Bone marrow adipose tissue (BMAT), also referred to as marrow adipose tissue (MAT), is a type of adipose tissue (fat deposit) found within the bone marrow. BMAT increases in conditions associated with low bone density, such as osteoporosis, anorexia nervosa and caloric restriction, and skeletal weightlessness such as that occurring during spaceflight. It has also been linked to certain anti-diabetic therapies.

Conversely, BMAT decreases in conditions such as anaemia, leukaemia, and hypertensive heart failure; in response to hormones including oestrogen, leptin, and growth hormone; with exercise-induced weight loss or bariatric surgery; following chronic cold exposure; and after treatment with 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. Another exception occurs in lipodystrophy, a condition with reduced overall adipose stores: exercise- induced anabolism is possible, even with minimal BMAT stores.

BMAT has been reported to have qualities of both white and brown fat. However, more-recent functional and -omics studies have shown that BMAT is a unique adipose depot that is molecularly and functionally distinct to WAT or BAT. Subcutaneous white fat contain excess energy, indicating a clear evolutionary advantage during times of scarcity. WAT is also the source of adipokines and inflammatory markers which have both positive (e.g., adiponectin) and negative effects on metabolic and cardiovascular endpoints. Visceral abdominal fat (VAT) is a distinct type of WAT that is "proportionally associated with negative metabolic and cardiovascular morbidity", regenerates cortisol, and recently has been tied to decreased bone formation Both types of WAT substantially differ from brown adipose tissue (BAT) as by a group of proteins that help BAT's thermogenic role. BMAT, by its "specific marrow location, and its adipocyte origin from at least LepR+ marrow MSC is separated from non-bone fat storage by larger expression of bone transcription factors", and likely indicates a different fat phenotype. Recently, BMAT was noted to "produce a greater proportion of adiponectin – an adipokine associated with improved metabolism – than WAT", suggesting an endocrine function for this depot, akin, but different, from that of WAT.

BMAT increases in states of bone fragility. BMAT is thought to result from preferential MSC differentiation into an adipocyte, rather than osteoblast lineage in osteoporosis based on the inverse relationship between bone and BMAT in bone-fragile osteoporotic states. An increase in BMAT is noted in osteoporosis clinical studies measured by MR spectroscopy. Estrogen therapy in postmenopausal osteoporosis reduces BMAT. Antiresorptive therapies like risedronate or zoledronate also decrease BMAT while increasing bone density, supporting an inverse relationship between bone quantity and BMAT. During aging, bone quantity declines and fat redistributes from subcutaneous to ectopic sites such as bone marrow, muscle, and liver. Aging is associated with lower osteogenic and greater adipogenic biasing of MSC. This aging-related biasing of MSC away from osteoblast lineage may represent higher basal PPARγ expression or decreased Wnt10b. Thus, bone fragility, osteoporosis, and osteoporotic fractures are thought to be linked to mechanisms which promote BMAT accumulation.^{[citation needed]}

BMAds secrete factors that promote HSC renewal in most bones.

Hematopoietic cells (also known as blood cells) reside in the bone marrow along with BMAds. These hematopoietic cells are derived from hematopoietic stem cells (HSC) which give rise to diverse cells: cells of the blood, immune system, as well as cells that break down bone (osteoclasts). HSC renewal occurs in the marrow stem cell niche, a microenvironment that contains cells and secreted factors that promote appropriate renewal and differentiation of HSC. The study of the stem cell niche is relevant to the field of oncology in order to improve therapy for multiple hematologic cancers. As such cancers are often treated with bone marrow transplantation, there is interest in improving the renewal of HSC.^{[citation needed]}