Determinants of bone marrow adiposity: The modulation of peroxisome proliferator-activated receptor-γ2 activity as a central mechanism

• Published in: Bone (New York, N.Y.) Vol. 56; no. 2; pp. 255 - 265
• Main Authors: Sadie-Van Gijsen, H, Hough, F.S, Ferris, W.F
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Inc 01.10.2013; Elsevier
• Subjects: Adipocytes; Adiposity - physiology; Animals; Biological and medical sciences; Bone Marrow - metabolism; Bone Marrow - physiopathology; Bone mineral density; Fundamental and applied biological sciences. Psychology; Humans; Investigative techniques, diagnostic techniques (general aspects); Marrow adiposity; Medical sciences; Orthopedics; Osteoarticular system. Muscles; Osteoblasts; PPAR gamma - metabolism; PPAR-γ2; Radiodiagnosis. Nmr imagery. Nmr spectrometry; Vertebrates: anatomy and physiology, studies on body, several organs or systems; Bone mineral density; Marrow adiposity; Adipocytes; PPAR-γ2; Osteoblasts; Adipocyte; Morphology; Bone marrow; Osteoblast; Mechanism; PPAR-γ2 receptor
• ISSN: 8756-3282; 1873-2763
• DOI: 10.1016/j.bone.2013.06.016

Abstract Although the presence of adipocytes in the bone marrow is a normal physiological phenomenon, the role of these cells in bone homeostasis and during pathological states has not yet been fully delineated. As osteoblasts and adipocytes originate from a common progenitor, with an inverse relationship existing between osteoblastogenesis and adipogenesis, bone marrow adiposity often negatively correlates with osteoblast number and bone mineral density. Bone adiposity can be affected by several physiological and pathophysiological factors, with abnormal, elevated marrow fat resulting in a pathological state. This review focuses on the regulation of bone adiposity by physiological factors, including aging, mechanical loading and growth factor expression, as well as the pathophysiological factors, including diseases such as anorexia nervosa and dyslipidemia, and pharmacological agents such as thiazolidinediones and statins. Although these factors regulate bone marrow adiposity via a plethora of different intracellular signaling pathways, these diverse pathways often converge on the modulation of the expression and/or activity of the pro-adipogenic transcription factor peroxisome proliferator-activated receptor (PPAR)-γ2, suggesting that any factor that affects PPAR-γ2 may have an impact on the fat content of bone.