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https://doi.org/10.5713/ab.21.0341    [Accepted] Published online October 29, 2021.
mTOR and ERK1/2 signaling participate in the process of acetate regulating lipid metabolism and HSL expression
Yujuan Li1,a  , Chunyan Fu1,3,a  , Lei Liu1,*  , Yongxu Liu2  , Fuchang Li1,* 
1Department of Animal Science, Shandong Agricultural University, Taian, Shandong 271018, China
2Qingdao Kangda Food Co., LTD., Qingdao, Shandong 266555, China
3Poultry Institute, Shandong Academy of Agricultural Science, Jinan, Shandong 250023, China
Correspondence:  Lei Liu, Tel: +86-0538-8242593-831, Fax: +86-538-8241419, Email: leiliu@sdau.edu.cn
Fuchang Li,Email: chlf@sdau.edu.cn
Received: 31 July 2021   • Revised: 3 September 2021   • Accepted: 1 October 2021
aThese authors contributed equally to this work.
Acetate plays an important role in host lipid metabolism. However, the network of acetate-regulated lipid metabolism remains unclear. Previous studies show that mitogen-activated protein kinases (MAPKs) and mechanistic target of rapamycin (mTOR) play a crucial role in lipid metabolism. We hypothesize that acetate could affect MAPKs and/or mTOR signaling and then regulate lipid metabolism. The present study investigated whether any cross talk occurs among MAPKs, mTOR and acetate in regulating lipid metabolism.
The ceramide C6 (an extracellular signaling-regulated kinases 1 and 2 (ERK1/2) activator) and MHY1485 (a mTOR activator) were used to treat rabbit adipose-derived stem cells (ADSCs) with or without acetate, respectively.
It indicated that acetate (9 mM) treatment for 48 h decreased the lipid deposition in rabbit ADSCs. Acetate treatment decreased significantly phosphorylated protein levels of ERK1/2 and mTOR but significantly increased mRNA level of hormone-sensitive lipase (HSL). Acetate treatment did not significantly alter the phosphorylated protein level of p38 MAPK and c-Jun aminoterminal kinase (JNK). Activation of ERK1/2 and mTOR by respective addition in media with ceramide C6 and MHY1485 significantly attenuated decreased lipid deposition and increased HSL expression caused by acetate.


Our results suggest that ERK1/2 and mTOR signaling pathways are associated with acetate regulated HSL gene expression and lipid deposition.
Keywords: Acetate; ERK1/2; Lipid Deposition; mTOR; Rabbit Adipose-derived Stem Cells
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