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Comparison of the metabolic effects of raloxifene and oral estrogen in postmenopausal and growth hormone-deficient women.

Artikel i vetenskaplig tidskrift
Författare James Gibney
Gudmundur Johannsson
Kin-Chuen Leung
Ken K Y Ho
Publicerad i The Journal of clinical endocrinology and metabolism
Volym 90
Nummer/häfte 7
Sidor 3897-903
ISSN 0021-972X
Publiceringsår 2005
Publicerad vid Institutionen för invärtesmedicin
Sidor 3897-903
Språk en
Länkar dx.doi.org/10.1210/jc.2005-0173
Ämnesord Adolescent, Adult, Cross-Over Studies, Energy Metabolism, drug effects, Estradiol, pharmacology, Female, Human Growth Hormone, blood, deficiency, Humans, Insulin-Like Growth Factor Binding Protein 3, blood, Insulin-Like Growth Factor I, analysis, Lipid Metabolism, Middle Aged, Oxidation-Reduction, Postmenopause, metabolism, Raloxifene, pharmacology, Sex Hormone-Binding Globulin, analysis
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

CONTEXT: The endocrine and metabolic functions of the liver are affected by estrogen. Oral estrogen reduces IGF-I and suppresses fat oxidation despite augmenting GH secretion. The aim of this study was to determine whether selective estrogen receptor modulators display similar effects and whether these effects are magnified in GH-deficient (GHD) women because of the loss of GH feedback. DESIGN: This was an open-label, randomized, two-period, crossover study comparing treatment (raloxifene vs. estradiol) and group (normal vs. GHD). SETTING: The setting of this study was a clinical research unit. PARTICIPANTS: Twelve postmenopausal women and 12 women with hypopituitarism participated in this study. INTERVENTION: Two 4-wk treatments with 17beta-estradiol (E2; 2 mg, followed by 4 mg) or raloxifene (60 mg, followed by 120 mg) were given, crossing over to the alternate treatment after a 4-wk washout period. OUTCOME MEASURES: Endocrine [GH, IGF-I, IGF-binding protein-3 (IGFBP-3), GH-binding protein, and SHBG] and metabolic (fat oxidation) end points were used as outcome measures. RESULTS: E2 reduced serum IGF-I levels in a dose-dependent manner in both groups, with effects greater (P < 0.05) than raloxifene. Raloxifene reduced IGF-I levels in the GHD group (P < 0.001), but not in the postmenopausal group. E2 reduced (P < 0.05), and raloxifene increased (P < 0.05), IGFBP-3 levels in both groups. E2, but not raloxifene, increased GH (P < 0.05) in postmenopausal women. The effects of E2 and raloxifene on IGF-I, IGFBP-3, IGF-I/IGFBP-3 molar ratio, GH-binding protein, and SHBG were significantly different (P < 0.05). E2 and raloxifene reduced (P < 0.05) fat oxidation equally in GHD, whereas the decrease in postmenopausal women was not significant. CONCLUSION: E2 and raloxifene exert different hepatic endocrine, but not lipid oxidative, effects. The greater effects seen in GHD women may be explained by the loss of endogenous GH feedback.

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