A team of researchers has identified the brain circuits controlling hunger that are influenced by a hormone called leptin. The research, published in Proceedings of the National Academy of Science, found that leptin reduced activation in regions of the brain linked to hunger, while enhancing activation in regions linked to inhibition and satiety. The study suggests possible new targets for the treatment of obesity.
Three Turkish adults who lacked the leptin (ob) hormone were used in the study, and magnetic resonance imaging (MRI) was used to measure brain activity before and after leptin supplementation in them. The subjects were shown images of food before and after leptin treatment, while MRI imaging was in progress.
After leptin replacement, the subjects had feelings of hunger induced by the images, and activity in brain regions associated with hunger—the insula, parietal and temporal cortex—were reduced, while brain activity increased in the prefrontal cortex, previously associated with feeling full.
Despite the limitations in having only three subjects with the ob mutation, Prof. London says, "We think knowing the mechanisms by which leptin alters brain function in congential leptin deficiency can provide understanding of normal leptin physiology. Ultimately, that may help identify new targets for the treatment of obesity and related metabolic disorders."
The research was conducted by Edythe London, a professor of psychiatry in the UCLA Semel Institute for Neuroscience & Human Behavior, and Kate Baicy, a graduate student in Professor London’s lab. Other authors involved with the study were ohn Monteroso, Tuncay Delibasi, and Anil Sharma from the Semel Institute and the UCLA David Geffen School of Medicine, and Ma-Li Wong and Julio Licinio of the University of Miami Miller School of Medicine. The research was supported in part by the National Institutes of Health and the UCLA General Clinical Research Center. During the course of this study Amgen, Inc. provided leptin; Amylin, Inc. now provides leptin to these patients. Neither Amgen, Inc., nor Amylin, Inc., contributed to the design, analysis, or writing of this study.
Source: Proceedings of the National Academy of Science,October 29, 2007
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