Qi Wu, Ph.D.
Qi Wu, Ph.D.
- Assistant Professor
Childrens Nutrition Research Center
Baylor College of Medicine
Houston, TX, US
- Children's Nutrition Research Center (Office)
Houston, TX 77030
- PhD from University of Georgia
- 12/2005 - Athens, Georgia, United States
- Molecular and Cellular Biology
- BS from Nanjing University
- 06/2000 - Nanjing, China
- Post-Doctoral Fellowship at University of Washington and HHMI
- 12/2011 - Seattle, Washington, United States
Honors & Awards
- Pew Scholar of Biomedical Sciences
- Pew Charitable Trust (07/2013)
- AAAS Excellence in Science Program Award
- American Association for the Advancement of Science (04/2010)
Professional StatementOur lab is studying neural control of feeding behavior and etiology of eating-associated disorders, such as obesity and anorexia nervosa, in genetic mouse models. Current treatment of obesity, one of the leading risk factors of type II diabetes, encounters severe challenges, partly because the process involves restoration of 2 fundamental aspects of daily life: food consumption and physical activity. Feeding behavior is tightly regulated at several levels in the central nervous system. 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. Our long term goals are to expand fundamental knowledge of the neural and molecular basis that underlie the control of feeding behavior. 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.
Current lab research primarily focuses on three areas:
1) Characterize functional connectivity of metabolic-sensing PBN neurons and their roles in control of feeding and energy homeostasis,
2) Identify a hindbrain neural circuit and associated signaling pathways that mediate feeding and energy expenditure, as well as addictive response to food in transgenic mouse models,
3) Characterize functional connectivity and relevant signaling systems between AgRP neurons and postsynaptic neurons in selective forebrain areas that mediate cognitive deficiency in obesity-associated neurological disorders. Publications
1) Meng, F., Srisai, D., Belakhov, V., Palmiter, R.D., Baasov, T. and Wu, Q. (2014) A novel gene targeting approach reveals differential roles of GABA from AgRP neurons in control of appetite and energy metabolism. (Manuscript under preparation)
2) Stewart, A., Maity, B., Wunsch, A.M., Meng, F., Wu, Q., Wemmie, J.A., and Fisher, R.A. (2014) Regulator of G protein signaling 6 (RGS6) promotes anxiety and depression by attenuating serotonin-mediated activation of the 5-HT1A receptor-adenylyl cyclase axis. FASEB J. doi: 10.1096/fj.12-235648
3) Wu, Q., Zhen, R., Srisai, D., McKnight, G.S. and Palmiter, R.D. (2013) The NR2B subunit of the NMDA glutamate receptor regulates appetite in the parabrachial nucleus. Proc. Natl. Acad. Sci. U.S.A. 110, 14765-14770.
4) Wu, Q., Clark, M. and Palmiter, R.D. (2012) Deciphering a neuronal circuit that mediates appetite. Nature 483, 594 – 597.
5) Wu, Q., Whiddon, B. and Palmiter, R.D. (2012) Ablation of AgRP (but not MCH) neurons of leptin-deficient mice restores normal metabolic functions and fertility. Proc. Natl. Acad. Sci. U.S.A. 109, 3155 – 3160.
6) Wu, Q. and Palmiter, R.D. (2010) GABAergic signaling by AgRP neurons prevents anorexia via a melanocortin-independent mechanism. Eur. J. Pharmacol. 660, 21-27.
7) Wu, Q., Boyle M.P. and Palmiter, R.D. (2009) Loss of GABAergic signaling by AgRP neurons to the parabrachial nucleus leads to starvation. Cell 137, 1225-1234.
8) Wu, Q., Howell M.P. and Palmiter, R.D. (2008) Ablation of AgRP neurons results in activation of Fos and glial markers in post-synaptic target regions in the brain. J. Neurosci. 28, 9218-9226.
9) Wu, Q., Howell M.P., Cowley, M.A. and Palmiter, R.D. (2008) Starvation after AgRP-neuron ablation is mediated by the hindbrain and is independent of melanocortin signaling. Proc. Natl. Acad. Sci. U.S.A. 105, 2687 – 2692.
10) Wu, Q. and Brown, M.R. (2006) Signaling and function of insulin-like peptides in insects. Annu. Rev. Entomol. 51, 1 – 24.
11) Wu, Q., Zhao, Z. and Shen, P. (2005). Regulation of aversion to noxious food by Drosophila neuropeptide Y- and insulin-like systems. Nat. Neurosci. 8, 1350 – 1355.
12) Wu, Q., Zhang, Y., Xu, J. and Shen, P. (2005) Regulation of hunger-driven behaviors by neural ribosomal S6 kinase in Drosophila. Proc. Natl. Acad. Sci. U.S.A. 102, 13289 – 13294.
13) Wen, T., Parrish, C.A., Xu, D., Wu, Q. and Shen, P. (2005) Drosophila neuropeptide F and its receptor NPFR1 define a neuronal pathway that acutely modulates alcohol sensitivity. Proc. Natl. Acad. Sci. U.S.A. 102, 2141 – 2146.
14) Wu, Q., Zhao, H. and Wen, T. (2004) The conserved signaling pathways and physiological functions of insulin-like peptides in insects. J. Shanghai Univ. 8, 227 – 234.
15) Wu, Q., Wen, T., Lee, G., Park, J.H., Cai, H.N. and Shen, P. (2003) Developmental control of foraging and social behavior by the Drosophila neuropeptide Y-like system. Neuron 39, 147 – 161.
16) Wen, T., Gu, P., Minning, T.A., Wu, Q., Liu, M., Chen, F., Liu, H. and Huang, H. (2002) Microarray analysis of neural stem cell differentiation in the striatum of the fetal rat. Cell Mol. Neurobiol. 22, 407 – 416.
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