Status of the Pituitary-Adrenocortical-Liver Axis following Partial Hepatectomy 1

Abstract

Since the liver is the primary site of steroid degradation and plasma binding protein synthesis, studies were undertaken to evaluate adrenocortical activity in partially hepatectomized (H) male rats. Two days after either 10, 30, 40, or 70% H, significant decreases in liver mass were observed, while elevations in total and free plasma corticosterone levels, adrenal corticosterone content, and adrenal weights were noted only in the 70% H group. Hepatic δ⁴-steroid hydrogenase activity was significantly depressed in both whole and microsomal, but not in the supernatant, fractions of the regenerating liver of the 70% H group. Although plasma ACTH levels were unchanged in these animals, the in vitro adrenocortical responsiveness to ACTH was increased. These data suggest that a portion of the increase in total plasma corticosterone levels post-70% H was due to a reduction in the hepatic capacity to inactivate corticosterone, while the remainder may be due to an increase in adrenocortical secretion as a result of an enhanced responsiveness of the adrenal gland to ACTH.