1Orthopaedic Surgery, Harvard Medical School, 2Center for Advanced Orthopaedic Studies, Beth Israel Deaconess Medical Center
Friday 2:00-2:15, Galleria South
Maternal overnutrition increases the risk of postnatal metabolic disease via perinatal developmental programming. Here we test the hypothesis that maternal diet induces skeletal programming that alters offspring skeletal acquisition. Methods: C57Bl/6J mothers were fed high-fat (HF, 45% fat) or normal (N, 10% fat) diet from 6 wks before breeding through gestation and lactation. At 3 wks of age we weaned male and female pups onto high-fat (HF-HF or N-HF) or normal diet (N-N). Outcomes at 12 and 20 wks of age included body mass, body fat, mass-adjusted bone mineral content (BMC/BM), and cortical and trabecular bone architecture at midshaft and distal femur. Results: HF diet caused obesity, with HF-HF more obese than N-HF (p<0.05), and impaired skeletal acquisition vs. N-N. By 20 wks of age, HF-HF had 20% lower mass-adjusted BMC and 36-50% higher body fat vs. N-N (p<0.05). N-HF had lower distal femur trabecular bone volume fraction (BV/TV) vs. N-N (p<0.05). In females, trabecular BV/TV was lower in HF-HF vs. N-HF; in males, it was higher. Midshaft femur cortical bone area was lower in N-HF and higher in HF-HF vs. N-N (p<0.05). Conclusions: Postnatal HF diet impaired bone mineral content and trabecular bone acquisition in both sexes. Maternal HF diet protected offspring cortical bone, and trabecular bone in males, from these effects, but worsened the effects of postnatal HF diet on trabecular bone in females. These data suggest that maternal diet may alter human skeletal phenotype and osteoporosis risk via developmental programming.
Funding for this project was provided by NIH RC1AR058389, T32DK007028, and F32HD060419.