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Published June 8, 2010 | Accepted Version + Supplemental Material
Journal Article Open

The Leucokinin Pathway and Its Neurons Regulate Meal Size in Drosophila


Background: Total food intake is a function of meal size and meal frequency, and adjustments to these parameters allow animals to maintain a stable energy balance in changing environmental conditions. The physiological mechanisms that regulate meal size have been studied in blowflies but have not been previously examined in Drosophila. Results: Here we show that mutations in the leucokinin neuropeptide (leuc) and leucokinin receptor (lkr) genes cause phenotypes in which Drosophila adults have an increase in meal size and a compensatory reduction in meal frequency. Because mutant flies take larger but fewer meals, their caloric intake is the same as that of wild-type flies. The expression patterns of the leuc and lkr genes identify small groups of brain neurons that regulate this behavior. Leuc-containing presynaptic terminals are found close to Lkr neurons in the brain and ventral ganglia, suggesting that they deliver Leuc peptide to these neurons. Lkr neurons innervate the foregut. Flies in which Leuc or Lkr neurons are ablated have defects identical to those of leucokinin pathway mutants. Conclusions: Our data suggest that the increase in meal size in leuc and lkr mutants is due to a meal termination defect, perhaps arising from impaired communication of gut distension signals to the brain. Leucokinin and the leucokinin receptor are homologous to vertebrate tachykinin and its receptor, and injection of tachykinins reduces food consumption. Our results suggest that the roles of the tachykinin system in regulating food intake might be evolutionarily conserved between insects and vertebrates.

Additional Information

© 2010 Elsevier Ltd. Received 18 December 2009; revised 12 March 2010; accepted 19 April 2010. Published online: May 20, 2010. Available online 20 May 2010. We thank J. Dow for anti-Lkr, M. Kankel for discussions, and L. Nicholson and E. Schwartz for editorial assistance. This work was supported by National Institutes of Health grants RO1 DK070154 and AG024366 to S.B. (later transferred to K.Z.) and RO1 NS028182 to K.Z. B.A. was partially supported by a Life Sciences Research Foundation grant provided by Bristol-Myers Squibb.

Attached Files

Accepted Version - nihms-202725.pdf

Supplemental Material - mmc1.pdf


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