Journal
AUTOPHAGY
Volume 13, Issue 11, Pages 1995-1997Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2017.1371394
Keywords
autophagy; lipid droplet; lipophagy; lipotoxicity; starvation
Categories
Funding
- Biomedical Research Training Program Fellowship, University of Kansas Medical Center
- [R01 AA020518]
- [R01 DK102142]
- [U01 AA024733]
- [P20GM103549]
- [P30GM118247]
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Fatty acids are an important cellular energy source under starvation conditions. However, excessive free fatty acids (FFAs) in the cytoplasm cause lipotoxicity. Therefore, it is important to understand the mechanisms by which cells mobilize lipids and maintain a homeostatic level of fatty acids. Recent evidence suggests that cells can break down lipid droplets (LDs), the intracellular organelles that store neutral lipids, via PNPLA2/adipose triglyceride lipase and a selective type of macroautophagy/autophagy termed lipophagy, to release FFAs under starvation conditions. FFAs generated from LD catabolism are either transported to mitochondria for beta-oxidation or converted back to LDs. The biogenesis of LDs under starvation conditions is mediated by autophagic degradation of membranous organelles and requires diacylglycerol O-acyltransferase 1, which serves as an adaptive cellular protective mechanism against lipotoxicity.
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