ESPE Abstracts

Marrow fat (BMAT) is an essential component of the bone marrow niche and plays a critical role during adaptive metabolism and stress responses. BMAT increases from birth and reaches a peak during adolescence and then is maintained until late in life when it increases again. Previous studies demonstrated a negative relationship between bone mineral density and BMAT; however those were predominantly cross sectional studies. New mouse models and inbred strains have provided novel insights into the function of BMAT. In particular, peak acquisition of bone mass is a time of maximal energy demands in the bone marrow, and also a time of marked adipogenesis in the appendicular marrow. Similarly during calorie restriction there is florid marrow adipogenesis which may be associated with a compensatory response to maintain some bone formation by stressed osteoblasts. We have previously shown that marrow adipocytes are a source of fatty acids in the niche during treatment with parathyroid hormone, a time of maximal bone formation. Similarly, peripheral fat cells can generate through lipolysis, energy for osteoblasts during growth and with PTH. We propose that bone marrow adipocytes may provide an important compensatory response to help osteoblasts when there are environmental and nutritional stresses and possibly with peak growth in the appendicular skeleton. Evidence to support this tenet will be demonstrated in both mouse models and human studies of fasting using -omics and genetic strategies.