TY - JOUR
T1 - Rat strain specific attenuation of estrogen action in the anterior pituitary gland by dietary energy restriction
AU - Harvell, Djuana M.E.
AU - Buckles, Linda K.
AU - Gould, Karen A.
AU - Pennington, Karen L.
AU - McComb, Rodney D.
AU - Shull, James D.
N1 - Funding Information:
This research was supported by grants R01-CA68529, R01-CA77876, T32-CA09476 and P30-CA36727 from the National Institutes of Health; grant 97A146 from the American Institutes for Cancer Research; and grant DAMD 17-00-1-0361 from the U.S. Army Breast Cancer Research Program.
PY - 2003/7
Y1 - 2003/7
N2 - The purpose of this study was to compare the effects of a 40% restriction of dietary energy consumption, relative to that consumed by rats allowed to feed ad libitum, on the ability of 17β-estradiol (E2) to induce pituitary tumorigenesis in two inbred rat strains, ACI and Copenhagen (COP), which are very closely related genetically. Ovary-intact ACI and COP rats were fed either a control or an energy-restricted diet beginning at 8 wk of age. Continuous treatment with E2, released from subcutaneous Silastic tubing implants, was initiated at 9 wk of age and the animals were killed 12 wk later. Estrogen-induced pituitary tumorigenesis is associated with rapid induction of lactotroph hyperplasia, increased pituitary mass, and hyperprolactinemia. E2 significantly increased pituitary mass and circulating prolactin (PRL) in both ACI and COP rats, and this response was significantly greater in ACI rats relative to COP. Dietary energy restriction did not inhibit E2-induced pituitary growth in the ACI rat. By contrast, E2-induced pituitary growth in COP rats was attenuated by dietary energy restriction, as evidenced by quantification of pituitary mass, pituitary weight to body weight ratio, circulating PRL, and pituitary cell proliferation. This study indicates that sensitivity to the inhibitory actions of dietary energy restriction on E2-induced pituitary tumorigenesis is genetically determined.
AB - The purpose of this study was to compare the effects of a 40% restriction of dietary energy consumption, relative to that consumed by rats allowed to feed ad libitum, on the ability of 17β-estradiol (E2) to induce pituitary tumorigenesis in two inbred rat strains, ACI and Copenhagen (COP), which are very closely related genetically. Ovary-intact ACI and COP rats were fed either a control or an energy-restricted diet beginning at 8 wk of age. Continuous treatment with E2, released from subcutaneous Silastic tubing implants, was initiated at 9 wk of age and the animals were killed 12 wk later. Estrogen-induced pituitary tumorigenesis is associated with rapid induction of lactotroph hyperplasia, increased pituitary mass, and hyperprolactinemia. E2 significantly increased pituitary mass and circulating prolactin (PRL) in both ACI and COP rats, and this response was significantly greater in ACI rats relative to COP. Dietary energy restriction did not inhibit E2-induced pituitary growth in the ACI rat. By contrast, E2-induced pituitary growth in COP rats was attenuated by dietary energy restriction, as evidenced by quantification of pituitary mass, pituitary weight to body weight ratio, circulating PRL, and pituitary cell proliferation. This study indicates that sensitivity to the inhibitory actions of dietary energy restriction on E2-induced pituitary tumorigenesis is genetically determined.
KW - ACI rat
KW - COP rat
KW - Estrogen
KW - Lactotroph
KW - Prolactin
KW - Tumorigenesis
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U2 - 10.1385/ENDO:21:2:175
DO - 10.1385/ENDO:21:2:175
M3 - Article
C2 - 12897383
AN - SCOPUS:0043207542
SN - 1355-008X
VL - 21
SP - 175
EP - 183
JO - Endocrine
JF - Endocrine
IS - 2
ER -