In recent years, environmental pollutants/endocrine disrupting chemicals (EDCs) have received special attention as metabolic disruptors that produce adverse developmental, reproductive, neurological, cardiovascular, metabolic and immune effects, including predisposition to metabolic syndrome, obesity and type 2 diabetes. Many EDCs are found in everyday products, such as plastic bottles, metal food cans, pesticides, detergents, toys, cosmetics, etc. The knowledge on cellular mechanisms behind the biological effect of EDCs exposure on the development of obesity and type2 diabetes is very limited. Bisphenol A (BPA) is one of the most abundant EDCs present in the environment. BPA is present in the tested samples of human serum and urine worldwide and is considered to be an “obesogene” that interferes with lipid and glucose metabolism (reviewed in Umar et al., 2013). We focused our study on the effects produced by the exposure to BPA on the expression of obesity-related genes using zebrafish as an experimental model. We have chosen the zebrafish model based on several criteria: 1) recent studies have used zebrafish as a model for studies of the effects of EDCs (Chow et al., 2012); 2) a review by Holtta-Vuori at al. (2010) described zebrafish as an excellent model organism for lipid research; 3) studies of diet-induced obesity show that zebrafish and mammals share common pathophysiological pathways (Oka et al., 2010). Our experiments showed that exposure of 7dpf zebrafish larvae to 5mg/L of BPA for 24 hours significantly decreased adiponectin and ghrelin mRNA expression (by 29±7% and 26±6 %, respectively, N=5, t-test p<0.05) assessed by quantitative RT-PCR using RPLO mRNA expression for the normalization. In the same experiments vitellogenin mRNA expression was increased (by 96±11%, N=5, t-test p<0.05) and there were no changes in the mRNA expression of PDK4, perilipin and UCP3. Exposure of 7dpf zebrafish larvae to 5mg/L of BPA for 72 hours decreased adiponectin and ghrelin mRNA expression by 56±4% and 38±5 %, respectively (N=5, t-test p<0.05). The data presented here are the first to show that exposure of zebrafish to BPA decreases adiponectin and ghrelin expression. Adiponectin increases fatty acid oxidation and glucose metabolism in muscle, reduces glucose output and enhances insulin sensitivity in liver, and exposure of mammalian adipocytes to BPA inhibits adiponectin release (reviewed in Ben-Jonathan et al., 2009). Ghrelin is involved in regulation of feeding and has potent growth hormone stimulation activity in zebrafish. Our data on increased vitellogenin mRNA expression correlate well with previously reported data on the zebrafish response to BPA (Chow et al., 2012). Overall our data suggest that exposure of zebrafish to BPA displays similarities with obesity-promoting effects of BPA previously documented in mammalian models.