TY - JOUR
T1 - Influence of estrogen administration on the growth response to growth hormone (GH) in GH-deficient mice
AU - Fintini, Danilo
AU - Alba, Maria
AU - Salvatori, Roberto
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2005/11
Y1 - 2005/11
N2 - In women who are growth hormone (GH) deficient, exogenous estrogens increase the dosage of GH that is needed to normalize circulating levels of insulin-like growth factor (IGF-1). Serum IGF-1 derives mostly from the liver, and it is unknown whether the peripheral effects of GH are also impaired by estrogens. Because the ultimate effect of GH is longitudinal growth, we have investigated the influence of estrogen administration on the growth response to recombinant mouse GH therapy in prepubertal GH-deficient (GHD) GHRH knockout (GHRHKO) female mice. Twenty-four GHRHKO female mice (4 animals/group) were treated for 4 weeks (from the second to sixth week of age) with the following schedules: Group I, GH only (25 μg/day); Group II, subcutaneous (sc) ethynil estradiol (EE) (0.035 μg/day); Group III, GH + scEE; Group IV, oral (po) EE (0.035 μg/day); Group V, GH + poEE; Group VI, placebo. At the end of the treatment period, we measured uterine weight, total body weight (TBW), body length (nose-anus, N-A), and femur length. In addition, serum IGF-1 levels were measured. Uteri of mice treated with oral or scEE showed similar increases in weight. There was no difference in the increase in longitudinal growth parameters between mice treated with GH alone or with GH in association with oral or scEE. Serum IGF-1 decreased in animals treated with GH + scEE, compared with GH group, but no group was significantly different from placebo. These results show that subcutaneous or oral EE does not reduce the growth response to GH in female GHD mice.
AB - In women who are growth hormone (GH) deficient, exogenous estrogens increase the dosage of GH that is needed to normalize circulating levels of insulin-like growth factor (IGF-1). Serum IGF-1 derives mostly from the liver, and it is unknown whether the peripheral effects of GH are also impaired by estrogens. Because the ultimate effect of GH is longitudinal growth, we have investigated the influence of estrogen administration on the growth response to recombinant mouse GH therapy in prepubertal GH-deficient (GHD) GHRH knockout (GHRHKO) female mice. Twenty-four GHRHKO female mice (4 animals/group) were treated for 4 weeks (from the second to sixth week of age) with the following schedules: Group I, GH only (25 μg/day); Group II, subcutaneous (sc) ethynil estradiol (EE) (0.035 μg/day); Group III, GH + scEE; Group IV, oral (po) EE (0.035 μg/day); Group V, GH + poEE; Group VI, placebo. At the end of the treatment period, we measured uterine weight, total body weight (TBW), body length (nose-anus, N-A), and femur length. In addition, serum IGF-1 levels were measured. Uteri of mice treated with oral or scEE showed similar increases in weight. There was no difference in the increase in longitudinal growth parameters between mice treated with GH alone or with GH in association with oral or scEE. Serum IGF-1 decreased in animals treated with GH + scEE, compared with GH group, but no group was significantly different from placebo. These results show that subcutaneous or oral EE does not reduce the growth response to GH in female GHD mice.
KW - Ethynil estradiol
KW - GHRH gene ablation
KW - Growth
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U2 - 10.1177/153537020523001004
DO - 10.1177/153537020523001004
M3 - Article
C2 - 16246898
AN - SCOPUS:27644584615
SN - 1535-3702
VL - 230
SP - 715
EP - 720
JO - Experimental Biology and Medicine
JF - Experimental Biology and Medicine
IS - 10
ER -