Bone marrow adipose tissue

Bone marrow adipose tissue (BMAT), sometimes referred to as marrow adipose tissue (MAT), is a type of fat deposit in bone marrow. It increases in states of low bone density -osteoporosis, anorexia nervosa/ caloric restriction, skeletal unweighting such as that which occurs in space travel, and anti-diabetes therapies. BMAT decreases in anaemia, leukaemia, and hypertensive heart failure; in response to hormones such as oestrogen, leptin, and growth hormone; with exercise-induced weight loss or bariatric surgery; in response to chronic cold exposure; and in response to pharmacological agents such as bisphosphonates, teriparatide, and metformin. Bone marrow adipocytes (BMAds) originate from mesenchymal stem cell (MSC) progenitors that also give rise to osteoblasts, among other cell types. Thus, it is thought that BMAT results from preferential MSC differentiation into the adipocyte, rather than osteoblast, lineage in the setting of osteoporosis. Since BMAT is increased in the setting of obesity and is suppressed by endurance exercise, or vibration, it is likely that BMAT physiology, in the setting of mechanical input/exercise, approximates that of white adipose tissue (WAT). The first study to demonstrate exercise regulation of BMAT in rodents was published in 2014; Now, exercise regulation of BMAT has been confirmed in a human, adding clinical importance. Several studies demonstrated exercise reduction of BMAT which occurs along with an increase in bone quantity. Since exercise increases bone quantity, reduces BMAT and increases expression of markers of fatty acid oxidation in bone, BMAT is thought to be providing needed fuel for exercise-induced bone formation or anabolism. A notable exception occurs in the setting of caloric restriction: exercise suppression of BMAT does not yield an increase in bone formation and even appears to cause bone loss. Indeed, energy availability appears to be a factor in the ability of exercise to regulate BMAT.