title: Oral estrogen antagonizes the metabolic actions of growth hormone in growth hormone-deficient women.
abstract: We have determined whether oral estrogen reduces the biological effects of growth hormone (GH) in GH-deficient (GHD) women compared with transdermal estrogen treatment. In two separate studies, eight GHD women randomly received either oral or transdermal estrogen for 8 wk before crossing over to the alternate route of administration. The first study assessed the effects of incremental doses of GH (0.5, 1.0, 2.0 IU/day for 1 wk each) on insulin-like growth factor I (IGF-I) levels during each estrogen treatment phase. The second study assessed the effects of GH (2 IU/day) on lipid oxidation and on protein metabolism using the whole body leucine turnover technique. Mean IGF-I level was significantly lower during oral estrogen treatment (P < 0.05) and rose dose dependently during GH administration by a lesser magnitude (P < 0.05) compared with transdermal treatment. Postprandial lipid oxidation was significantly lower with oral estrogen treatment, both before (P < 0.05) and during (P < 0.05) GH administration, compared with transdermal treatment. Protein synthesis was lower during oral estrogen both before and during GH administration (P < 0.05). Oral estrogen antagonizes several of the metabolic actions of GH. It may aggravate body composition abnormalities already present in GHD women and attenuate the beneficial effects of GH therapy. Estrogen replacement in GHD women should be administered by a nonoral route.
authors.affiliation: The Garvan Institute of Medical Research, St. Vincent's Hospital and Biomedical Mass Spectrometry Unit, University of New South Wales, Sydney, New South Wales 2010, Australia.
authors.forename: T
authors.initials: T
authors.lastname: Wolthers
authors.forename: D M
authors.initials: DM
authors.lastname: Hoffman
authors.forename: A G
authors.initials: AG
authors.lastname: Nugent
authors.forename: M W
authors.initials: MW
authors.lastname: Duncan
authors.forename: M
authors.initials: M
authors.lastname: Umpleby
authors.forename: K K
authors.initials: KK
authors.lastname: Ho
mesh_terms: D000279:Administration, Cutaneous; D000284:Administration, Oral; D000328:Adult; D018592:Cross-Over Studies; D004305:Dose-Response Relationship, Drug; D004311:Double-Blind Method; D004958:Estradiol / Q000008:administration & dosage / Q000494:pharmacology; D004967:Estrogens / Q000008:administration & dosage / Q000494:pharmacology*; D005260:Female; D013006:Growth Hormone / Q000037:antagonists & inhibitors* / Q000627:therapeutic use*; D019382:Human Growth Hormone / Q000172:deficiency*; D006801:Humans; D007018:Hypopituitarism / Q000188:drug therapy; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D007930:Leucine / Q000378:metabolism; D050356:Lipid Metabolism; D008525:Medroxyprogesterone / Q000008:administration & dosage / Q000494:pharmacology; D008875:Middle Aged; D045167:Progesterone Congeners / Q000494:pharmacology; D011506:Proteins / Q000378:metabolism
chemical_list: D004967:Estrogens; D045167:Progesterone Congeners; D011506:Proteins; D019382:Human Growth Hormone; D004958:Estradiol; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D007930:Leucine; D008525:Medroxyprogesterone