Lysosome Inhibition Reduces Basal and Nutrient-Induced Fat Accumulation in Caenorhabditis elegans

Rui Lu; Juan Chen; Fangbin Wang; Lu Wang; Jian Liu; Yan Lin

doi:10.14348/molcells.2022.0073

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자료유형: 학술저널

저자정보: Rui Lu (Hefei University of Technology) Juan Chen (Hefei University of Technology) Fangbin Wang (Hefei University of Technology) Lu Wang (Hefei University of Technology) Jian Liu (Hefei University of Technology) Yan Lin (Hefei University of Technology)

저널정보: 한국분자세포생물학회 Molecules and Cells Molecules and Cells 제45권 제9호

발행연도: 2022.9

수록면: 649 - 659 (11page)

DOI: 10.14348/molcells.2022.0073

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A long-term energy nutritional imbalance fundamentally causes the development of obesity and associated fat accumulation. Lysosomes, as nutrient-sensing and lipophagy centers, critically control cellular lipid catabolism in response to nutrient deprivation. However, whether lysosome activity is directly involved in nutrient-induced fat accumulation remains unclear. In this study, worm fat accumulation was induced by 1 mM glucose or 0.02 mM palmitic acid supplementation. Along with the elevation of fat accumulation, lysosomal number and acidification were also increased, suggesting that lysosome activity might be correlated with nutrient-induced fat deposition in Caenorhabditis elegans. Furthermore, treatments with the lysosomal inhibitors chloroquine and leupeptin significantly reduced basal and nutrient-induced fat accumulation in C. elegans. The knockdown of hlh-30, which is a critical gene in lysosomal biogenesis, also resulted in worm fat loss. Finally, the mutation of aak-2, daf-15, and rsks-1showed that mTORC1 (mechanistic target of rapamycin complex-1) signaling mediated the effects of lysosomes on basal and nutrient-induced fat accumulation in C. elegans. Overall, this study reveals the previously undescribed role of lysosomes in overnutrition sensing, suggesting a new strategy for controlling body fat accumulation.

#Caenorhabditis elegans #fat accumulation #lysosome #nutrient

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