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Estrogen signaling in arcuate Kiss1 neurons suppresses a sex-dependent female
circuit promoting dense strong bones.
Authors Herber CB, Krause WC, Wang L, Bayrer JR, Li A, Schmitz M, Fields A, Ford B,
Zhang Z, Reid MS, Nomura DK, Nissenson RA, Correa SM, Ingraham HA
Submitted By Submitted Externally on 1/25/2019
Status Published
Journal Nature communications
Year 2019
Date Published 1/1/2019
Volume : Pages 10 : 163
PubMed Reference 30635563
Abstract Central estrogen signaling coordinates energy expenditure, reproduction, and in
concert with peripheral estrogen impacts skeletal homeostasis in females. Here,
we ablate estrogen receptor alpha (ERa) in the medial basal hypothalamus and
find a robust bone phenotype only in female mice that results in exceptionally
strong trabecular and cortical bones, whose density surpasses other reported
mouse models. Stereotaxic guided deletion of ERa in the arcuate nucleus
increases bone mass in intact and ovariectomized females, confirming the central
role of estrogen signaling in this sex-dependent bone phenotype. Loss of ERa in
kisspeptin (Kiss1)-expressing cells is sufficient to recapitulate the bone
phenotype, identifying Kiss1 neurons as a critical node in this powerful
neuroskeletal circuit. We propose that this newly-identified female
brain-to-bone pathway exists as a homeostatic regulator diverting calcium and
energy stores from bone building when energetic demands are high. Our work
reveals a previously unknown target for treatment of age-related bone disease.


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