title: Effects of different oral oestrogen formulations on insulin-like growth factor-I, growth hormone and growth hormone binding protein in post-menopausal women.
abstract: OBJECTIVE
  Insulin like growth factor-I (IGF-I) levels in post-menopausal women are reduced by oral administration of the synthetic oestrogen ethinyl oestradiol but increased by transdermal delivery of 17 beta-oestradiol. Since these oestrogen types are different, the aim of this study was to clarify whether reduction in IGF-I is a specific effect of ethinyl oestradiol or common to other oral oestrogen formulations.
  
  
  METHODS
  Randomized cross-over study comparing one month of treatment with ethinyl oestradiol (20 micrograms), conjugated equine oestrogen (1.25 mg Premarin) and oestradiol valerate (2 mg).
  
  
  METHODS
  Six healthy post-menopausal women, age 60.3 +/- 5.6 years.
  
  
  METHODS
  Mean 24 hour GH (from hourly sampling), IGF-I, GH binding protein (GHBP), pituitary (LH, FSH) and hepatic function (SHBG and angiotensinogen) were measured.
  
  
  RESULTS
  All three oestrogen formulations resulted in a significant reduction in IGF-I levels compared to baseline and significant elevations of GH and GHBP (P < 0.05). The percentage increase in GH during oestrogen treatment was significantly related to the percentage decrease in IGF-I levels (P = 0.04). All three oestrogen formulations resulted in significant suppression of LH and FSH and induction of the hepatic proteins, SHBG and angiotensinogen (P < 0.05). GHBP increased in parallel with other hepatic proteins.
  
  
  CONCLUSIONS
  Reduction in IGF-I levels is an intrinsic effect of oral oestrogen therapy and increased GH levels may occur as a result of reduced feedback inhibition by IGF-I. Since GHBP activity is not changed by transdermal oestrogen, we conclude that the liver is a major source of circulating GHBP and that GHBP is an oestrogen sensitive protein.
authors.affiliation: Garvan Institute of Medical Research, St Vincent's Hospital, Sydney, Australia.
authors.forename: J J
authors.initials: JJ
authors.lastname: Kelly
authors.forename: I A
authors.initials: IA
authors.lastname: Rajkovic
authors.forename: A J
authors.initials: AJ
authors.lastname: O'Sullivan
authors.forename: C
authors.initials: C
authors.lastname: Sernia
authors.forename: K K
authors.initials: KK
authors.lastname: Ho
mesh_terms: D000368:Aged; D000808:Angiotensinogen / Q000097:blood; D002352:Carrier Proteins / Q000097:blood*; D004958:Estradiol / Q000031:analogs & derivatives / Q000494:pharmacology; D004967:Estrogens / Q000494:pharmacology*; D004966:Estrogens, Conjugated (USP) / Q000494:pharmacology; D004997:Ethinyl Estradiol / Q000494:pharmacology; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D013006:Growth Hormone / Q000097:blood*; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000032:analysis*; D008099:Liver / Q000187:drug effects; D007986:Luteinizing Hormone / Q000097:blood; D008593:Menopause / Q000378:metabolism*; D008875:Middle Aged; D012738:Sex Hormone-Binding Globulin / Q000032:analysis
chemical_list: D002352:Carrier Proteins; D004967:Estrogens; D004966:Estrogens, Conjugated (USP); D012738:Sex Hormone-Binding Globulin; D000808:Angiotensinogen; D004997:Ethinyl Estradiol; D004958:Estradiol; D007334:Insulin-Like Growth Factor I; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013006:Growth Hormone; C051815:somatotropin-binding protein