Department of Internal Medicine, Nephrology Division, Universidade de São Paulo, São Paulo, Brazil.
Inserm Unit 1018, Team 5, Centre de Recherche en Épidémiologie et Santé des Populations (CESP), Hôpital Paul Brousse, Paris-Sud University and Versailles Saint-Quentin-en-Yvelines University (Paris-Ile-de-France-Ouest University), Villejuif, France.
Kidney Int. 2016 Mar;89(3):529-31. doi: 10.1016/j.kint.2015.12.031.
Chronic metabolic acidosis stimulates bone resorption, resulting in loss of calcium and bicarbonate from bone. Both osteoblasts and osteoclasts sense extracellular H(+) by the G-protein coupled receptor, OGR1, whose activation leads to increased bone resorption as well as decreased bone formation. Krieger et al. examined the effect of OGR1 knockout in mice. They found an unexpected increase in bone resorption, but nevertheless an increase in bone volume linked to enhanced bone formation. This discovery opens a window of opportunity to explore potential new anabolic treatments for patients with low bone mass.
慢性代谢性酸中毒刺激骨吸收，导致钙和碳酸氢根从骨骼中流失。成骨细胞和破骨细胞都能通过 G 蛋白偶联受体 OGR1 感知细胞外 H(+)，其激活可导致骨吸收增加和骨形成减少。Krieger 等人研究了 OGR1 基因敲除对小鼠的影响。他们发现骨吸收意外增加，但骨量增加与骨形成增强有关。这一发现为探索治疗低骨量患者的潜在新型合成代谢治疗方法提供了机会。
