**Adipogenic differentiation**

Adipogenesis is the process of cell differentiation from stem cells to adipocytes. During this process, the ASCs will divide into two cells, where one cell keeps the stemness and the other cell can commit to the adipogenic lineage and become preadipocyte. The preadipocytes are fibroblast-like cells that are morphologically indistinguishable from the mesenchymal precursors but they lose their capacity to differentiate into other cell types (osteocytes, chondrocytes, myocytes, etc. The preadipocyte can terminal differentiate and acquire the characteristics of mature adipocytes, including lipid synthesis, insulin sensitivity, and the secretion of adipocyte-specific proteins. The terminally-differentiated adipocytes are characterized by a large unilocular lipid droplet and their main function is energy storage [11].

Adipogenesis is a well-orchestrated process that requires sequential activation of numerous transcription factors, including the CCAAT gene family/enhancerbinding protector (C/EBP) and peroxisomal proliferator-activated receptor-γ (PPAR-γ) [12]. The molecular mechanisms of adipogenesis involve stimulators and inhibitors. Adipogenic stimulators are represented by peroxisome proliferatoractivated γ receptor (PPAR γ), insulin-like growth factor I (IGF-1), macrophage colony-stimulating factor, fatty acids, prostaglandins, and glucocorticoids. The inhibitors are Wnt, transforming growth factor-β (TGF-β), inflammatory cytokines, and growth hormone. Adipogenesis could be also influenced by age, gender, adipose depot, and lifestyle [13].

*In vitro* studies showed that mRNA expression level of CD10 of subcutaneous-ASCs increased after adipogenic stimuli, and this increase positively correlated with those of adipogenic markers, PPARG and aP2. In contrast, the CD200 level decreased after adipogenesis was initiated and exhibited a negative correlation with adipogenic markers [10].
