A Visual Circuit Linked To The Lateral Hypothalamus Mediates The Food Consumption-Suppressing And Weight Gain-Attenuating Effects Of Bright Light Treatment

In addition to its well-established role in vision, environmental light also plays a crucial role in non-image-forming visual functions, including the regulation of instinctive behaviors such as feeding. Clinical evidence suggests that bright light therapy can alleviate symptoms in individuals with obesity. However, the neural mechanisms underlying the influence of light on feeding behaviors remain poorly understood. In this study, we demonstrate that bright light treatment effectively reduces food intake and mitigates weight gain in mice through a visual circuit involving the lateral hypothalamic area (LHA). Specifically, a subset of SMI-32-expressing ON-type retinal ganglion cells (RGCs) innervate GABAergic neurons in the ventral lateral geniculate nucleus (vLGN), which in turn inhibits GABAergic neurons in the LHA. Activation of both vLGN-projecting RGCs and the vLGN-to-LHA pathway is sufficient to suppress food consumption and attenuate weight gain. Importantly, we provide direct evidence that the suppressive effects of bright light treatment on food consumption and weight gain rely on the activation of the retina-vLGN-LHA pathway. Together, our results delineate an LHA-related visual circuit underlying the food consumption-suppressing and weight gain-attenuating effects of bright light treatment.