Objective: Managing the complications of metabolic syndrome is one of the major issues in the daily practice of plastic surgery. Thus, a better understanding of molecular mechanism in development and function of adipose tissues should help us managing the problems of the metabolic syndrome. YULINK was discovered as an essential regulator in Drosophila oogenesis in the first decade of the 21st century. Recently, YULINK has been reported to serve as an upstream positive regulator for mTORC1 signalling in amino acid regulation. However, whether and how YULINK functions in adipogenesis and glucose metabolism is still not clear.
Materials and Methods: In this study, both mouse preadipocytes 3T3L1 and human adipose-derived stromal cells (hASCs) were examined in response to insulin-stimulating adipogenesis or glucose uptake with or without YULINK silencing. Raft and non-raft domains of the cell membrane were studied for functional analysis of the YULINK. The roles of YULINK were also explored in the insulin signalling by western blot analysis.
Results: A gradually increase of YULINK expression accompanied with increased adipogenic markers during adipogenesis in both 3T3L1 cells and hASCs have also been noted. Knockdown of YULINK resulted in markedly decreased lipid accumulation and failed to undergo adipogenesis in either 3T3L1 or hASCs. YULINK was demonstrated to co-localize with flotillin-1 on lipid raft in response to insulin treatment. In addition, YULINK might be associated with insulin-stimulating PI3K-AKT signalling and its downstream SREBP1, PPAR expression in adipogenesis. YULINK was demonstrated to interact with GLUT4 and to regulate its translocation from cytosol to membrane in 3T3L1 adipocytes.
Conclusion: YULINK might participate in adipogenesis in preadipocytes as well as glucose uptake in 3T3L1 adipocytes via insulin-stimulating PI3K-AKT signalling.
Key words: YULINK; insulin signalling; GLUT4; lipid rafts; glucose uptake; adipogenesis

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