The metabolic effects of estriol in female rat liver.
10.3346/jkms.1999.14.3.277
- Author:
Jin Mo YANG
1
;
Sung Soo KIM
;
Jin Il KIM
;
Byung Min AHN
;
Sang Wook CHOI
;
Jae Kwang KIM
;
Chang Don LEE
;
Kyu Won CHUNG
;
Hee Sik SUN
;
Doo Ho PARK
;
Ronald G THURMAN
Author Information
1. Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul. jmyang@sph.cuk.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Estriol;
Metabolism;
Kupffer cells;
Oxygen Consumption;
Calcium
- MeSH:
3-Hydroxybutyric Acid/metabolism;
Acetoacetates/metabolism;
Animal;
Calcium/metabolism;
Carbohydrates/metabolism;
Carbon/metabolism;
Cells, Cultured;
Colloids/metabolism;
Estriol/pharmacology*;
Estriol/metabolism;
Ethanol/pharmacology;
Female;
Gadolinium/pharmacology;
Glucose/biosynthesis;
Intracellular Fluid/metabolism;
Kupffer Cells/metabolism;
Kupffer Cells/cytology;
Lactates/metabolism;
Lipids/metabolism;
Liver/metabolism;
Liver/drug effects*;
Oxygen Consumption;
Phagocytosis;
Pyruvic Acid/metabolism;
Rats;
Rats, Sprague-Dawley
- From:Journal of Korean Medical Science
1999;14(3):277-285
- CountryRepublic of Korea
- Language:English
-
Abstract:
The effects of estriol on oxygen uptake, glucose release, lactate and pyruvate production, beta-hydroxybutyrate and acetoacetate production in perfused rat liver as well as, carbon uptake in rat liver and intracellular calcium in isolated Kupffer cells were investigated. Basal oxygen consumption of perfused liver increased significantly in estriol or ethanol-treated rats. But these increased effects were blocked by gadolinium chloride pretreatment. In a metabolic study, pretreatment with estriol resulted in a decrease in glucose production and in glycolysis while an increase in ketogenesis. A more oxidized redox state of the mitochondria was indicated by increased ratios of perfusate [lactate]/[pyruvate] and decreased ratios of perfusate [beta-hydroxybutyrate]/[acetoacetate]. Carbon uptake of Kupffer-cell increased significantly in estriol-treated rats. But these increased uptake were not shown in rats pre-treated by gadolinium chloride blocking phagocytosis. In isolated Kupffer cells from estriol-treated rats, intracellular calcium was more significantly increased after addition of lipopolysaccharide (LPS) than in controls. These findings suggest that the metabolic effects of estriol (two mg per 100 mg body wt) can be summarized to be highly toxic in rat liver, and these findings suggest that oral administration of estrogens may induce hepatic dysfunctions and play a role in the development of liver disease.
