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Published on: November 30, 2017
Mechanisms Involved in Childhood Obesity-Related Bone Fragility
Maria Felicia Faienza1, Gabriele D'Amato2, Mariangela Chiarito1
1Department of Biomedical Sciences and Human Oncology, University of Bari Aldo Moro, Bari, Italy.
Insights
Childhood obesity increases inflammation and alters key molecules, potentially leading to osteoporosis and fractures in children. This review explores the cellular links between excess fat and weakened bone health.
Area of Science:
- Endocrinology
- Bone Biology
- Pediatric Health
Background:
- Childhood obesity is a significant health issue in Western countries.
- Excess adipose tissue triggers inflammation, oxidative stress, and mitochondrial dysfunction.
- Obesity is linked to severe comorbidities like type 2 diabetes, liver steatosis, cardiovascular, and neurodegenerative diseases.
Purpose of the Study:
- To review the cellular mechanisms connecting obesity to osteoporosis and bone fractures in children.
- To explore the growing understanding of the interplay between adipose tissue and bone metabolism.
- To examine how obesity-associated inflammation impacts bone health.
Main Methods:
- Literature review of cellular and molecular mechanisms.
- Analysis of studies on obesity, inflammation, and bone metabolism.
- Synthesis of current research on adipokines and bone health.
Main Results:
- Obesity induces low-grade inflammation, altering critical signaling molecules (e.g., leptin, TNFα).
- These molecular changes can negatively affect bone metabolism, increasing osteoporosis risk.
- Adipose tissue's influence on bone may be fat-depot specific, requiring further investigation.
Conclusions:
- Obesity in children presents a significant risk factor for developing osteoporosis and fractures.
- Understanding the cellular pathways is crucial for developing targeted interventions.
- Further research is needed to fully elucidate the complex relationship between adipose tissue and bone health.
Abstract:
Childhood obesity is one of the major health problems in western countries. The excessive accumulation of adipose tissue causes inflammation, oxidative stress, apoptosis, and mitochondrial dysfunctions. Thus, obesity leads to the development of severe co-morbidities including type 2 diabetes mellitus, liver steatosis, cardiovascular, and neurodegenerative diseases which can develop early in life. Furthermore, obese children have low bone mineral density and a greater risk of osteoporosis and fractures. The knowledge about the interplay bone tissue and between adipose is still growing, although recent findings suggest that adipose tissue activity on bone can be fat-depot specific. Obesity is associated to a low-grade inflammation that alters the expression of adiponectin, leptin, IL-6, Monocyte Chemotactic Protein 1 (MCP1), TRAIL, LIGHT/TNFSF14, OPG, and TNFα. These molecules can affect bone metabolism, thus resulting in osteoporosis. The purpose of this review was to deepen the cellular mechanisms by which obesity may facilitate osteoporosis and bone fractures.
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