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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.
Pubmed ID: 29890821
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View all literature mentionsCell line 3T3-L1 is a Spontaneously immortalized cell line with a species of origin Mus musculus (Mouse)
View all literature mentionsDrosophila melanogaster with name fliI[3] from BDSC.
View all literature mentionsDrosophila melanogaster with name w[1118] from BDSC.
View all literature mentionsDrosophila melanogaster with name fliI[14]/FM6 from BDSC.
View all literature mentionsDrosophila melanogaster with name w[1118]; P{w[+mW.hs]=Switch1}106 from BDSC.
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