溶酶体活性影响秀丽隐杆线虫脂肪沉积的作用

文章通过在秀丽隐杆线虫的生长培养基（nematode growth medium，NGM）中补充1 mmol/L葡萄糖或0.02 mmol/L棕榈酸诱导线虫的脂肪沉积，结果发现，随着线虫脂肪沉积的增加，其溶酶体数量和酸化水平显著提升，说明溶酶体可能参与了营养物诱导的线虫脂肪沉积；用溶酶体抑制剂氯喹和溶酶体生物合成关键转录因子hlh-30的突变体抑制线虫溶酶体活性，结果发现线虫脂肪沉积水平显著降低；利用线虫溶酶体营养感应和脂代谢相关信号关键分子aak-2、daf-15和rsks-1的突变体，发现mTORC1信号通路在上述溶酶体影响的线虫脂肪沉积中发挥关键作用，结果表明，溶酶体通过mTORC1信号通路影响线虫能量营养过剩所导致的脂肪沉积。

In this paper, 1 mmol/L glucose or 0.02 mmol/L palmitic acid was added to nematode growth medium (NGM) to induce Caenorhabditis elegans fat deposition. Along with the increased fat deposition, lysosomal numbers and acidification levels were also elevated. This suggests that lysosome might regulate nutrient-induced fat deposition. Using lysosomal inhibitor chloroquine and the mutant of hlh-30 that is a key gene involving in lysosomal biosynthesis to inhibit the activity of lysosome, this paper found that lysosome inhibition significantly reduced C. elegans fat deposition. Utilizing various mutants of aak-2, daf-15 and rsks-1, which are key factors in lysosomal nutrient sensing and lipid metabolism-related signaling pathways, the paper explored that mTORC1 signaling pathway mediated the effect of lysosome on nutrient-induced fat deposition in C. elegans. The results show the role of lysosomal activity in nutrient-induced C. elegans fat deposition.