Combating osteoporosis and obesity with exercise: leveraging cell mechanosensitivity.


Journal

Nature reviews. Endocrinology
ISSN: 1759-5037
Titre abrégé: Nat Rev Endocrinol
Pays: England
ID NLM: 101500078

Informations de publication

Date de publication:
06 2019
Historique:
pubmed: 1 3 2019
medline: 18 7 2019
entrez: 1 3 2019
Statut: ppublish

Résumé

Osteoporosis, a condition of skeletal decline that undermines quality of life, is treated with pharmacological interventions that are associated with poor adherence and adverse effects. Complicating efforts to improve clinical outcomes, the incidence of obesity is increasing, predisposing the population to a range of musculoskeletal complications and metabolic disorders. Pharmacological management of obesity has yet to deliver notable reductions in weight and debilitating complications are rarely avoided. By contrast, exercise shows promise as a non-invasive and non-pharmacological method of regulating both osteoporosis and obesity. The principal components of exercise - mechanical signals - promote bone and muscle anabolism while limiting formation and expansion of fat mass. Mechanical regulation of bone and marrow fat might be achieved by regulating functions of differentiated cells in the skeletal tissue while biasing lineage selection of their common progenitors - mesenchymal stem cells. An inverse relationship between adipocyte versus osteoblast fate selection from stem cells is implicated in clinical conditions such as childhood obesity and increased marrow adiposity in type 2 diabetes mellitus, as well as contributing to skeletal frailty. Understanding how exercise-induced mechanical signals can be used to improve bone quality while decreasing fat mass and metabolic dysfunction should lead to new strategies to treat chronic diseases such as osteoporosis and obesity.

Identifiants

pubmed: 30814687
doi: 10.1038/s41574-019-0170-1
pii: 10.1038/s41574-019-0170-1
pmc: PMC6520125
mid: NIHMS1019691
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

339-355

Subventions

Organisme : NICHD NIH HHS
ID : P2C HD086843
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR073264
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK056350
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL127522
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR066616
Pays : United States

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Auteurs

Gabriel M Pagnotti (GM)

School of Medicine, Division of Endocrinology, Indiana University, Indianapolis, IN, USA.

Maya Styner (M)

Department of Medicine, Division of Endocrinology and Metabolism, University of North Carolina, Chapel Hill, NC, USA.

Gunes Uzer (G)

College of Mechanical and Biomedical Engineering, Boise State University, Boise, ID, USA.

Vihitaben S Patel (VS)

Department of Biomedical Engineering, Stony Brook University, Stony Brook, NY, USA.

Laura E Wright (LE)

School of Medicine, Division of Endocrinology, Indiana University, Indianapolis, IN, USA.

Kirsten K Ness (KK)

Department of Epidemiology and Cancer Control, St. Jude Children's Research Hospital, Memphis, TN, USA.

Theresa A Guise (TA)

School of Medicine, Division of Endocrinology, Indiana University, Indianapolis, IN, USA.

Janet Rubin (J)

Department of Medicine, Division of Endocrinology and Metabolism, University of North Carolina, Chapel Hill, NC, USA.

Clinton T Rubin (CT)

Department of Biomedical Engineering, Stony Brook University, Stony Brook, NY, USA. Clinton.rubin@stonybrook.edu.

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