Maternal High-Fat Diet Induces Long-Lasting Defects in Bone Structure in Rat Offspring Through Enhanced

Priyanka Kushwaha1, Seva G Khambadkone2,3, Mengni Li2

  • 1Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, 720 Rutland Avenue, Ross 209, Baltimore, MD, 21205, USA.

Insights

Maternal high-fat diet (HFD) exposure during pregnancy impacts offspring bone health. Male offspring showed significant bone loss due to increased osteoclast activity, suggesting long-term skeletal health risks.

Area of Science:

  • Reproductive Biology
  • Endocrinology
  • Skeletal Biology

Background:

  • Maternal stress during pregnancy and lactation can affect offspring chronic disease risk.
  • High-fat diet (HFD) is a common maternal stressor with potential long-term health implications for offspring.
  • Prenatal and perinatal nutrition significantly influences developmental programming and adult health outcomes.

Purpose of the Study:

  • To investigate the impact of maternal high-fat diet (HFD) exposure on skeletal homeostasis in rat offspring.
  • To determine sex-specific effects of maternal HFD on bone development and maintenance.
  • To elucidate the cellular mechanisms underlying diet-induced skeletal changes in offspring.

Main Methods:

  • Utilized a rat model with maternal HFD exposure during gestation and lactation.
  • Assessed skeletal parameters in offspring at young (3 weeks) and adult (15 weeks) stages using histomorphometry.
  • Isolated and cultured bone marrow stromal cells and osteoclastic precursors from offspring for in vitro differentiation assays.

Main Results:

  • Maternal HFD led to transient increases in trabecular bone volume in young offspring, followed by sustained bone loss in males by 15 weeks.
  • Male offspring from HFD dams exhibited significantly reduced trabecular bone volume fraction, attributed to a threefold increase in osteoclasts.
  • Osteoclastic precursors from male offspring of HFD dams showed enhanced differentiation and increased sensitivity to RANKL, while osteoblastic differentiation was unaffected.

Conclusions:

  • Maternal HFD exposure during critical developmental periods has persistent, sex-specific detrimental effects on offspring skeletal health.
  • Increased osteoclastogenesis, driven by heightened precursor sensitivity to RANKL, is a key mechanism for HFD-induced bone loss in male offspring.
  • These findings suggest that maternal dietary interventions may be crucial for preventing long-term skeletal morbidities like osteopenia and osteoporosis in offspring.