Adipoq, encoding adiponectin, is a gene with a preponderant role in the homeostasis of glucose and fatty acids. Adiponectin is a fat-derived protein hormone, and its associated pathways likely involve energy metabolism, glucose and lipid regulation, which are crucial for overall metabolic health [2]. Genetic models, such as gene knockout (KO) or conditional knockout (CKO) mouse models, can be valuable for studying Adipoq's function.

In bone marrow, Adipoq-lineage progenitors (cells expressing Adipoq) are a major cellular source of M-CSF. Deficiency of M-CSF in bone marrow Adipoq-lineage progenitors in mice drastically reduces the generation of bone marrow macrophages and osteoclasts, leading to severe osteopetrosis. Also, osteoporosis in ovariectomized mice can be significantly alleviated by the absence of M-CSF in these progenitors, revealing their crucial contribution to bone homeostasis and pathological bone loss [1]. Depletion of Shn3 in Adipoq-lineage progenitors in mice results in a significant increase in trabecular bone mass and bone formation in vivo, and enhances bone fracture healing under pathological conditions, suggesting a role of Adipoq-lineage progenitors in osteogenesis [3].

In conclusion, Adipoq is essential for metabolic homeostasis, especially in glucose and fatty acid regulation. Mouse models with genetic manipulation of Adipoq-lineage progenitors have revealed its significance in bone-related biological processes, such as bone marrow macrophage development, osteoclastogenesis, and bone mass regulation, providing insights into potential treatments for bone-loss related disorders [1,3].