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Area of Science:

  • Hepatology
  • Bone Biology
  • Metabolic Diseases

Background:

  • Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) is a prevalent condition with serious risks.
  • Osteoporosis and fractures are emerging comorbidities of MASLD, with unknown underlying mechanisms.
  • The sexually dimorphic nature of these bone complications requires further investigation.

Purpose of the Study:

  • To investigate the skeletal phenotype in male mice with diet-induced MASLD.
  • To identify potential molecular mechanisms linking MASLD to bone loss.
  • To explore sex differences in MASLD-associated bone disease.

Main Methods:

  • Utilized DIAMOND mice exposed to Western or control diets for up to 48 weeks.
  • Assessed skeletal parameters including trabecular and cortical bone, and mechanical integrity.
  • Employed NicheNet analysis of hepatic gene expression and a PTH-induced bone loss model.

Main Results:

  • Male DIAMOND mice with MASLD exhibited progressive bone loss, affecting trabecular and cortical bone, and leading to mechanical fragility by 48 weeks.
  • Female mice were protected from MASLD-associated bone loss and skeletal fragility.
  • Identified Ctgf, Rarres2, Anxa2, Fgf21, and Mmp13 as potential liver-secreted mediators of bone resorption.

Conclusions:

  • This study provides the first preclinical evidence of bone loss in MASLD and its progression.
  • Ctgf, Rarres2, Anxa2, Fgf21, and Mmp13 are suggested as novel molecular drivers of MASLD-associated bone pathology.
  • Findings highlight potential therapeutic targets for managing bone complications in MASLD.