina, núcleo paraventricular, núcleo del tracto solitario y tejido adiposo marrón (BAT).
La activación inducida por la luz de este circuito suprimió la termogénesis BAT, lo que condujo a una tolerancia reducida a la glucosa.
Se observó una modulación similar de la tolerancia a la glucosa por la luz en humanos a temperaturas en las que la MTD está activa.

Conclusiones:

Un nuevo eje neuronal retina-SON-BAT regula el metabolismo de la glucosa en respuesta a la luz.
Esta vía explica cómo la luz artificial puede interrumpir la homeostasis metabólica.
Los hallazgos sugieren posibles estrategias terapéuticas para los trastornos metabólicos dirigidos a este eje.

Palabras clave:

circuito del cerebro tejido adiposo marrón metabolismo de la glucosa Las GCRP la luz Núcleo supraóptico

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