Other studies have suggested that when sufficient glucose is present not only will gluconeogenesis be inhibited but corticosterone can antagonize the effects of insulin and increase glucose storage [28], [29] and [30]. Our data support this theory and provide evidence in laying hens that corticosterone will not induce gluconeogenesis unless the concentration of glucose in the liver has been depleted. In addition, when there is sufficient glucose in the liver corticosterone may induce glucose storage as evidenced by the increased glycogenesis in experiment 1. These data should be interpreted with caution as one limitation of our research is that we could not attribute causation. Although there were strong associations between corticosterone and glucose metabolism we could not conclude that the corticosterone caused the changes in glucose metabolism. Regardless, increased corticosterone was only associated with increased gluconeogenesis when glucose in the liver was depleted, and increased corticosterone was associated with increased glycogenesis when glucose in the liver was not depleted. This finding validates our methods and supports the need to extend our investigation of the stress response to the site of corticosterone action.