Mol. Cells 2018; 41(6): 603~611  https://doi.org/10.14348/molcells.2018.0120
Flightless-I Controls Fat Storage in Drosophila
Jung-Eun Park1, Eun Ji Lee1, Jung Kwan Kim2, Youngsup Song1, Jang Hyun Choi2, and Min-Ji Kang1,*
1Department of Biomedical Sciences, University of Ulsan College of Medicine, Seoul 05505, Korea, 2Department of Biological
Sciences, Ulsan National Institute of Science and Technology, Ulsan 44919, Korea
*Correspondence: mjkang@amc.seoul.kr
Received April 14, 2018; Revised April 4, 2018; Accepted May 21, 2018.; Published online June 12, 2018.
© Korean Society for Molecular and Cellular Biology. All rights reserved.

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. To view a copy of this license, visit (http://creativecommons.org/licenses/by-nc-sa/3.0/).
ABSTRACT
Triglyceride homeostasis is a key process of normal development and is essential for the maintenance of energy metabolism. Dysregulation of this process leads to metabolic disorders such as obesity and hyperlipidemia. Here, we report a novel function of the Drosophila flightless-I (fliI) gene in lipid metabolism. Drosophila fliI mutants were resistant to starvation and showed increased levels of triglycerides in the fat body and intestine, whereas fliI overexpression decreased triglyceride levels. These flies suffered from metabolic stress indicated by increased levels of trehalose in hemolymph and enhanced phosphorylation of eukaryotic initiation factor 2 alpha (eIF2α). Moreover, upregulation of triglycerides via a knockdown of fliI was reversed by a knockdown of desat1 in the fat body of flies. These results indicate that fliI suppresses the expression of desat1, thereby inhibiting the development of obesity; fliI may, thus, serve as a novel therapeutic target in obesity and metabolic diseases.
Keywords: desaturase-1, Drosophila, fat storage, flightless-1, lipid metabolism


Current Issue

30 June 2018 Volume 41,
Number 6, pp. 495~611

This Article


Cited By Articles
  • CrossRef (0)

Social Network Service
Services

Indexed in

  • Science Central
  • CrossMark