Bright light exposure suppresses feeding and weight gain via a visual circuit linked to the lateral hypothalamus.

Environmental light regulates nonimage-forming functions like feeding, and bright light therapy shows anti-obesity potential, yet its neural basis remains unclear. Here we show 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 innervate GABAergic neurons in the ventral lateral geniculate nucleus (vLGN), which in turn inhibits GABAergic neurons in the LHA. Activation of both vLGN-projecting retinal ganglion cells and the vLGN-to-LHA projection is sufficient to suppress food consumption and attenuate weight gain. Notably, 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.