J Clin Invest. 2022 Feb 15;132(4). doi: 10.1172/JCI157200.
Osteocalcin is a hormone produced in bones by osteoblasts during bone formation. Numerous studies have demonstrated that adrenal gland-derived glucocorticoids inhibit osteocalcin production, which can ultimately cause deleterious bones loss. This loss establishes a unidirectional endocrine relationship between the adrenal glands and bone, however, whether osteocalcin reciprocally regulates glucocorticoid secretion remains unclear. In this issue of the JCI, Yadav and colleagues address how bone-derived osteocalcin influences adrenal organogenesis and function. Using a large variety of animal models, the authors established that embryonic osteocalcin signaling, specifically through the GPR158 receptor, regulates postnatal adrenal steroid concentrations throughout life. This work has translational potential, and we await future investigations that determine whether modulating osteocalcin levels could promote endogenous adrenocortical function in adrenocortical hypoplasia and glucocorticoid deficiency.
骨钙素是成骨细胞在骨形成过程中产生的一种激素。许多研究表明,肾上腺源性糖皮质激素抑制骨钙素的产生,这最终可能导致有害的骨质流失。这种流失在肾上腺和骨骼之间建立了一种单向的内分泌关系,然而,骨钙素是否反过来调节糖皮质激素的分泌尚不清楚。在本期 JCI 中,Yadav 及其同事探讨了骨钙素如何影响肾上腺的发生和功能。作者使用了多种动物模型,证实了胚胎骨钙素信号,特别是通过 GPR158 受体,调节了整个生命过程中出生后的肾上腺类固醇浓度。这项工作具有转化潜力,我们期待未来的研究能够确定调节骨钙素水平是否可以促进肾上腺皮质发育不全和糖皮质激素缺乏症中的内源性肾上腺皮质功能。