As a postdoctoral researcher in Dr. Jeffrey Friedman’s lab, I am driven by a deep curiosity about how the brain regulates energy balance and behavior. Our recent Nature paper identifying lepR/BNC2 neurons revealed an uncharted neural pathway in leptin signaling, with potential implications for treating obesity and related diseases. This discovery reaffirmed my belief that foundational research can open doors to transformative medical advances.
Being nominated by Dr. Friedman to the Hong Kong Laureate Forum is an incredible honor. I see the Forum as more than an academic gathering—it is a catalyst for global collaboration and visionary thinking. I hope to engage with leading scientists and passionate young researchers across disciplines, to learn from their perspectives, and to challenge and refine my own ideas.
I believe that addressing complex scientific challenges—from metabolic disease to climate-driven health impacts—requires cross-cultural, cross-disciplinary dialogue. The Forum embodies this spirit, and I am excited to contribute my voice while learning from others. I hope to leave not only inspired, but also more connected to a global scientific community committed to discovery, collaboration, and societal impact.

Rockefeller University

Leptin, a hormone derived from fat, is essential for maintaining energy balance through its action on leptin receptor (LepR)-expressing neurons in the brain, particularly the hypothalamus. Despite its importance, the mechanisms by which leptin influences diverse neuronal populations remain poorly understood. Using high-throughput multiplexed snRNA-seq and snATAC-seq, I mapped transcriptomic and chromatin accessibility changes across hypothalamic subregions in response to leptin. This analysis revealed a novel population of LepR neurons marked by Basonuclin 2 (Bnc2), which rapidly suppress appetite by counterbalancing hunger-promoting AGRP neurons, redefining feeding regulation. Additionally, leptin-induced changes highlighted cell-type-specific molecules critical for its function. These findings uncover key neural and molecular pathways for leptin action and provide new therapeutic targets for addressing obesity and leptin resistance.