Sebastien Bouret, Ph.D. is a tenured Associate Professor of Pediatrics at the University of Southern California. He is also a research investigator at the Division of Endocrinology, Diabetes and Metabolism at Children’s Hospital Los Angeles. Dr. Bouret has a broad background in the field of metabolic programming and the neurobiology of obesity. His research has directly led to several breakthroughs in the understanding of the complex hormonal signals and neurodevelopmental substrates responsible for appetite and glucose regulation.
Dr. Bouret has published more than 65 articles, reviews, and book chapters. In addition, Dr. Bouret has served on numerous journal editorial boards, organizing committees and grant review panels (he is currently a member of the NNRS study section of the NIH) and has been invited to lecture internationally.
University of Lille, France, Neuroscience, Ph.D. (Neuroscience), Highest Honors, 2001
University of Lille, France, M.S. (Physiology), High Honors, 1998
Postdoctoral Fellow, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, Oregon. Dr. Richard B. Simerly Laboratory. 2001-2004
Bouret SG, Draper SJ, & Simerly RB. Trophic action of leptin on hypothalamic neurons that regulate feeding. Science, 2004; 304(5667):108-110. (News & Views, p. 63-64; Science Editor’s Choice; also Nature Medicine, 12(1):52-53, 2006; and NIH 2004 Strategic Plan for NIH Obesity Research)
Bouret SG, Gorski JN, Kirigiti MA, Levin BE, & Simerly RB. Hypothalamic neural projections are permanently disrupted in diet-induced obese rats. Cell Metabolism, 2008; 7(2):179-185. (cover illustration; also 2009 Dana Alliance’s top findings in brain research)
Steculorum SM & Bouret SG. Maternal diabetes compromises the organization of hypothalamic feeding circuits and impairs leptin sensitivity in offspring. Endocrinology, 2011; 152(11):4171-4179. (also News & Views p. 4007-4009)
Coupe B, Ishii Y, Dietrich MO, Komatsu M, Horvath TL, & Bouret SG. Loss of autophagy in proopiomelanocortin neurons perturbs axon growth and causes metabolic dysregulation. Cell Metabolism, 2012; 15(2):247-255. (also Cell Cycle (Perspective), 2012, 11(8): 1477-1478).
Collden G, Balland E, Parkash J, Caron E, Langlet F, Prevot V, & Bouret SG. Neonatal overnutrition causes early alterations in the central response to peripheral ghrelin. Molecular Metabolism, 4(1):15-24, 2015.
Steculorum SM, Collden G, Coupe B, Croizier S, Lockie S, Andrews Z, Jarosch F, Klussmann S, & Bouret SG. Ghrelin programs development of hypothalamic feeding circuits. The Journal of Clinical Investigation, 125(2), 846-858, 2015 (also J Clin Invest (commentary), 490-492, 2015).
Bouret S, Levin BE, & Ozanne SE. Gene-environment interactions controlling energy and glucose homeostasis and the developmental origins of obesity. Physiological Reviews, 95(1):47-82, 2015
Maillard J, Park S, Croizier S, Vanacker C, Cook J, Prevot V, Tauber M, Bouret SG. Loss of Magel2 impairs the development of hypothalamic anorexigenic circuits. Human Molecular Genetics, 25(15): 3208-3215, 2016
Croizier SM, Prevot V, Bouret SG. Leptin controls parasympathetic wiring of the pancreas during embryonic life. Cell Reports, 15(1):36-44, 2016
The general research interest of Dr. Bouret’s laboratory is to understand how early life events program lifelong obesity and metabolism. His research program in the Saban Research Institute at Children's Hospital Los Angeles is focused on the role of hormones and nutrition during critical periods of development on the organization and plasticity of brain circuits that control appetite and glucose regulation. His lab also interested in studying the neurodevelopmental substrates of Prader-Willi Syndrome, a genetic disorder characterized by excessive hyperphagia, which can lead to life-threatening obesity.
Visit the Bouret Laboratory.
The growing prevalence of obesity and associated type II diabetes is a major health concern, particularly among children. There is growing appreciation that developmental malprogramming of neuroendocrine systems during critical periods of life is a potential cause for obesity and associated metabolic diseases in later life. Dr. Bouret’s research has directly led to several breakthroughs in the understanding of the complex hormonal signals and neurodevelopmental substrates responsible for appetite and glucose regulation. Most notably, he discovered that metabolic hormones such as leptin and ghrelin play a crucial role in hypothalamic development and lifelong body weight regulation (Bouret et al., Science, 304:108-110, 2004; Steculorum et al., J Clin Invest, 125(2): 846-858, 2015) . More recently, his lab has discovered an unanticipated inhibitory role for prenatal leptin in the wiring of insulin-producing cells of the pancreas (Croizier et al., Cell Reports, 15:1-9, 2016). He also recently published that loss of Magel 2, one of the genes that are inactivated in Prader-Willi Syndome, causes a perturbations in the development of hypothalamic anorexigenic circuits (Maillard et al., Hum Mol Genet, 25:3208-3215, 2016).
R01 National Institute of Health (NIDDK), DK084142: Leptin and the nutritional programming of obesity and diabetes. The project is designed to study the role of the fat-derived hormone leptin in the wiring of the pancreas in a context of maternal obesity.
R01 National Institute of Health (NIDDK), DK102780: Hypothalamic miRNAs in the pathogenesis of obesity. The long-range goal of this proposal is to study the role of small non-coding RNAs in the development and function of neurons known to be involved in the regulation of food intake, body weight, and glucose homeostasis.
Foundation for Prader-Willi Research: Development of appetite-related neural circuits in a mouse model for Prader-Willi Syndrome. The long-term of this project is to investigate the development of hypothalamic appetite-related circuits in a mouse model for Prader-Willi Syndrome.