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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
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Peroxisome proliferator activated receptor-γ in osteoblasts controls bone formation and fat mass by regulating

Soohyun P Kim1, Avery H Seward1, Jean Garcia-Diaz1

  • 1Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

Iscience
|August 3, 2023
PubMed

Insights

Peroxisome proliferator activated receptor-γ (PPARγ) links skeletal and metabolic functions. Modulating sclerostin action may prevent bone loss from anti-diabetic drugs and enhance their metabolic benefits.

Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Bone Biology

Background:

  • Nuclear receptor PPARγ regulates adipogenesis and insulin sensitivity, crucial for metabolic health.
  • PPARγ also negatively impacts skeletal homeostasis, creating a dichotomy in its physiological roles.

Purpose of the Study:

  • To investigate the link between the skeletal and metabolic actions of PPARγ.
  • To determine if PPARγ's effects on bone and fat are interconnected.

Main Methods:

  • Genetic ablation of PPARγ (Pparg) in osteoblasts and osteocytes.
  • Analysis of bone mass, osteoblast activity, subcutaneous fat mass, and fatty acid metabolism.
  • Assessment of sclerostin (Sost) expression and serum levels.

Main Results:

  • Pparg ablation in bone cells led to high bone mass and reduced subcutaneous fat.
  • These phenotypes were linked to PPARγ's regulation of sclerostin production.
  • Reduced sclerostin levels in mutants normalized both skeletal and metabolic parameters.
  • Disrupting sclerostin production synergized with a PPARγ agonist, preventing bone loss and enhancing metabolic effects.

Conclusions:

  • PPARγ's skeletal and metabolic actions are interconnected through sclerostin regulation.
  • Modulating sclerostin offers a potential strategy to mitigate bone loss associated with anti-diabetic therapies.
  • Targeting sclerostin may enhance the metabolic benefits of PPARγ agonists.
Keywords:
Cell biologyMolecular physiology

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