Adipogenesis corresponds to the commitment and differentiation of AT progenitor cells into adipocytes. Human AT progenitor cells are CD34+/CD31- and have adipogenic potential under pharmacological PPARγ agonist treatment (1). However in human endogenous signals leading to adipogenic commitment are not clearly known. In mice, BMP2/BMP4 and BMP7 induce the commitment in white and brown adipogenesis respectively (2-3). A third type of adipocytes has been described, brite adipocytes which are white adipocytes with some brown characteristics (4). The present study was undertaken to characterize the effects of these BMPs on human native AT progenitor cells white and brown/brite adipogenesis. Human subcutaneous AT cell populations (adipocytes, immune cells, endothelial cells, and progenitor cells) were isolated by immunoselection/depletion approaches. BMPs gene expressions were determined by RT-qPCR analyses in the different AT cell populations (n=6). BMP receptor gene expressions were performed by RT-qPCR on isolated human AT progenitor cells (n=5). AT progenitor cells were treated (or not, control (ctl)) for 48 hours by BMP2, BMP4 or BMP7 (50ng/ml) then cultured in basal adipogenic medium (without PPARγ agonist) for 9 days (n=7). At day 9, adipogenesis was evaluated by lipid accumulation quantification and RT-qPCR analyses on white and brown/brite adipocyte gene markers were performed (n=6). BMP2 gene expression is higher in immune and endothelial cells compared to adipocytes and progenitor cells (1.5 and 5 fold increase respectively, p<0.05), BMP4 and BMP7 gene expressions are higher in progenitor cells than in others (3 and 50 fold increase respectively, p<0.05). Human AT progenitor cells express BMP receptors ALK2, ALK3, ALK6, BMPR2 and ACVR2. Early BMP2, BMP4 or BMP7 treatment on human AT progenitor cells increases lipid accumulation (3 fold increase vs ctl, p<0.001) and induces the expression of common adipogenic gene markers such as PPARγ, LEPTIN and PERILIPIN 1 after 9 days (3 fold increase vs ctl, p<0.05). However only BMP7 induces the expression of the common brown/brite adipocyte gene marker UCP1 (3.5 fold increase vs ctl, p<0.05). Classical brown adipocyte genes as PRDM16, CIDEA and PGC1α are not significantly induced by BMP7 treatment. Our study shows that human AT progenitor cells express BMP receptors and that early BMPs treatment induces the commitment and/or differentiation of human AT progenitor cells into adipocyte. BMP2 and BMP4 are white adipogenesis inducers whereas BMP7 induces brown-like/brite adipogenesis. These results suggest that human AT progenitor cells might have brown-like/brite potential and represent a target to fight against obesity-associated pathologies. Finally, BMPs could be produced locally by AT cells and could be endogenous adipogenic signals regulating human white and brite adipogenesis and obesity.