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C. elegans ACAT regulates lipolysis and its related lifespan in fasting through modulation of the genes in lipolysis and insulin/IGF-1 signaling.
Biofactors ( IF 6 ) Pub Date : 2020-07-08 , DOI: 10.1002/biof.1666
Juan Bai 1, 2 , Renalison Farias-Pereira 3 , Yuan Zhang 2, 4 , Miran Jang 2 , Yeonhwa Park 3 , Kee-Hong Kim 2, 5
Affiliation  

Overly active acyl‐coenzyme A: cholesterol acyltransferases (ACATs) are known to contribute to the development of atherosclerosis, cancer cell proliferation and de novo lipogenesis. However, the role of ACAT in systemic lipid metabolism and its consequence of aging is unknown. Using avasimibe, a clinically proven ACAT inhibitor, and mboa‐1 mutant strain, a homologous to mammalian ACAT, herein, we found that Ava treatment and mboa‐1 mutant exhibited a decreased fat accumulation during feeding and increased lipolysis with extended lifespan of C. elegans during fasting. Our study highlights the essential role of ACAT inhibitor and mboa‐1 in fat mobilization and the survival of C. elegans in fasting through the modulation of the genes involved in lipolysis and insulin/IGF‐1 signaling.

中文翻译:

秀丽隐杆线虫 ACAT 通过调节脂解和胰岛素/IGF-1 信号传导中的基因来调节禁食中的脂解及其相关寿命。

过度活跃的酰基辅酶 A:已知胆固醇酰基转移酶 (ACAT) 有助于动脉粥样硬化的发展、癌细胞增殖和从头脂肪生成。然而,ACAT 在全身脂质代谢中的作用及其衰老后果尚不清楚。使用临床证明的 ACAT 抑制剂avasimibe 和与哺乳动物ACAT同源的mboa-1突变株,我们发现 Ava 处理和mboa-1突变在喂养期间表现出减少的脂肪积累和增加的脂解,延长了C.禁食期间的秀丽隐杆线虫。我们的研究强调了 ACAT 抑制剂和mboa-1在脂肪动员和秀丽隐杆线虫存活中的重要作用 通过调节参与脂肪分解和胰岛素/IGF-1 信号传导的基因来禁食。
更新日期:2020-07-08
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