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This Article Full Text Full Text (PDF) All Versions of this Article: 295/5/E1172    most recent 90507.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Govoni, K. E. Articles by Mohan, S. Search for Related Content PubMed PubMed Citation Articles by Govoni, K. E. Articles by Mohan, S.

Prepubertal OVX increases IGF-I expression and bone accretion in C57BL/6J mice

¹Jerry L. Pettis Veterans Affairs Medical Center, Loma Linda; and ²Loma Linda University, Loma Linda, California

Submitted 13 June 2008 ; accepted in final form 21 September 2008

It is generally well accepted that the pubertal surge in estrogen is responsible for the rapid bone accretion that occurs during puberty and that this effect is mediated by an estrogen-induced increase in growth hormone (GH)/insulin-like growth factor (IGF) action. To test the cause and effect relationship between estrogen and GH/IGF, we evaluated the consequence of ovariectomy (OVX) in prepubertal mice (C57BL/6J mice at 3 wk of age) on skeletal changes and the GH/IGF axis during puberty. Contrary to our expectations, OVX increased body weight (12–18%), bone mineral content (11%), bone length (4%), bone size (3%), and serum, liver, and bone IGF-I (30–50%) and decreased total body fat (18%) at 3 wk postsurgery. To determine whether estrogen is the key ovarian factor responsible for these changes, we performed a second experiment in which OVX mice were treated with placebo or estrogen implants. In addition to observing similar results compared with our first experiment, estrogen treatment partially rescued the increased body weight and bone size and completely rescued body fat and IGF-I levels. The increased bone accretion in OVX mice was due to increased bone formation rate (as determined by bone histomorphometry) and increased serum procollagen peptide. In conclusion, contrary to the known estrogen effect as an initiator of GH/IGF surge and thereby pubertal growth spurt, our findings demonstrate that loss of estrogen and/or other hormones during the prepubertal growth period effect leads to an increase in IGF-I production and bone accretion in mice.

osteoporosis; estrogen; puberty; bone size; bone mineral density