New Study Links Metabolic Genes to Bone-To-Fat Ratio in Bone Marrow

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Researchers from University of California – Los Angeles (UCLA) found that auxiliary metabolic genes (AMG) control the equilibrium of bone and fat in bone marrow.

Peroxisome proliferator-activated receptor-γ coactivator (PGC-1α) was primarily known to regulate reactions that convert and sustain energy for human cells. The study led by Dr. Cun-Yu Wang, professor of oral biology and medicine, and Dr. Bo Yu, assistant professor of restorative dentistry, at UCLA School of Dentistry suggest that PGC-1α may actually impact cellular reprograming by  converting stem cells into fat cells or bone marrow cells. The process reveals that PGC-1α controls the bone-to-fat balance in bone marrow. The research published online in the journal Cell Stem Cell on July 12, 2018, could lead to promising therapeutic targets in the treatment of osteoporosis and skeletal aging.

Bone marrow is a semi-solid tissue composed of blood cells, marrow adipose tissue and supportive stromal cells. It is found within the spongy or cancellous portions of bones. The inverse relationship between bone mass and fat cells in bone marrow is observed in many clinical trials. It depicts that an increase in marrow fat often decreases bone mass in aging as well as osteoporosis and other metabolic disorders. Osteoblasts that are bone-forming cells and adipocytes that are fat-forming cells are derived from a common pool of mesenchymal stem cells. These mesenchymal stem cells are stromal cells that can transform into several different types of cells. The composition of osteoblasts and adipocytes suggests a tradeoff between the two cell types. Furthermore, it reveals the abnormality of a cell to express its final type of mesenchymal stem cell in skeletal aging and osteoporosis. However, the molecular mechanism of the phenomenon is poorly understood. Human and mouse bone marrows showed that the expression of the PGC-1α gene drastically decreased as both the subjects aged. Furthermore, PGC-1α directly activated the expression of tafazzin (TAZ), which is involved in the metabolism of cardiolipin and promotes bone formation while inhibiting fat cell differentiation of mesenchymal stem cells. The researchers stated that further study of inverse relationship of bone loss to fat formation may lead to new treatments for these conditions.

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