id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
work_6m7txdktbjf47fo425ow5r47ge	Truc B. Nguyen	Lipid droplets and lipotoxicity during autophagy	2017	3	.pdf	application/pdf	1387	103	38	macroautophagic/autophagic breakdown of membranous organelles are packaged and stored in new LDs selectively channeled by DGAT1 (diacylglycerol O-acyltransferase 1) into triacylglycerol (TAG)-rich LDs. These DGAT1-dependent LDs sequester FAs and prevent the accumulation of acylcarnitines, which cellular response to periods of high autophagic flux that provide a lipid buffering system to mitigate Starvation-induced increase in LDs is observed in multiple cell autophagic flux and autophagy-dependent LD biogenesis, even DGAT1-dependent lipid droplet biogenesis protects mitochondrial function during starvation-induced autophagy. https://doi.org/10.1080/15548627.2017.1359451 https://doi.org/10.1080/15548627.2017.1359451 DGAT1 inhibition, indicating that the decrease in mitochondrial functional parameters is not due to increased mitophagy DGAT1-dependent LD biogenesis during starvation is required LDs in preventing lipotoxic cellular damage during autophagy (Figure 1). Olzmann http://orcid.org/0000-0001-7751-8316 (B) In the absence of LD biogenesis, such as during inhibition of DGAT1, autophagy-released FAs can no longer be sequestered as TAGs and instead accumulate as acylcarnitine (AC), which disrupts mitochondrial membrane integrity and impairs http://orcid.org/0000-0001-7751-8316	./cache/work_6m7txdktbjf47fo425ow5r47ge.pdf	./txt/work_6m7txdktbjf47fo425ow5r47ge.txt