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Erratum Free access | 10.1172/JCI81812

Osteocalcin regulates murine and human fertility through a pancreas-bone-testis axis

Franck Oury, Mathieu Ferron, Wang Huizhen, Cyrille Confavreux, Lin Xu, Julie Lacombe, Prashanth Srinivas, Alexandre Chamouni, Francesca Lugani, Herve Lejeune, T. Rajendra Kumar, Ingrid Plotton, and Gerard Karsenty

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Published May 1, 2015 - More info

Published in Volume 125, Issue 5 on May 1, 2015
J Clin Invest. 2015;125(5):2180–2180. https://doi.org/10.1172/JCI81812.
Copyright © 2015, American Society for Clinical Investigation
Published May 1, 2015 - Version history
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Related article:

Osteocalcin regulates murine and human fertility through a pancreas-bone-testis axis
Franck Oury, … , Ingrid Plotton, Gerard Karsenty
Franck Oury, … , Ingrid Plotton, Gerard Karsenty
Research Article

Osteocalcin regulates murine and human fertility through a pancreas-bone-testis axis

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Abstract

The osteoblast-derived hormone osteocalcin promotes testosterone biosynthesis in the mouse testis by binding to GPRC6A in Leydig cells. Interestingly, Osteocalcin-deficient mice exhibit increased levels of luteinizing hormone (LH), a pituitary hormone that regulates sex steroid synthesis in the testes. These observations raise the question of whether LH regulates osteocalcin’s reproductive effects. Additionally, there is growing evidence that osteocalcin levels are a reliable marker of insulin secretion and sensitivity and circulating levels of testosterone in humans, but the endocrine function of osteocalcin is unclear. Using mouse models, we found that osteocalcin and LH act in 2 parallel pathways and that osteocalcin-stimulated testosterone synthesis is positively regulated by bone resorption and insulin signaling in osteoblasts. To determine the importance of osteocalcin in humans, we analyzed a cohort of patients with primary testicular failure and identified 2 individuals harboring the same heterozygous missense variant in one of the transmembrane domains of GPRC6A, which prevented the receptor from localizing to the cell membrane. This study uncovers the existence of a second endocrine axis that is necessary for optimal male fertility in the mouse and suggests that osteocalcin modulates reproductive function in humans.

Authors

Franck Oury, Mathieu Ferron, Wang Huizhen, Cyrille Confavreux, Lin Xu, Julie Lacombe, Prashanth Srinivas, Alexandre Chamouni, Francesca Lugani, Herve Lejeune, T. Rajendra Kumar, Ingrid Plotton, Gerard Karsenty

×

Original citation: J Clin Invest. 2013;123(6):2421–2433. doi:10.1172/JCI65952.

Citation for this erratum: J Clin Invest. 2015;125(5):2180. doi:10.1172/JCI81812.

During the preparation of this manuscript, the genotype of the control animals was labeled incorrectly in Figure 5. The correct figure and legend are below.

Insulin signaling in osteoblasts favors testosterone production.Figure 5

Insulin signaling in osteoblasts favors testosterone production. (A) Testis size, and (B) testis, (C) epididymal, and (D) seminal vesicle weights normalized to BW (mg/g of BW); (E) sperm count; (F) circulating testosterone levels in InsRosb–/– versus InsRfl/fl (Cre–) male mice. (G) qPCR analysis of the expression of StAR, Cyp11a, Cyp17, 3β-HSD, Cyp19, and HSD-17 genes in testes of InsRosb–/– (n = 10) and InsRfl/fl (n = 12) mice. All analyses presented were performed on nonbreeder mix background (129/Sv: 87.5%; 129/Sv: 12.5%) mice. *P < 0.05; **P < 0.01.

The JCI regrets the error.

Footnotes

See the related article beginning on page 2421.

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