Qili Liu

Qili Liu, PhD, is an Assistant Professor in the Department of Anatomy at the University of California, San Francisco (UCSF). Her research investigates the neuronal mechanisms underlying food selection and nutrient-specific appetites using Drosophila as a model organism to uncover conserved biological principles of motivated behavior.

Dr. Liu's educational background includes:

• PhD in Plant Physiology and Ecology from the Shanghai Institute of Plant Physiology and Ecology, Chinese Academy of Sciences, focusing on stem cell maintenance in plants.
• Postdoctoral training at Johns Hopkins University with Dr. Mark Wu, transitioning from plant biology to neuroscience through research on circadian rhythms and feeding behavior.

Her research centers on nutritional neuroscience, examining how internal biological factors drive food choices through molecular and neural mechanisms. She investigates nutrient-specific appetites (e.g., protein, salt) using genetic and behavioral approaches in Drosophila, revealing how neural plasticity encodes hunger signals and how different appetites compete to regulate balanced nutrient intake. Her work bridges molecular biology, genetics, and behavioral neuroscience to understand homeostatic set points for nutrient consumption.

Analysis of Dr. Liu's publications shows a clear evolution from plant biology to neuroscience, with recent work dominated by circadian regulation of sleep, dopamine circuit function in feeding behavior, and protein appetite mechanisms. Her Drosophila-based research consistently identifies molecular pathways that govern nutrient-specific hunger, demonstrating how neural plasticity creates competition between different appetites (e.g., protein vs. sugar) with implications for understanding obesity.

The Liu Lab at UCSF employs advanced genetic tools in Drosophila to dissect neural circuits controlling food selection. Current research explores sex- and mating status-dependent variations in protein appetite, aiming to define molecular set points for nutrient intake that could inform therapeutic interventions for metabolic disorders by reprogramming biological hunger signals.