Over-accumulation of fat leads to obesity, one of the major public health problems. Obesity is a high-risk factor of obesity-associated disorders, e.g. insulin resistance, cardiovascular disease, dyslipidaemia. Obesity is accompanied by low-grade inflammation (1, 2). Inflammation promotes synthesising and releasing proinflammatory adipokines, and cytokines from adipocytes, e.g. leptin, IL-6, TNFα (3). Inflammation may be induced during treatment preadipocytes with lipopolysaccharides (LPS). Adropin, peptide encoded by Energy Homeostasis Associated gene, is involved in lipid metabolism and body weight gain. Adropin deficiency in mice leads to increased adiposity and dyslipidaemia (4). There is negative correlation between adropin plasma level and BMI in human (5). The role of adropin in adipose tissue inflammation was unknown. The aim of the study was to evaluate the effects of adropin on proliferation, viability, and cell death of LPS-treated preadipocytes. Murine 3T3-L1 cell line as a model of fat precursor cells treated with LPS (from bacteria E.coli) or adropin was used. Preadipocyte proliferation was studied using BrdU assay. Viability of preadipocytes was assessed by MTT assay. Cell death was determined by Cell Death ELISA kit. Statistical analysis was performed using ANOVA followed by the Bonferroni post hoc test. Data are shown as mean ± SEM. Preadipocyte proliferation increased after adropin 100 nM and LPS 500 ng/ml treatment for 24h (0.16±0.02, 0.15±0.01 vs. 0.08±0.01 OD 450-690, p<0.05). Adropin failed to affect the effects observed after treatment with LPS. LPS treatment (250, 500 ng/ml) increased viability of 3T3-L1 preadipocytes after 24h of incubation (0.84±0.02, 0.86±0.02 vs. 0.71±0.17 OD 570-650, p<0.05). Viability also increased after treatment with both adropin 100 nM and LPS 500 ng/ml (0.80±0.01, p<0.05). Moreover, viability of preadipocytes increased after 48h of incubation with 100 nM adropin, LPS 500 and 1000 ng/ml (0.69±0.02, 0.79±0.04, 0.70±0.02 vs. 0.57±0.02, p<0.05). Viability was also greater after incubation with both LPS 500 or 1000 ng/ml and adropin 100 nM (0.84±0.02, 0.74±0.03 vs. 0.57±0.02, p<0.05). Cell death was decreased by 100 nM adropin (0.82±0.02 vs. 1.18±0.01), and LPS (100 and 500 ng/ml) (0.71±0.01, 0.66±0.06 vs. 1.18±0.01 OD 405-490, p<0.05) treatment after 24h of incubation. Similar effect was observed after incubation both with adropin 100 nM and LPS 100 or 500 ng/ml (0.85±0.04, 0.67±0.04 vs. 1.18±0.01, p<0.05). Adropin 100 nM (1.15±0.04) and LPS 500 ng/ml (1.08±0.06 vs. 1.41±0.07, p<0.05) were also effective after 48h. Obtained data suggest that short-term induced inflammatory may enhance proliferation, and viability, and prevent preadipocyte cell death. Adropin failed to modify the effects observed after LPS treatment. Further studies are required to determine the role of adropin in adipose tissue inflammation.