Researchers from Brown University and other institutions discovered that reducing a protein called opsin 3 in mice leads to lower food intake. This intriguing finding has sparked conversations about potentially using similar approaches to tackle diabetes and obesity in humans.
Opsin 3, often abbreviated as OPN3, belongs to the opsin protein family, which is mainly known for helping animals detect light. However, unlike visual opsins, OPN3 doesn’t participate in vision. According to Hala Haddad, the lead author of the study, OPN3 is present in the hypothalamus, the brain region responsible for hunger, temperature regulation, and sleep. In contrast, visual opsins are located in the eyes.
Haddad collaborated with Professor Elena Oancea and other researchers in Oancea’s lab. They teamed up with scientists from Cincinnati Children’s Hospital Medical Center, Stanford University, and the Instituto Multidisciplinario de Biología Celular in Argentina.
Using mice without OPN3, the team observed significant changes in their eating habits. Richard Lang, director of the Visual Systems Group at Cincinnati Children’s, mentioned that these mice consumed less food. Furthermore, the absence of OPN3 made neurons in the hypothalamus more responsive to external signals, allowing them to react faster.
Haddad expressed a desire to investigate how OPN3 functions in other brain areas, like the cerebellum and hippocampus, which are key for memory and navigation. Lang is also curious about how OPN3 works with other non-visual opsins, such as OPN5, which plays a role in regulating body temperature.
Lang shared his excitement about exploring how OPN3 and OPN5 might work together to maintain energy balance, control food intake, and manage body temperature. Although their findings may one day help address human health issues like obesity and diabetes, both Lang and Oancea emphasized that more research is needed to confirm whether these processes occur in humans and what they might mean for treatment strategies.
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