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White adipose tissue (WAT) stores triglycerides and is crucial to maintaining the body's energy balance. Attributed to its plasticity, WAT can undergo dynamic remodeling in response to chronic energy excess. As obesity increases, alterations in the quantity and function of progenitor and immune cells result in fibrosis and inflammation in the WAT. Hence, metabolic dysfunction becomes more severe. In a recent study, HFD feeding significantly increased the gene expressions of bone morphogenetic protein 2 (BMP2), acidic fibroblast growth factor (FGF1), and basic fibroblast growth factor (FGF2) in macrophages. It was found in a fibrotic environment that the factors stimulated the growth of progenitor cells and the expression of fibrotic genes but suppressed adipogenesis. We looked at how these ligands affect fat metabolism, including adipogenesis, fibrosis, and thermogenesis. We also found out how these ligands affect the way progenitor cells change. By conducting proliferation and differentiation experiments on the 3T3-L1 cell model in vitro with these ligands supplemented at different phases, we demonstrated these ligands' influence 3T3-L1 preadipocytes and adipocytes genotype and phenotype. Based on this research, it was found that BMP2 stimulates adipogenesis by making cells multiply and differentiate. FGF1 exhibits different phasic influences on adipogenesis. FGF1 suppresses the preadipocyte differentiation phase but promotes cell proliferation, which increases the cell confluence speed and might lead to earlier differentiation of adipocytes. FGF2 added in the proliferation phase did not have much effect on adipogenesis. FGF2 might promote preadipocyte commitment during the adipocyte-genesis stage of differentiation phase but the comprehensive effect remains ambiguous.