Adipose tissue is a specialized connective tissue composed mostly of fat cells (adipocytes), which play a pivotal role in the storage of excess energy as a fat. Moreover, adipose tissue is known as a metabolic organ which regulates energy homeostasis and serves as an endocrine gland. Adipocytes express and release several biologically active molecules, known as adipokines [1]. The proliferation and differentiation of adipocytes is regulated by, among others, adropin [2]. Adropin is a peptide encoded by Enho gene [3]. It is known that adropin affects the modulation of body mass as well as lipid metabolism [4]. However, the potential role of adropin on rodent mature adipocyte biology was unknown. Therefore, our research aimed to evaluate the effects of adropin on the expression of adipokines in rodent adipocytes. To conduct the study we utilised two different cell types, namely 3T3-L1 cells (a cell model to study white adipocyte function [5]) and rat primary preadipocytes. Rat primary white preadipocytes were collected from epididymal adipose tissue depots of male Wistar rats. After reaching confluency, cells were differentiated into mature adipocytes, and then incubated in the presence or absence of adropin (10 or 100 nmol/L) for 3 or 24 h. To evaluate the expression of selected adipokines (adiponectin, resistin and visfatin), we used real-time PCR. Data was analysed using one-way ANOVA followed by the Bonferroni post hoc test, and results are shown as mean ± SEM, n = 6. All experiments were conducted at least two times. We found that adropin (10 and 100 nmol/L) promoted the expression of adiponectin mRNA in rat adipocytes after 3 h (3.81±0.58 and 4.97±0.20 vs. 2.14±0.37, p<0.05, respectively), but not after 24 h (1.11±0.07 and 0.81±0.08 vs. 0.96±0.05, p<0.05, respectively). By contrast, adropin (10 and 100 nmol/L) downregulated the expression of resistin (after 3 h – 0.34±0.08 and 0.34±0.07 vs. 1.13±0.05; after 24 h – 0.69±0.09 and 0.31±0.02 vs. 1.03±0.08), and visfatin (after 3 h – 0.43±0.08 and 0.41±0.04 vs. 0.96±0.04; after 24 h – 0.64±0.09 and 0.39±0.02 vs. 0.92±0.10, p<0.05, respectively) in rat adipocytes. Furthermore, adropin (10 and 100 nmol/L) effectively upregulated adiponectin mRNA expression in 3T3-L1 adipocytes exposed to adropin for 3 h (1.38±0.05 and 1.49±0.06 vs. 0.95±0.05) and 24 h (1.27±0.09 and 1.29±0.05 vs. 1.04±0.02, p<0.05, respectively). No effects were found in the expression of resistin (1.13±0.21 and 0.96±0.10 vs. 1.23±0.08) and visfatin (1.07±0.18 and 1.06±0.08 vs. 0.91±0.05, p<0.05) in 3T3-L1 adipocytes exposed to adropin (10 and 100 nmol/L, respectively) for 3 h. However, adropin (100 nmol/L) suppressed mRNA expression of resistin (0.72±0.03 vs. 0.90±0.04) and visfatin (0.63±0.04 vs. 0.95±0.02, p<0.05) in 3T3-L1 adipocytes after 24 h of incubation. To conclude, we found that adropin stimulates adiponectin mRNA expression, but suppresses the expression of resistin and visfatin in rodent adipocytes. Our results indicate that adropin may modulate adipokine expression in rodent adipocytes.