Adipsin is a molecular marker of obesity in rodents. Content of adipsin protein in blood and mRNA in adipocytes is significantly reduced in several genetic and experimentally induced obese models. It has been suggested that this reduction in adipsin is causative to obesity development. Insulin reduces adipsin expression in vitro and is negatively correlated with adipsin expression in vivo. Because bovine somatotropin (bST) opposes many actions of insulin and can reduce body fat content, we tested the hypothesis that bST enhances adipsin expression. In two experiments using 210 rats, bST and a similar hormone, bovine placental lactogen (bPL), both caused a small (14 to 27%) but statistically significant reduction in circulating adipsin protein. Because exogenous bST can increase circulating insulin we next used a diabetic model to test the bST effect on adipsin. In rats treated with streptozotocin and injected daily with insulin (STZ+I), bST had no effect on circulating adipsin. Additional variables related to growth were influenced differently by bST in normal vs. STZ+I animals. In conclusion, the drop in circulating adipsin following bST administration in normal rats is dependent upon the animals' ability to secrete insulin.