Objective: To investigate the effect of Alamandine, a peptide derived from the decarbonization of Angiotensin（1-7）,on the adipogenic differentiation of adipose-derived mesenchymal stem cells (ADSCs) in rats, and the mechanism of Alamandine regulating lipogenic differentiation. Methods：Rat ADSCs were treated with Alamandine at different concentrations (0.1μM, 1μM, 10μM), lipid droplets were observed by light microscopy, intracellular triglyceride and total cholesterol were determined, the degree of lipid differentiation was detected by oil red O staining, and the protein associated with adipogenic differentiation was detected by Western blot. After determining the optimal concentration, 10μM Alamandine was used to detect the adipogenic differentiation degree of rat ADSCs in different days. Angiotensin II (Ang Ⅱ) and Alamandine dealt with rats ADSCs, same method to detect a concomitant with differentiation, detect the effect of AngII and Alamandine on adipogenic differentiation. Rat ADSCs were treated with Mas associated G protein coupled receptor D(MrgD) antagonist D-pro7, and adipogenic differentiation was detected by the same method, so as to further verify the role of Alamandine in promoting adipogenic differentiation. Results :Alamandine treatment of rat ADSCs with different concentrations showed that Alamandine promoted adipogenic differentiation of rat ADSCs in an obvious dose-dependent manner. ADSCs of rats treated with 10 μM Alamandine were detected at 1, 3, 6 and 10 days, respectively. With the increase of treatment days, the degree of adipogenic differentiation gradually increased and reached its peak on the 10th day. Ang Ⅱ single processing rat ADSCs inhibits adipogenticdifferentiation and the effect of Alamandine contributing to fat differentiation is weakened with AngII. MrgD antagonist D- Pro7 also inhibited the lipid differentiation effect of Alamandine on rat ADSCs. Conclusion: Alamandine promotes lipid differentiation through MrgD on rat ADSCs. This may provide a new way to treat obesity.