Mediation of the Acute Stress Response by the Skeleton

Julian Meyer Berger, Parminder Singh, Lori Khrimian, Donald A. Morgan, Subrata Chowdhury, Emilio Arteaga-Solis, Tamas L. Horvath, Ana I. Domingos, Anna L. Marsland, Vijay Kumar Yadav,Kamal Rahmouni, Xiao-Bing Gao, and Gerard Karsenty

Cell Metabolism (2019) 30: 1 – 13

We hypothesized that bone evolved, in part, to enhance the ability of bony vertebrates to escape danger in the wild. In support of this notion, we show here that a bone-derived signal is necessary to develop an acute stress response (ASR). Indeed, exposure to various types of stressors in mice, rats (rodents), and humans leads to a rapid and selective surge of circulating bioactive osteocalcin because stressors favor the uptake by osteoblasts of gluta- mate, which prevents inactivation of osteocalcin prior to its secretion. Osteocalcin permits manifesta- tions of the ASR to unfold by signaling in post-synap- tic parasympathetic neurons to inhibit their activity, thereby leaving the sympathetic tone unopposed. Like wild-type animals, adrenalectomized rodents and adrenal-insufficient patients can develop an ASR, and genetic studies suggest that this is due to their high circulating osteocalcin levels. We propose that osteocalcin defines a bony-vertebrate-specific endocrine mediation of the ASR. 

Full text of Dr Julian Berger’s  article is available from HERE

Julian Berger
First Author

Columbia University, USA

Jonathan Gustafson

Rush University, USA.