Qi Wu, PhD

Wu, Qi
Assistant Professor
Summary statement: 

Neural regulation of feeding behavior and energy metabolism

Office phone: 
(319) 384-4729
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Office building: 
Lab phone: 
(319) 335-6762
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Our lab is studying neural control of feeding behavior and etiology of eating-associated disorders, such as obesity and anorexia nervosa, in genetic mouse models. Feeding behavior is tightly regulated at several levels in the central nervous system. Peripheral hormonal and nutritional signals impinge onto several hypothalamic and brainstem nuclei to regulate appetite and energy metabolism in a largely subconscious manner. Meanwhile, higher cognitive centers also modulate food intake. A challenging question is how neural circuits that underlie the basic drive to feed interact with those representing conscious wish to mediate feeding-related activities. Hypothalamic AgRP neurons are critical for regulation of feeding and body weight, as acute ablation of these cells in adult mice leads to anorexia and profound weight loss. We demonstrated that such anorexic phenotype is fully reversible with the aid of a GABA-A receptor agonist and that GABA release from AgRP neurons onto neurons in the lateral parabrachial nucleus (PBN) is essential for maintenance of appetite and body weight. Therefore, we proposed that a novel hindbrain circuit and associated signaling pathways underlie neural adaptive control of anorexia and obesity through bi-directional modulation.

Current projects:

(1)  Characterize functional connectivity of metabolic-sensing PBN neurons and their roles in control of feeding and energy homeostasis. We would expect to reveal the anatomical and functional organization of the PBN and how it interacts with other brain regions to promote compensatory adaptation after ablation of AgRP neurons. Moreover, we would expect to establish precise physiological roles and pivotal signaling mechanisms of distinct subpopulations of the PBN neurons in control of appetite and body weight.

(2)  Identify a hindbrain neural circuit and associated signaling pathways that mediate feeding and addictive response to food in transgenic mouse models. Our preliminary results indicated that a hindbrain neural circuit might be functionally organized by several critical signaling pathways that integrate metabolic inputs from the hypothalamus along with gustatory and vagal stimuli to promote long-term adaptation to different homeostatic level. The potential outcome will illuminate a more complete feeding circuitry in the mammalian brain and novel adaptive mechanisms at synapse level that might contribute to developing therapeutic approaches against obesity and eating disorders.

“The neuroscience program at the university has a unique blend of cognitive and molecular neuroscience that appeals to my own diverse interests for studying the brain. Most other programs place emphasis on one side or the other of these two broad disciplines.”