The role of PPARγ in childhood obesity-induced fractures

Matthew R McCann1,2, Anusha Ratneswaran2,3,4

  • 11Sydney Medical School, University of Sydney, Sydney, NSW 2006 Australia.

Genes & Nutrition
|December 5, 2019
PubMed

Insights

Childhood obesity lowers bone density and increases fracture risk. Targeting the PPARγ pathway may reduce fat, improve bone health, and treat obesity-related skeletal issues in children.

Area of Science:

  • Pediatric Endocrinology
  • Bone Biology
  • Metabolic Disorders

Background:

  • Global obesity rates are rising, affecting children and leading to musculoskeletal issues.
  • Childhood obesity is linked to chronic conditions, including significant skeletal disorders.
  • Adiposity impacts bone density, necessitating a deeper understanding of underlying mechanisms.

Purpose of the Study:

  • To review the effects of childhood adiposity on bone density.
  • To describe slipped capital femoral epiphysis and Blount's disease in obese children.
  • To explore the role of PPARγ in adipogenesis and bone remodeling.

Main Methods:

  • Analysis of clinical studies on childhood obesity and bone density.
  • Review of literature on bone remodeling and cellular mediators of bone growth.
  • Examination of the transcriptional factor peroxisome proliferator-activated receptor gamma (PPARγ).

Main Results:

  • Childhood obesity is associated with decreased bone density and increased risk of skeletal conditions.
  • PPARγ is a key regulator of adipocyte differentiation and influences osteoblast populations.
  • Higher PPARγ expression in obesity correlates with increased adipocytes and reduced bone density.

Conclusions:

  • Modulating PPARγ signaling can shift mesenchymal stem cells towards osteoblastogenesis, enhancing bone mineral density.
  • PPARγ presents a potential therapeutic target for reducing adiposity and increasing bone density in obese children.
  • Targeting PPARγ may offer a novel treatment strategy for obesity-induced bone fractures in pediatric populations.

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