Advanced
Identification of a neural pathway governing satiety in Drosophila
Identification of a neural pathway governing satiety in Drosophila
BMB Reports. 2016. Mar, 49(3): 137-138
Copyright © 2016, Korean Society for Biochemistry and Molecular Biology
This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
  • Received : March 04, 2016
  • Published : March 31, 2016
Download
PDF
e-PUB
PubReader
PPT
Export by style
Article
Author
Metrics
Cited by
About the Authors
Soohong Min
msh2001560011@empas.com
Jongkyeong Chung
msh2001560011@empas.com

Abstract
Satiety cues a feeding animal to cease further ingestion of food, thus protecting it from excessive energy gain. Impaired control of satiety is often associated with feeding-related disorders such as obesity. In our recent study, we reported the identification of a neural pathway that expresses the myoinhibitory peptide (MIP), critical for satiety responses in Drosophila. Targeted silencing of MIP neuron activity strikingly increased the body weight (BW) through elevated food intake. Similarly, genetic disruption of the gene encoding MIP also elevated feeding and BW. Suppressing the MIP pathway behaviorally transformed the satiated flies to feed similar to the starved ones, with augmented sensitivity to food. Conversely, temporal activation of MIP neuron markedly reduced the food intake and BW, and blunted the sensitivity of the starved flies to food as if they have been satiated. Shortly after termination of MIP neuron activation, the reduced BW reverted to the normal level along with a strong feeding rebound. Together our results reveal the switch-like role of the MIP pathway in feeding regulation by controlling satiety. [BMB Reports 2016; 49(3): 137-138]
Keywords
Acknowledgements
J.C. was supported by the National Creative Research Initiatives grant through the National Research Foundation of Korea (NRF) funded by Ministry of Science, ICT and Future Planning, Korea (NRF-2010-0018291). S.M. was supported by NRF-2012-Global Ph.D. Fellowship Program and the fellowship from Seoul National University for Fundamental Academic Fields, and an awardee of the HumanTech Paper Award hosted by Samsung Electronics. S.M. and J.C. were supported by BK21 Plus Program from Ministry of Education, Korea.
References