Molecular Mechanisms of Obesity-Induced Osteoporosis and Muscle Atrophy

Obesity and osteoporosis are two alarming health disorders prominent among middle and old age populations, and the numbers of those affected by these two disorders are increasing. It is estimated that more than 600 million adults are obese and over 200 million people have osteoporosis worldwide. Int...

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Main Authors:	Roy, Bipradas, Curtis, Mary E., Fears, Letimicia S., Nahashon, Samuel N., Fentress, Hugh M.
Format:	Online
Language:	English
Published:	Frontiers Media S.A. 2016
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5040721/

id	pubmed-5040721
recordtype	oai_dc
spelling	pubmed-50407212016-10-14 Molecular Mechanisms of Obesity-Induced Osteoporosis and Muscle Atrophy Roy, Bipradas Curtis, Mary E. Fears, Letimicia S. Nahashon, Samuel N. Fentress, Hugh M. Physiology Obesity and osteoporosis are two alarming health disorders prominent among middle and old age populations, and the numbers of those affected by these two disorders are increasing. It is estimated that more than 600 million adults are obese and over 200 million people have osteoporosis worldwide. Interestingly, both of these abnormalities share some common features including a genetic predisposition, and a common origin: bone marrow mesenchymal stromal cells. Obesity is characterized by the expression of leptin, adiponectin, interleukin 6 (IL-6), interleukin 10 (IL-10), monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), macrophage colony stimulating factor (M-CSF), growth hormone (GH), parathyroid hormone (PTH), angiotensin II (Ang II), 5-hydroxy-tryptamine (5-HT), Advance glycation end products (AGE), and myostatin, which exert their effects by modulating the signaling pathways within bone and muscle. Chemical messengers (e.g., TNF-α, IL-6, AGE, leptins) that are upregulated or downregulated as a result of obesity have been shown to act as negative regulators of osteoblasts, osteocytes and muscles, as well as positive regulators of osteoclasts. These additive effects of obesity ultimately increase the risk for osteoporosis and muscle atrophy. The aim of this review is to identify the potential cellular mechanisms through which obesity may facilitate osteoporosis, muscle atrophy and bone fractures. Frontiers Media S.A. 2016-09-29 /pmc/articles/PMC5040721/ /pubmed/27746742 http://dx.doi.org/10.3389/fphys.2016.00439 Text en Copyright © 2016 Roy, Curtis, Fears, Nahashon and Fentress. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Roy, Bipradas Curtis, Mary E. Fears, Letimicia S. Nahashon, Samuel N. Fentress, Hugh M.
spellingShingle	Roy, Bipradas Curtis, Mary E. Fears, Letimicia S. Nahashon, Samuel N. Fentress, Hugh M. Molecular Mechanisms of Obesity-Induced Osteoporosis and Muscle Atrophy
author_facet	Roy, Bipradas Curtis, Mary E. Fears, Letimicia S. Nahashon, Samuel N. Fentress, Hugh M.
author_sort	Roy, Bipradas
title	Molecular Mechanisms of Obesity-Induced Osteoporosis and Muscle Atrophy
title_short	Molecular Mechanisms of Obesity-Induced Osteoporosis and Muscle Atrophy
title_full	Molecular Mechanisms of Obesity-Induced Osteoporosis and Muscle Atrophy
title_fullStr	Molecular Mechanisms of Obesity-Induced Osteoporosis and Muscle Atrophy
title_full_unstemmed	Molecular Mechanisms of Obesity-Induced Osteoporosis and Muscle Atrophy
title_sort	molecular mechanisms of obesity-induced osteoporosis and muscle atrophy
description	Obesity and osteoporosis are two alarming health disorders prominent among middle and old age populations, and the numbers of those affected by these two disorders are increasing. It is estimated that more than 600 million adults are obese and over 200 million people have osteoporosis worldwide. Interestingly, both of these abnormalities share some common features including a genetic predisposition, and a common origin: bone marrow mesenchymal stromal cells. Obesity is characterized by the expression of leptin, adiponectin, interleukin 6 (IL-6), interleukin 10 (IL-10), monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), macrophage colony stimulating factor (M-CSF), growth hormone (GH), parathyroid hormone (PTH), angiotensin II (Ang II), 5-hydroxy-tryptamine (5-HT), Advance glycation end products (AGE), and myostatin, which exert their effects by modulating the signaling pathways within bone and muscle. Chemical messengers (e.g., TNF-α, IL-6, AGE, leptins) that are upregulated or downregulated as a result of obesity have been shown to act as negative regulators of osteoblasts, osteocytes and muscles, as well as positive regulators of osteoclasts. These additive effects of obesity ultimately increase the risk for osteoporosis and muscle atrophy. The aim of this review is to identify the potential cellular mechanisms through which obesity may facilitate osteoporosis, muscle atrophy and bone fractures.
publisher	Frontiers Media S.A.
publishDate	2016
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5040721/
_version_	1613664389195366400

Molecular Mechanisms of Obesity-Induced Osteoporosis and Muscle Atrophy

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