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Department of Neurology & Neurosciences

Barry Levin, M.D.

Interim Chair, Department of Neurology and Neurosciences
Professor

Department of Neurology & Neurosciences
levin@umdnj.edu
 

Medical Science Building (MSB)
185 South Orange Avenue Room H506
Newark, NJ 07101
Phone: (973) 973-5209

Clinical Info

Medical Expertise

General Neurology

 

Biography

Education

M.D., 1967, Emory University School of Medicine (Magna Cum Laude)

 

 

Publications

Relevant Publications:

Patterson, C. M., S. G. Bouret, et al. (2009). "Three-weeks of post-weaning exercise in DIO rats produces prolonged increases in central leptin sensitivity and signaling." Am J Physiol Regul Integr Comp Physiol 296(3): 90859.2008.
Patterson, C. M. and B. E. Levin (2008). "Role of exercise in the central regulation of energy homeostasis and in the prevention of obesity." Neuroendocrinology 87(2): 65-70.
Bouret, S. G., J. N. Gorski, et al. (2008). "Hypothalamic neural projections are permanently disrupted in diet-induced obese rats." Cell Metab 7(2): 179-85.
Dunn-Meynell, A. A., N. M. Sanders, et al. (2009). "Relationship among brain and blood glucose levels and spontaneous and glucoprivic feeding." J. Neurosci. 29(21): 7015-7022.
Levin, B. E., T. C. Becker, et al. (2008). "Ventromedial hypothalamic glucokinase is an important mediator of the counterregulatory response to insulin-induced hypoglycemia." Diabetes 57(5): 1371-9.
Levin, B.E., Magnan, C., Dunn-Meynell, A.A., Le Foll, C., “Metabolic sensing and the brain : Who, what where and how ?”, Endocrinology 152 (7): 2252-2257, 2011.
Migrenne, S., Le Foll, C., Levin, B.E., Magnan, C., “Brain lipid sensing and nervous control of energy balance”, Diabetes Metab.37 (2): 83-88, 2011.
Levin, B.E., “Developmental gene x environment interactions affecting systems regulating energy homeostasis and obesity”, Front. Neuroendocrinol. 31(3): 270-283, 2010
Yang, L., Isoda, F., Yen, K., Kleopoulos, S.P., Janssen, W. Fan, X., Mastaitis, J, Dunn-Meynell, A.A., Levin, B.E., McCrimmon, R., Sherwin, R. Musatov, S. and Mobbs, C. V., “ Hypothalamic Fkbp51 is induced by fasting and elevated hypothalamic expression promotes obese phenotypes”, Am J. Physiol, Endo Metabol, 302 (8): E987-E991, 2012.

 

Current Research

Neuronal control of energy homeostsasis in obesity and diabetes

Using a polygenic model of diet-induced obesity (DIO)that mimics many of the characteristics of obesity and type 2 diabetes mellitus in humans, we examine the factors that predispose individuals who carry the genes for obesity to become obese. Current focus is on the effects of manipulating the maternal and postnatal environments to prevent the development of DIO. This includes altering maternal nutritional status, the hormonal milieu of the pups and postweaning exercise. In addition, we study the role that specialized metabolic sensing neurons in the brain play in the regulation of energy and glucose homeostasis. This includes neurons which alter their activity when ambient levels of glucose and long chain fatty acids change in their environment. These neurons appear to be critical sensors that allow the brain to monitor and then alter the metabolic status of the body.



 

 

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