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From the Cover
BIOLOGICAL SCIENCES / NEUROSCIENCE
Leptin replacement alters brain response to food cues in genetically leptin-deficient adults
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Department of Psychiatry and Biobehavioral Sciences and Semel Institute, and Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, Los Angeles, CA 90024; ||Center for Pharmacogenomics, Department of Psychiatry and Behavioral Sciences, University of Miami Miller School of Medicine, Miami, FL 33136; and Biomedical Engineering Interdepartmental Faculty, University of California, Los Angeles, CA 90024
Edited by Marcus E. Raichle, Washington University School of Medicine, St. Louis, MO, and approved August 21, 2007 (received for review July 10, 2007)
A missense mutation in the ob gene causes leptin deficiency and morbid obesity. Leptin replacement to three adults with this mutation normalized body weight and eating behavior. Because the neural circuits mediating these changes were unknown, we paired functional magnetic resonance imaging (fMRI) with presentation of food cues to these subjects. During viewing of food-related stimuli, leptin replacement reduced brain activation in regions linked to hunger (insula, parietal and temporal cortex) while enhancing activation in regions linked to inhibition and satiety (prefrontal cortex). Leptin appears to modulate feeding behavior through these circuits, suggesting therapeutic targets for human obesity.
functional MRI | obesity | hunger | prefrontal cortex | insula
The authors declare no conflict of interest.
This article is a PNAS Direct Submission.
¶To whom correspondence should be addressed. E-mail: elondon{at}mednet.ucla.edu
© 2007 by The National Academy of Sciences of the USA
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