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ARS Home Plains Area Grand Forks, North Dakota Grand Forks Human Nutrition Research Center Dietary Prevention of Obesity-related Disease Research Research Publications at this Location





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Title:   Author  item
                                            COLAIANNI, GRAZIANA - Mount Sinai School Of Medicineitem
                                            SUN, LI - Mount Sinai School Of Medicineitem
                                            DI BENEDETTO, ANDRIANA - Mount Sinai School Of Medicineitem
                                            TAMMA, ROBERTO - University Of Bariitem
                                            ZHU, LING-LING - University Of Bariitem
                                            Cao, Jayitem
                                            GRANO, MARIA - University Of Bariitem
                                            YUAN, TONY - Mount Sinai School Of Medicineitem
                                            COLUCCI, SYLVA - University Of Bariitem
                                            CUSCITO, CONCETTA - Mount Sinai School Of Medicineitem
                                            MANCINI, LUCIA - University Of Bariitem
                                            LI, JINHUA - Mount Sinai School Of Medicineitem
                                            NISHIMORI, KATSUHIKO - Tokyo University Of Agriculture & Technologyitem
                                            BAB, ITAI - University Of Jerusalemitem
                                            LEE, HEON-JIN - Kyungpook National Universityitem
                                            IQBAL, JAMEEL - Mount Sinai School Of Medicineitem
                                            YOUNG, W. SCOTT - University Of Bariitem
                                            ROSEN, CLIFFORD - Maine Medical Center Research Institute (MMCRI)item
                                            ZALLONE, ALBERTA - University Of Bariitem
                                            ZAIDI, MONE - Mount Sinai School Of Medicine
  Submitted to: Proceedings of the National Academy of Sciences (PNAS)
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 5/18/2012
                                    Publication  Date: 8/17/2012
                                    Citation: Colaianni, G., Sun, L., Di Benedetto, A., Tamma, R., Zhu, L., Cao, J.J., Grano, M., Yuan, T., Colucci, S., Cuscito, C., Mancini, L., Li, J., Nishimori, K., Bab, I., Lee, H., Iqbal, J., Young, W., Rosen, C., Zallone, A., Zaidi, M. 2012. Bone marrow oxytocin mediates the anabolic action of estrogen on the skeleton. Proceedings of the National Academy of Sciences. 287(34):29159-29167.Interpretive Summary: Oxytocin (OT) is a nanopeptide synthesized in the hypothalamus and released into circulation by the posterior pituitary. Its primary function is to mediate the milk ejection reflex in nursing mammals1. It also augments uterine contraction during parturition2. Serum OT levels peak during late pregnancy and lactation. These periods correspond, respectively, to maximal fetal and post-natal bone growth, because of which, the mother must loose ~120g of calcium from her skeleton3,4. Hormonal adaptations, including low estrogen and elevated PTHrP levels,
permit this maternal hyper-resorption and intergenerational calcium transfer5. However, it is surprising that shortly after these periods of profound bone loss, the mother’s skeleton is rapidly repleted; if not, pregnancy- and lactation-associated osteoporosis ensues. The mechanisms for this dramatic skeletal recovery remain poorly understood.
                                Technical Abstract: Estrogen withdrawal in women due to natural or artificial menopause is followed by rapid bone
loss, osteoporosis, and a high fracture risk. Replacement with estrogen prevents this bone loss
and reduces the risk of fracture. Estrogen uses two mechanisms to exert this effect: it inhibits
bone resorption by osteoclasts and stimulates bone formation by osteoblasts. While the antiresorptive
actions of estrogen arise from the inhibition of the MAP kinase JNK, the mechanism
of its effect on the osteoblast remains unclear. Here we show that the osteoblast-directed
anabolic action of estrogen occurs, at least in part, through an intermediary, oxytocin (OT),
produced by bone marrow osteoblasts in response to estrogen.


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