Qingchun Tong, Ph.D.
Associate Professor, Center for Metabolic and Degenerative DiseaseQingchun.Tong@uth.tmc.edu
Synopsis The Tong lab studies how neurocircuitry in the brain controls feeding, energy expenditure and glucose homeostasis. To tackle the complexity in the hypothalamic neural network in the regulation of energy balance, Dr. Tong’s group will generate mouse models with gene-deletion restricted to defined groups of brain neurons using Cre-loxP technology. Using these animal models, as well as an array of techniques including immunohistochemistry, in situ hybridization, neuronal tracing and stereotaxic delivery, his group will try to delineate neural pathways in the brain underlying food intake, body weight homeostasis and glucose homeostasis, and provide a framework for an effective drug design against the current epidemics of obesity and its associated syndromes.
B.S.: Anhui Normal University, China, 1996
M.S.: Shanghai Institute of Physiology, Chinese Academy of Sciences, 1999
PhD: SUNY Downstate Medical Center, 2003
Postdoc training: Beth Israel Deaconess Medical Center and Harvard Medical School, 2003-2008
Instructor: Harvard Medical School, 2008-2009
In 2009, Dr. Tong started his own lab in the Institute of Molecular Medicine of the University of Texas at Houston, where he will continue to investigate the role of fast-acting neurotransmitter from novel groups of hypothalamic neurons. In addition, he will extend this line of research by generating mice with inducible region-specific disruption of glutamate or GABA release to investigate the role of these neurotransmitters in the adult state without a potential compensation. By using tracing studies and animal surgeries on these animal models, specific neural pathways underlying specific physiologic functions (body weight, glucose homeostasis, etc.) will also be investigated.
Pilot and Feasibility Award, Boston Area Diabetes and Endocrinology Research Center (BADERC). 2009
Pilot and Feasibility Award, Boston Obesity and Nutrition Research Center (BONRC) 2007
Young Investigator Award, NAASO 2007
Keystone Symposia Travel Scholarship Award 2007
Career Development Award, AHA 2010.
Research Interests Obesity and its associated complications are imposing a huge burden to our society, while its effective treatment is still lacking. A better understanding of the mechanisms regulating energy balance is required to develop new therapeutic strategies. Neurons in the hypothalamus receive and integrate nutritional status signals, and then adjust food intake and energy expenditure accordingly to maintain energy balance. Previous research has identified important functions of a few groups of hypothalamic neurons (e.g. POMC neurons, AgRP neurons, etc.) and a few hypothalamic genes (POMC, AgRP and MC4R, etc.). However, the mechanisms with which the hypothalamus regulates energy balance are not well understood.
The research focus of my group is to understand how neurocircuitry in the hypothalamus regulates energy balance. My current research focus is to understand the role of glutamate and GABA release from hypothalamic neurons in the regulation of energy balance. Glutamate and GABA are the main excitatory and inhibitory neurotransmitters, respectively, in the brain. However, research efforts that address the mechanisms underlying energy balance have been largely focusing on the roles of neuropeptides, while the roles of glutamate and GABA have been overlooked. To study the roles of glutamate and GABA release, we generated mice with floxed vesicular glutamate transporter 2 (Vglut2, required for presynaptic glutamate release in the hypothalamus) and floxed vesicular GABA transporter (Vgat, required for presynaptic GABA release). These mice will be crossed with transgenic mouse lines that express Cre only in a subset of hypothalamic neurons to generate mice with disruption of glutamate (lox-Vglut2) or GABA (lox-Vgat) release only from the Cre-expressing neurons. These models will then used to study the function of neural pathways in which these glutamatergic or GABAergic neurons engage to regulate energy balance. Recently, we have incorporated optogenetics and DREADD techniques in our research. Ultimately we try to delineate specific neural pathways underlying specific physiologic functions.
In addition, we are also interested in understanding how the brain controls energy expenditure and mediates responses to high-caloric, high-fat diet (HFD) feeding through communicating with peripheral metabolic tissues with an aim to identify key tissues/mediators that are important to mediate appropriate responses to HFD feeding and could be used to better cope with HFD feeding.
The Tong lab is currently funded by AHA, JDRF and NIH, and has open positions for postdocs and graduate students. Please email Dr. Tong with your interest.
Publications (within last 10 years):
- Wu Z, Kim ER, Sun H, Xu Y, Mangieri LR, Li DP, Pan HL, Xu Y, Arenkiel AR and Tong Q. GABAergic projections from lateral hypothalamus to paraventricular hypothalamic nucleus promote feeding. J. Neurosci., 2015, in press. Corresponding author.
- Zheng H, Fu J, Xue P, Zhao R, Dong J, Liu D, Yamamoto M, Tong Q, Teng W, Qu W, Zhang Q, Andersen ME, Pi J. CNC-bZIP protein Nrf1-dependent regulation of glucose-stimulated insulin secretion. Antioxid Redox Signal. 2015 Jan 4. [Epub ahead of print], PMID: 25556857.
- Cao X, Xu P, Oyola MG, Xia Y, Yan X, Saito K, Zou F, Wang C, Yang Y, Hinton A Jr, Yan C, Ding H, Zhu L, Yu L, Yang B, Feng Y, Clegg DJ, Khan S, DiMarchi R, Mani SK, Tong Q, Xu Y. Estrogens stimulate serotonin neurons to inhibit binge-like eating in mice. J Clin Invest. 2014, 124(10):4351-62. PMID: 25157819.
- Xu Y, Kim ER, Fang S, Xia Y, Huang C, Xu Y and Tong Q. Profound and Rapid Body Temperature Reduction by the Melanocortin Receptor Agonists. Biochemical and Biophysical Research Communication, 2014, 451(2): 184-189. PMID: 25065745. Corresponding author.
- Xu Y, Wu Z, Sun H, Zhu Y, Kim ER, Arenkiel RA, Lowell BB, Xu Y and Tong Q. Glutamate Mediates the PMID: 24315371. Function of MC4Rs on Sim1 Neurons in Body Weight Regulation. Cell Metabolism. 2013, 18 (6): 860-870. Corresponding author.
- Shi X, Zhou F, Li X, Chang B, Li D, Wang Y, Tong Q, Xu Y, Fukuda M, Zhao JJ, Li D, Burrin DG, Chan L, Guan X. Central GLP-2 Enhances Hepatic Insulin Sensitivity via Activating PI3K Signaling in POMC Neurons. Cell Metabolism. 2013, 18 (1) 86-98. PMID: 23823479.
- Kong D*, Tong Q*, Ye C, Koda S, Fuller PM, Krashes MJ, Vong L, Olson DP, Lowell BB. GABAergic Rip-Cre neurons in the arcuate nucleus selectively regulate energy expenditure. *: Co-first authors, Cell, 2012, 151(3) 645-658.
- Xu Y, Kim ER, Zhao R, Myers MG, Munzberg H and Tong Q, Glutamate release mediates leptin action on energy expenditure, Mol. Metabolism, 2013, 2(2): 109-115. Corresponding author.
- Liu T, Wang Q, Berglund, ED and Tong Q. Action of neurotransmitters, a key to unlock the AgRP feeding neurocircuit. Front. Neuroscience. 2012, 6:200. Corresponding author.
- Tong Q and Xu Y. Central regulation of Leptin in obesity and reproduction. Current Obesity Reports, 2012, 1 (4): 236-244. Corresponding author.
- Wu Z, Xu Y, Zhao R, Olson DP, Lowell BB, Tong Q. An obligate role of oxytocin neurons in energy expenditure regulation. PLOS One, 2012, 7(9) e45167, PMID: 23028821, Corresponding author.
- Xu Y, O’Brien W, Lee C-C, Myers MG, and Tong Q. Role of GABA release from leptin-recpeor-expressing neurons in body weight regulation. Endocrinology, 2012, 153(5): 2223-2233, PMID: 22334723. Corresponding author.
- Xu Y and Tong Q Expanding neurotransmitters in the hypothalamic neurocircuitry for energy balance regulation. Protein & Cell, 2011, 2 (10): 800-813,
- Tong, Q.: Synaptotagmin 4: A New Anti-obesity Target? Neuron, 2011, 69(3): 401-403, PMID: 21315251.
- Song, J., Xu, Y., Hu, X., Choi, B., and Tong, Q.: Brain Expression of Cre Recombinase Driven by Pancreas-specific Promoters. Genesis, 2010, 48(11): 628-634. Corresponding author.
- Liu, Y., Samad, O.A., Zhang, L., Duan, B., Tong, Q., Lopes, C., Ji, R-R., Lowell, B.B., and Ma, Q.: VGLUT2-dependent glutamate release from nociceptors is required to sense pain and suppress itch. Neuron, 2010, 68(3):543-546
- Kong, D., Vong, L., Parton, L.E., Ye, C., Tong, Q., Hu, X., Choi, B., Bruning, J.C., and Lowell, B.B.: Glucose Stimulation of Hypothalamic MCH neurons involves KATP channels, is modulated by UCP2, and regulates peripheral glucose homeostasis. Cell Metabolism, 2010, 12(5): 545-552.
- Zhou, L., Podolsky, N., Sang, Z., Ding, Y., Fan, X., Tong, Q., Levine, B.E., and McCrimmon, R.J.: The medial amygadalar nucleus: A novel glucose-sensing region that modulates the counter-regulatory response to hypoglycemia. Diabetes, 2010, 59(10): 2646-2652.
- Vetrivelan R, Fuller P, Tong Q. and Lu J. Medullary circuitry regulating rapid eye movement (REM) sleep and motor atonia. J Neurosci., 2009, 29 (29): 9361-9369.
- Tong Q, Ye C, Jones JE, Elmquist JK and Lowell BB. Synatpic GABA Release by AgRP neurons is Required for Normal Regulation of Energy Balance. Nature Neuroscience 11:998-1000, 2008.
- Tong Q, Ye C, McCrimmon RJ, Dhillon H, Choi B, Kramer MD, Yu J, Yang Z, Christiansen LM, Lee CE, Choi CS, Zigman JM, Shulman GI, Sherwin RS, Elmquist JK and Lowell BB. Synaptic Glutamate Release by Ventromedial Hypothalamic Neurons is Part of the Neurocircuitry that Prevents Hypoglycemia. Cell Metabolism 5(5):383-393, 2007.