title: Gastric estrogen increases pituitary estrogen receptor α and prolactin mRNAs during the different pathological conditions of the liver.
abstract: Mammalian liver is an estrogen-responsive tissue mediated by hepatic estrogen receptors. Although Ueyama et al. (Endocrinology 143:3162-3170, 2002) have reported the presence of aromatase and active production of gastric 17β-estradiol in parietal cells, there are a few studies on gastric 17β-estradiol exploring the relationship between gastro-hepato function and the gastro-pituitary-gonadal axis. The alteration of gastric 17β-estradiol flow into the systemic circulation by portal vein ligation (PVL) or partial hepatectomy (PH), and the effect of gastric 17β-estradiol on the pituitary function was investigated. In the PVL rats, arterial 17β-estradiol increased 9.5 times that of controls on day 3, and gradually decreased near to control levels in the portal vein by 4 weeks, which was still 5 times higher than those in the arteries of the control rats. In the PH rats, arterial 17β-estradiol increased 2 times that of controls on day 3, and gradually decreased to the control levels. Regeneration and growth of the liver remnants were observed about 2 weeks after PH. In the PVL and PH animals, pituitary ERα and prolactin mRNAs levels increased, positively correlating with an increase of arterial 17β-estradiol levels. Both reduced LHβ mRNA. It is apparent that hepatic dysfunction causes changes in gastric 17β-estradiol levels in the systemic circulation; and that elevated gastric 17β-estradiol affects pituitary function(s). This data suggest that gastric 17β-estradiol has a pivotal role in the regulation of the gastro-hepato-pituitary axis.
authors: Department of Anatomy and Structural Science, Yamagata University Faculty of Medicine, 2-2-2 Iida-nishi, Yamagata, 990-9585, Japan. kob-h@med.id.yamagata-u.ac.jp
authors: Hiroto
authors: H
authors: Kobayashi
authors: Saori
authors: S
authors: Yoshida
authors: Ying-Jie
authors: YJ
authors: Sun
authors: Nobuyuki
authors: N
authors: Shirasawa
authors: Akira
authors: A
authors: Naito
mesh_terms: D000818:Animals; D015536:Down-Regulation; D004958:Estradiol / Q000097:blood / Q000378:metabolism*; D047628:Estrogen Receptor alpha / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D005753:Gastric Mucosa / Q000378:metabolism*; D006498:Hepatectomy / Q000009:adverse effects; D048550:Hepatic Insufficiency / Q000097:blood / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D008026:Ligation; D008099:Liver / Q000473:pathology / Q000502:physiology / Q000601:surgery; D037101:Luteinizing Hormone, beta Subunit / Q000235:genetics / Q000378:metabolism; D008297:Male; D010903:Pituitary Gland, Anterior / Q000378:metabolism* / Q000473:pathology; D011168:Portal System / Q000503:physiopathology; D011169:Portal Vein / Q000601:surgery; D011388:Prolactin / Q000097:blood* / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012038:Regeneration; D015854:Up-Regulation
chemical_list: D047628:Estrogen Receptor alpha; D037101:Luteinizing Hormone, beta Subunit; D012333:RNA, Messenger; D004958:Estradiol; D011388:Prolactin