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Endocrine Abstracts (2016) 41 S9.1 | DOI: 10.1530/endoabs.41.S9.1

France.


Bone Marrow Adipose Tissue (BMAT) has only recently become an emerging topic in both medical and basic research. As secretory cells found either packed or scattered within the BM, these adipocytes are likely contributors to haematopoiesis- or bone- related diseases. Indeed, clinical studies have consistently reported that BMAT amount is associated with bone loss in diverse types of osteoporosis such as that of ageing, post-menopause and anorexia nervosa. Since BM adipocytes and osteoblasts (the bone forming cells) arise from the resident Mesenchymal Stem Cells (MSC), the process of adipogenesis per se is often viewed as a competitive process for osteoblastogenesis. Indeed, various endocrine and local factors that usually alter osteoblastogenesis promote adipogenesis. However, studies from other groups and ours qualify this view. Moreover, the functional phenotype of BM adipocytes is also suggested to be a key determinant in bone fragility. As shown by us and others, coculture of osteoblasts with adipocytes compromises the phenotype, function or survival of osteoblasts. Owing to the impact of the adipokines adiponectin and leptin on bone formation, a few groups like ours have started to explore the capacity of BM adipocytes to release factors involved in bone remodeling. Indeed, compared to classical extramedullary adipocytes; primary mature BM adipocytes exhibit low expression levels of typical adipokines with high expression levels of anti-osteoblastogenic factors (such as Wnt signaling inhibitors) and pro-osteoclastogenic factors (such as RANKL). These first findings obtained both in human samplings and mouse models strengthen the detrimental involvement of BMAT in bone remodeling.

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