Exercise and Diet: Uncovering Prospective Mediators of Skeletal Fragility in Bone and Marrow Adipose Tissue.

Marrow adipocytes accumulate in the bone in the setting of not only hypercaloric intake (calorie excess; e.g., diet-induced obesity) but also with hypocaloric intake (calorie restriction; e.g., anorexia), despite the fact that these states affect bone differently. With hypercaloric intake, bone quantity is largely unaffected, whereas with hypocaloric intake, bone quantity and quality are greatly diminished. Voluntary running exercise in rodents was found to lower MAT and promote bone in eucaloric and hypercaloric states, while degrading bone in hypocaloric states, suggesting differential modulation of MAT and bone, dependent upon whole-body energy status. Energy status alters bone metabolism and bioenergetics via substrate availability or excess, which plays a key role in the response of bone and MAT to mechanical stimuli. Marrow adipose tissue (MAT) is a fat depot with a potential role in-as well as responsivity to-whole-body energy metabolism. Understanding the localized function of this depot in bone cell bioenergetics and substrate storage, principally in the exercised state, will aid to uncover putative therapeutic targets for skeletal fragility.