Adipsin is a molecular marker of obesity in rodents. Content of adipsi
n protein in blood and mRNA in adipocytes is significantly reduced in
several genetic and experimentally induced obese models. It has been s
uggested that this reduction in adipsin is causative to obesity develo
pment. Insulin reduces adipsin expression in vitro and is negatively c
orrelated 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 tw
o experiments using 210 rats, bST and a similar hormone, bovine placen
tal lactogen (bPL), both caused a small (14 to 27%) but statistically
significant reduction in circulating adipsin protein. Because exogenou
s bST can increase circulating insulin we next used a diabetic model t
o test the bST effect on adipsin. In rats treated with streptozotocin
and injected daily with insulin (STZ+I), bST had no effect on circulat
ing adipsin. Additional variables related to growth were influenced di
fferently 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.