Endothelium-specific depletion of LRP1 improves glucose homeostasis through inducing osteocalcin.

平衡 细胞生物学 脂质代谢 低密度脂蛋白受体
作者
Hua Mao,Luge Li,Qiying Fan,Aude Angelini,Pradip K. Saha,Cristian Coarfa,Kimal Rajapakshe,Dimuthu Perera,Jizhong Cheng,Huaizhu Wu,Christie M. Ballantyne,Zheng Sun,Liang Xie,Xinchun Pi
出处
期刊:Nature Communications [Springer Nature]
卷期号:12 (1): 5296- 被引量:2
标识
DOI:10.1038/s41467-021-25673-6
摘要

The vascular endothelium is present within metabolic organs and actively regulates energy metabolism. Here we show osteocalcin, recognized as a bone-secreted metabolic hormone, is expressed in mouse primary endothelial cells isolated from heart, lung and liver. In human osteocalcin promoter-driven green fluorescent protein transgenic mice, green fluorescent protein signals are enriched in endothelial cells lining aorta, small vessels and capillaries and abundant in aorta, skeletal muscle and eye of adult mice. The depletion of lipoprotein receptor-related protein 1 induces osteocalcin through a Forkhead box O -dependent pathway in endothelial cells. Whereas depletion of osteocalcin abolishes the glucose-lowering effect of low-density lipoprotein receptor-related protein 1 depletion, osteocalcin treatment normalizes hyperglycemia in multiple mouse models. Mechanistically, osteocalcin receptor-G protein-coupled receptor family C group 6 member A and insulin-like-growth-factor-1 receptor are in the same complex with osteocalcin and required for osteocalcin-promoted insulin signaling pathway. Therefore, our results reveal an endocrine/paracrine role of endothelial cells in regulating insulin sensitivity, which may have therapeutic implications in treating diabetes and insulin resistance through manipulating vascular endothelium. The vascular endothelium contributes to metabolic regulation, however, the underlying mechanisms are not fully understood. Here the authors show that endothelial low-density lipoprotein receptor-related protein 1 regulates glucose homeostasis via osteocalcin expression.
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