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Published August 13, 2009 | Supplemental Material + Accepted Version
Journal Article Open

Obesity-Blocking Neurons in Drosophila


In mammals, fat store levels are communicated by leptin and insulin signaling to brain centers that regulate food intake and metabolism. By using transgenic manipulation of neural activity, we report the isolation of two distinct neuronal populations in flies that perform a similar function, the c673a-Gal4 and fruitless-Gal4 neurons. When either of these neuronal groups is silenced, fat store levels increase. This change is mediated through an increase in food intake and altered metabolism in c673a-Gal4-silenced flies, while silencing fruitless-Gal4 neurons alters only metabolism. Hyperactivation of either neuronal group causes depletion of fat stores by increasing metabolic rate and decreasing fatty acid synthesis. Altering the activities of these neurons causes changes in expression of genes known to regulate fat utilization. Our results show that the fly brain measures fat store levels and can induce changes in food intake and metabolism to maintain them within normal limits.

Additional Information

© 2009 Elsevier. Accepted 7 July 2009; published: August 12, 2009; available online 12 August 2009. We would like to acknowledge M. Brown for providing the anti-DILP antibody. We would also like to acknowledge Erich Schwarz, Louise Nicholson, and Mary Lynn Formanack for their editorial assistance. This work was supported by an R01 grant to S.B., DK070154.

Attached Files

Accepted Version - nihms137983.pdf

Supplemental Material - mmc1.pdf


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