What is it about?

This review is focused on understanding how exercise -mediated signals can be leveraged to improve bone quality while decreasing fat mass and metabolic dysfunction and promoting new strategies to treat chronic diseases such as osteoporosis and obesity.

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Why is it important?

1. Aging and inactivity each contribute towards a local and systemic environment conducive to poor bone quality, increased systemic adiposity, marrow adipogenesis and inflammation. 2. Mesenchymal stem cells and their lineage-differentiated progeny (for example, osteoblasts) are mechanosensitive, such that increased mechanical signals (such as exercise) stimulate muscle and bone anabolism. 3. Mechanical signals suppress obesity end points, including fat gain, adipocyte lipid acquisition, chronic inflammation and indices associated with type 2 diabetes mellitus. 4. Transduction of mechanical signals across the plasma membrane of stem cells into the nucleus activates signalling cascades and cytoskeletal adaptations to initiate osteogenic, chondrogenic and myogenic differentiation and inhibit adipocyte differentiation. 5. Mechanical signals, such as those induced through low-intensity vibration, need not be large in magnitude, or long in duration, to influence bone or fat phenotypes.


This is a review of the effect of excercise/ mechanical strain on bone and fat in-vitro as well as in-vivo.

Dr Maya Styner
University of North Carolina at Chapel Hill, Department of Medicine, Division of Endocrinology

Read the Original

This page is a summary of: Combating osteoporosis and obesity with exercise: leveraging cell mechanosensitivity, Nature Reviews Endocrinology, February 2019, Springer Science + Business Media,
DOI: 10.1038/s41574-019-0170-1.
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