The Regulation of mTOR Signaling Pathway on Adipogenesis
10.13865/j.cnki.cjbmb.2022.04.1548
- Author:
Ming-Kun CHAO
1
;
Xu-Dong YI
1
;
Wei-Jun PANG
1
Author Information
1. College of Animal Science and Technology, Animal Fat Deposition and Muscle Development Laboratory, Northwest A&F University
- Publication Type:Journal Article
- Keywords:
adipogenesis;
mammalian target of rapamycin (mTOR);
micro RNA (miRNA);
signaling pathways
- From:
Chinese Journal of Biochemistry and Molecular Biology
2022;38(11):1477-1485
- CountryChina
- Language:Chinese
-
Abstract:
Adipose tissue is a major energy storage and endocrine organ. Adipogenesis is a complex process of cell differentiation, which is regulated by nutrient levels, hormones and metabolites, etc. The mammalian target of rapamycin (mTOR) complex includes two protein complexes, mammalian target of rapamycin complex 1 (mTORC1) and mTORC2. The lipid kinase-like domain contained in the mTOR complex lays the foundation for the mTOR pathway to regulate adipogenesis. Research on some components of mTORC1 and mTORC2 has verified the roles of mTOR in the regulation of adipogenesis. Based on previous studies, we reviewed the research of miR-199a-3p, miR-103, miR-188, Src-associated substrate in mitosis of 68 kD (Sam68), endostatin and other substances in the regulation of adipogenesis through mTORC1 and mTORC2. At the same time, we had further constructed the adipogenesis network regulated by mTOR signaling pathway, including insulin/IGF pathway, PI3K-AKT pathway, amino acid pathway, AMPK pathway, cAMP pathway, cGMP pathway, NOTCH pathway, and the modulation of bta-miR-150, 4-O-methylasochlorin and a variety of proteins. This article mainly reviewed the characteristics of mTOR complex and the latest research progress in the regulation of adipogenesis by mTOR pathway. It was pointed out that mTORC2 can regulate lipid uptake, lipolysis and regulate the function of mTORC1. However, there are fewer studies on mTORC2 compared to mTORC1, so further researches on adipogenesis and lipid metabolism may be more focused on mTORC2.
