Fig. 1

Heterogeneity and plasticity of adipose precursors in white and beige adipogenesis. Adipogenesis is a process involving two phases, lineage commitment and terminal differentiation. The former is the commitment of adipose stem cells to adipose precursors. The latter is terminal differentiation of adipose precursors to matured adipocytes. Interestingly, the precursors in different WAT depots have complex populations and characteristics. In vWAT, there are two subpopulations of PDGFRβ+ progenitors, LY6C-CD9- and LY6C+ populations. Among them, LY6C-CD9-PDGFRβ+ cells are adipose progenitors, with the ability of commitment to white adipocytes. LY6C+ PDGFRβ+ progenitors representing FIPs that have lost the ability to differentiate into adipocytes, but gain the ability to promote tissue inflammation and fibrosis. Using scRNA-seq, DPP4+ progenitor cells in sWAT can be converted to ICAM1+ committed preadipocytes, and CD142+ ABCG1+ Aregs that act as brake in adipogenesis. During obesity in rodents, the remodeling of vWAT is attributed to hyperplasia and hypertrophy, while the expansion of sWAT is mainly relied on hypertrophy. Importantly, the excessive expansion in vWAT is closely linked to metabolically unhealthy obesity, whereas sWAT expansion to certain extend is expected to improve lipid storage stress and metabolic status. In addition, the PDGFRα+ CD81+ beige adipose precursors existing in sWAT contribute to the de novo beige adipogenesis upon long-term cold exposure and β3-adrenergic receptor activation. Meanwhile, short-term stimuli can convert mature white adipocytes into beige adipocytes. These browning strategies hold the promise to combat obesity and related metabolic disorders