IGF-1 from bone marrow Adipoq-lineage cells stimulates endocortical bone formation in mature female mice.
Bertels. Joshua C JC; Sawall. Jasmin Koehnken JK; Dulmovits. Brian B; Liu. Xiaobin X; Phan. Ashley A; Ji. Xing X; Song. Fangfang F; Thom. Christopher C; Long. Fanxin F
Key Findings
- Adipoq+ stromal cells in bone marrow are a major source of IGF‑1 in post‑natal mice
- Deleting IGF‑1 in these cells lowers endocortical bone formation and cortical bone mass in mature female mice
- Trabecular bone and hematopoietic function were unchanged, and male mice were not affected
Practical Outcomes
- For biohackers, the work suggests that simply boosting systemic IGF‑1 may not target cortical bone health as effectively as influencing local IGF‑1 pathways. At present there’s no direct human protocol, but maintaining overall IGF‑1 through diet, sleep, and resistance training remains the most practical approach for bone strength.
Summary
The study shows that a specific type of bone‑marrow cell makes IGF‑1, which helps build the outer part of bone in adult female mice. When IGF‑1 was removed from those cells, the mice had weaker cortical bone, but their inner spongy bone and blood‑cell production stayed the same. This points to a local, bone‑specific role for IGF‑1 rather than a whole‑body effect.
Abstract
Insulin-like growth factor 1 (IGF-1) is an anabolic signal promoting growth, differentiation and function of both embryonic and postnatal tissues. Both endocrine and paracrine functions of IGF-1 have been documented to regulate bone growth and bone marrow hematopoiesis. Local production of IGF-1 from various cell types may contribute differently to the overall bioactivity of IGF-1 in bone, but relevant sources and mechanisms are yet to be fully elucidated. Here we report that the Adipoq<sup>+</sup> stromal cells are a notable source of IGF-1 in the bone marrow of postnatal mice. Deletion of IGF-1 with Adipoq-Cre diminished endocortical bone formation and cortical bone mass in mature female mice. On the other hand, the trabecular bone parameters or hematopoietic properties were not affected in mutant mice of either sex. The study uncovers a local source of IGF-1 in the bone marrow microenvironment that contributes to bone anabolic regulation in a site-specific manner.
Study Information
pubmed
2025
2025-11-06T00:00:00.000Z
10.1101/2025.11.05.686616
38