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Absorption and metabolism of estrogens from the stomach and duodenum of pigs
Affiliation:1. Copenhagen Cystic Fibrosis Center, Department of Infectious Diseases, Rigshospitalet, Copenhagen University Hospital, Blegdamsvej 9, DK2100 Copenhagen, Denmark;2. Dept. of Medicine, Endocrine Division, Zealand University Hospital, Lykkebaekvej 1, DK4600 Koege, Denmark;3. Dept. of Clinical Physiology, Nuclear Medicine and PET, Rigshospitalet, Blegdamsvej 9, Copenhagen University Hospital, DK2100 Copenhagen, Denmark;4. Copenhagen Cystic Fibrosis Center, Danish Pediatric Pulmonary Service, Copenhagen University Hospital, Juliane Maries Vej 6, DK2100 Copenhagen, Denmark;5. Dept of Clinical Biochemistry, Rigshospitalet, Copenhagen University Hospital, Valdemar Hansens Vej 13, 2600 Glostrup, Copenhagen, Denmark;6. Dept. of Clinical Microbiology, Rigshospitalet, Copenhagen University Hospital, Ole Maaløes Vej, 26, DK2200 Copenhagen, Denmark;7. Institute for Inflammation Research, Center for Rheumatology and Spine Diseases, Copenhagen University Hospital, Rigshospitalet, Blegdamsvej 9, DK2100 Copenhagen, Denmark;8. The Centre of Inflammation and Metabolism (CIM), Centre for Physical Activity Research (CFAS), Rigshospitalet, Copenhagen University Hospital, Blegdamsvej 9, DK2100 Copenhagen, Denmark
Abstract:To determine the absorption and metabolism of 17β-estradiol (E2) by the stomach and liver of the pig, crystalline E2 was placed in the stomach of prepubertal gilts. Blood samples were subsequently obtained from the hepatic portal and jugular veins and plasma was assayed for E2, estrone (E1), 17β-estradiol-glucuronide (E2G), estrone-glucuronide (E1G) and estrone-sulfate (E1S). Concentrations of E2, E1, E2G and E1S rose in the hepatic portal vein within five min and remained elevated for several hr. Concentration of E2 represented only 6% of the total estrogen detected in the hepatic portal vein during the sampling period, indicating that most of the E2 was converted or conjugated prior to entering the hepatic portal vein. The metabolism of E2 presumably occurred in the stomach mucosa because food had been withheld for 26 hr before infusion of E2. Concentrations of E2G, E1G and E1S, but not E2 and E1, rose in the jugular vein and remained elevated for several hr. The lack of a rise in E2 and E1 in the jugular vein indicates that the E2 and E1 from the hepatic portal vein were completely converted and/or removed by the liver. Most of E2 was converted to E1 and then to E1G. The infusion of bile containing normal estrogens from pregnant gilts into the duodenum of prepubertal gilts resulted in a peak of E1G and E2G in the hepatic portal and jugular veins within a few minutes. This was followed in about 180 min by a second sustained rise. The first peak was essentially abolished by extracting E1 and E2 from the bile before infusion. The second peak failed to occur in gilts given antibiotics orally to reduce gut bacteria before infusion of bile.
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