C. elegans ACAT regulates lipolysis and its related lifespan in fasting through modulation of the genes in lipolysis and insulin/IGF-1 signaling.
Juan BaiRenalison Farias-PereiraYuan ZhangMiran JangYeonhwa ParkKee-Hong KimPublished in: BioFactors (Oxford, England) (2020)
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.
Keyphrases
- adipose tissue
- insulin resistance
- blood glucose
- type diabetes
- cell proliferation
- glycemic control
- fatty acid
- pi k akt
- cardiovascular disease
- wild type
- dna repair
- dna damage
- skeletal muscle
- growth hormone
- genome wide
- cell cycle
- free survival
- low density lipoprotein
- signaling pathway
- combination therapy
- transcription factor
- replacement therapy
- weight loss
- genome wide analysis