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Updated: Feb 9, 2026
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High Fat Diet Feeding and High Throughput Triacylglyceride Assay in Drosophila Melanogaster
Published on: September 13, 2017
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Flightless-I Controls Fat Storage in Drosophila
Jung-Eun Park1, Eun Ji Lee1, Jung Kwan Kim2
1Department of Biomedical Sciences, University of Ulsan College of Medicine, Seoul 05505, Korea.
Molecules and Cells
|June 13, 2018
Summary
The flightless-I (fliI) gene regulates triglyceride levels in Drosophila. FliI deficiency increases triglycerides and obesity, suggesting fliI as a potential therapeutic target for metabolic disorders.
Area of Science:
- * Molecular genetics
- * Metabolic research
- * Drosophila melanogaster model systems
Background:
- * Triglyceride homeostasis is crucial for energy metabolism and development.
- * Dysregulation of lipid metabolism contributes to obesity and hyperlipidemia.
- * The role of the flightless-I (fliI) gene in lipid metabolism is largely unexplored.
Purpose of the Study:
- * To investigate the function of the Drosophila flightless-I (fliI) gene in lipid metabolism.
- * To determine the impact of fliI on triglyceride levels and metabolic stress.
- * To explore the potential of fliI as a therapeutic target for obesity.
Main Methods:
- * Generation and analysis of Drosophila fliI mutants and overexpression lines.
- * Measurement of triglyceride levels in fat body and intestine.
- * Assessment of metabolic stress markers, including hemolymph trehalose and eIF2α phosphorylation.
- * Genetic manipulation (knockdown) of desat1 in the fat body.
Main Results:
- * Drosophila fliI mutants exhibited starvation resistance and elevated triglyceride levels.
- * fliI overexpression led to decreased triglyceride levels.
- * fliI knockdown flies showed signs of metabolic stress (increased trehalose, eIF2α phosphorylation).
- * Knockdown of desat1 reversed triglyceride upregulation caused by fliI knockdown.
Conclusions:
- * Drosophila fliI plays a suppressive role in triglyceride accumulation.
- * fliI acts by inhibiting the expression of desat1.
- * fliI is a novel regulator of lipid metabolism and a potential therapeutic target for obesity and related metabolic diseases.
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