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Journal of Lipids
Volume 2013, Article ID 297932, 7 pages
Research Article

Reduction of Cellular Lipid Content by a Knockdown of Drosophila PDP1γ and Mammalian Hepatic Leukemia Factor

Department of Psychiatry, Psychiatric Institute, University of Illinois at Chicago, Chicago, IL 60612, USA

Received 22 March 2013; Accepted 19 July 2013

Academic Editor: Philip W. Wertz

Copyright © 2013 Svetlana Dzitoyeva and Hari Manev. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


In exploring the utility of double-stranded RNA (dsRNA) injections for silencing the PAR-domain protein 1 (Pdp1) gene in adult Drosophila, we noticed a dramatic loss of fat tissue lipids. To verify that our RNAi approach produced the expected Pdp1 knockdown, the abdominal fat tissues sections were stained with PDP1 antibodies. PDP1 protein immunostaining was absent in flies injected with dsRNA targeting a sequence common to all known Pdp1 isoforms. Subsequent experiments revealed that lipid staining is reduced in flies injected with dsRNA against Pdp1γ (fat body specific) and not against Pdp1ε (predominantly involved in circadian mechanisms). Drosophila PDP1γ protein shows a high homology to mammalian thyrotroph embryonic factor (TEF), albumin D site-binding protein (DBP), and hepatic leukemia factor (HLF) transcription factors. In an in vitro model of drug- (olanzapine-) induced adiposity in mouse 3T3-L1 cells, the mRNA content of HLF but not TEF and DBP was increased by the drug treatment. A knockdown of the HLF mRNA by transfecting the cultures with HLF dsRNA significantly reduced their lipid content. Furthermore, the HLF RNAi prevented olanzapine from increasing the cell lipid content. These results suggest that the PDP1/HLF system may play a role in physiological and drug-influenced lipid regulation.