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Robert Lustig, MD

University of California, san francisco

 

Dr. Lustig is a nationally-recognized authority in the field of neuroendocrinology, with a specific emphasis on the regulation of energy balance by the central nervous system. He is currently investigating the contribution of biochemical, neural, hormonal, and genetic influences in the expression of the current obesity epidemic both in children and adults. He has defined a syndrome of vagally-mediated beta-cell hyperactivity which leads to insulin hypersecretion and obesity, and which is treatable by insulin suppression. This phenomenon may occur in up to 20% of the obese population. He is interested in the hypothalamic signal transduction of insulin and leptin, how these two systems interact, and how hyperinsulinemia contributes to leptin resistance. He is studying the cardiovascular morbidity associated with hyperinsulinemia, and developing methods to evaluate and prevent this phenomenon in children. He is also analyzing the contribution of the autonomic nervous system to insulin secretion and insulin resistance in obese children, and the utility of assessing insulin dynamics in targeting obesity therapy. Lastly, he is researching the role of specific macronutrients in fomenting liver insulin resistance and the metabolic syndrome, both in childhood and before birth.

Dr. Lustig graduated from MIT, and received his M.D. from Cornell University Medical College. He performed his pediatric residency at St. Louis Children's Hospital, and his clinical fellowship at UCSF. From there, he spent six years as a post-doctoral fellow in neuroendocrinology at The Rockefeller University in New York.

Dr. Lustig has authored over 85 research articles and 45 chapters. He is the former Chairman of the Obesity Task Force of the Pediatric Endocrine Society, a member of the Obesity Task force of The Endocrine Society, and on the Steering Committee of the International Endocrine Alliance to Combat Obesity. He is the Editor of the volume "Obesity before birth: maternal and prenatal effects on the offspring.