Discussion and Conclusions
These two randomized, crossover studies show that oral estrogen replacement therapy suppresses the biological actions of growth hormones in GH-deficient women:
- In the first study, mean IGF-I across all three GH doses was significantly lower, and the rise in IGF-I during oral estrogen was significantly less than that observed during transdermal therapy.
- In the metabolic study, postprandial lipid oxidation and leucine incorporation into protein were stimulated by GH treatment but remained significantly lower during the oral estrogen phase.
Moreover, the route-dependent effects of estrogen on IGF-I, fat oxidation, and protein metabolism were evident even before GH administration. Thus, in GH-deficient, hypogonadal women, oral estrogen exhibits intrinsic metabolic actions that are opposite those of GH and are not overcome by replacement doses of GH currently used in clinical practice, indicating the physiological importance of these observations.
The findings demonstrate for the first time that the impact of oral estrogen extends beyond effects on circulating IGF-I levels in that GH-induced stimulation of fat oxidation and protein metabolism are also affected. Although fat oxidation was stimulated by GH, it remained suppressed to a greater degree postprandially during the oral estrogen treatment. Similarly, although GH stimulated protein metabolism, leucine incorporation into protein was significantly lower during oral estrogen therapy. These observations in postmenopausal women strongly suggest that similar detrimental chan
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Contact: Donna Krupa
djkrupa1@aol.com
703-527-7357
American Physiological Society
30-Nov-2001