Adropin is a secreted protein encoded by Energy Homeostasis Associated (Enho) gene. Enho mRNA is abundantly expressed in the liver and brain (1). There is evidence indicating that biological effects of adropin are mediated trough GPR19 receptor (2). It was shown that in mice adropin deficiency leads to increased adiposity, impaired glucose production and dyslipidaemia (3). Adropin overexpression or adropin administration attenuates insulin resistance, reduces lipogenic genes expression and protects from body weight gain (1). These data suggested that adropin is involved in lipid metabolism and body weight regulation. However, the role of adropin in modulation of adipose tissue biology including adipogenesis remains unknown. In the present work we studied the effects of adropin on proliferation and differentiation of white preadipocytes into adipocytes. The influence of adropin on proliferation and differentiation of preadipocytes was studied using primary preadipocytes isolated from Wistar male rats (weighing 80-100 g) and murine 3T3-L1 cells. Cell proliferation was assessed by BrdU assay. Gene mRNA expression and protein phosphorylation were determined by Real Time PCR and Western blot. Triacylglycerol level was evaluated by Oil Red O staining. Statistical analysis was performed using ANOVA followed by the Bonferroni post hoc test. Data are shown as mean ± SEM. Enho and Gpr19 mRNA expression was detected in the rat primary preadipocytes and 3T3-L1 cells. Adropin (100 nmol/l) increased proliferation of rat preadipocytes (0.45±0.02 vs. 0.54±0.01 OD 450-690 nm) and 3T3-L1 cells (0.47±0.02 vs. 0.58±0.02 OD 450-690 nm, p<0.05). Furthermore, adropin (100 nmol/l) stimulated AKT (1.0±0.42 vs. 3.68±0.71 arb. u., p<0.05) and ERK1/2 (1.0±0.02 vs. 1.82±0.20 arb. u., p<0.05) phosphorylation in 3T3-L1 cells. Adropin failed to induce cell proliferation in the presence of AKT and ERK1/2 inhibitors. In addition, adropin (100 nmol/l) decreased mRNA expression of adipogenic genes in rat preadipocytes (Pparγ 4.96±0.17 vs. 3.67±0.29 arb. u., Fabp4 6.43±0.28 vs. 4.46±0.38 arb. u. and Cebpa 1.84±0.23 vs. 1.23±0.59 arb. u., p<0.05). Similar effect was also observed in 3T3-L1 adipocytes (Pparγ 19.69±2.33 vs. 13.26±1.31 arb. u., Fabp4 1499±167.2 vs. 803±158.7 arb. u., p<0.05). Furthermore, lower level of intracellular triacylglycerol was found in rat preadipocytes (0.43±0.01 vs. 0.35±0.008 OD 520 nm, p<0.05) and 3T3-L1 cells (0.22±0.003 vs. 0.18±0.002 OD 520 nm, p<0.05) differentiated for 7 days in the presence of adropin (100 nmol/l). These results showed that adropin stimulates preadipocytes proliferation via ERK1/2- and AKT-dependent mechanisms. Furthermore, we provide evidence that adropin suppresses differentiation of preadipocytes into mature adipocytes. These data suggest that adropin may contribute to controlling energy homeostasis by modulation of white adipogenesis.