17β-Estradiol in the systemic circulation derives mainly from the parietal cells in cholestatic female rats.

Abstract

Estrogenic symptoms of liver disease patients including biliary tract disorder with high frequency is observed in clinical cases. However, the origin of 17β-estradiol which is abundant enough to cause symptoms remains uncertain. In male rats, it has been reported that the parietal cells which have an abundance of aromatase-synthesized 17β-estradiol, and a part of 17β-estradiol secreted into the portal vein, may flow into the systemic circulation under a pathophysiological condition of the liver including bile duct ligation (BDL). The aim of this study is to reveal the origin of 17β-estradiol increment in female rats and to investigate the effect of BDL on the ovary during the estrus cycle. Wistar female rats were used, and the common bile duct was ligated twice and transected completely at 7 days before termination. Serum portal venous and arterial 17β-estradiol levels, Cyp19a1 expressions, aromatase protein levels, and estrogen receptor (ER) α levels in the liver were measured during the estrus cycle. Both arterial and portal venous 17β-estradiol levels increased 2.9 times at proestrus and maintained constant levels during the cycle. The expression of Cyp19a1 and aromatase protein in the stomach maintained constant levels, and significantly decreased during the estrus cycle in the ovary. Hepatic ERα protein and Esr1 expressions decrease by BDL in all stages. These results suggest that the increment of serum 17β-estradiol levels in obstructive cholestasis induced by BDL is derived from 17β-estradiol secreted from the parietal cells in females as well as males.