Perinatal programming of the skeleton

Osteoporosis and obesity are increasingly prevalent diseases with many men and women predicted to suffer an osteoporotic fracture in their remaining lifetime with a large number of adults and children being overweight or obese.

The recent discovery of interactions between bone, fat, and the brain raises the possibility that these diseases may share common origins that could start in the perinatal environment. Previous studies have demonstrated that maternal high fat (HF) diet induces perinatal developmental programming of of metabolic diseases, such as obesity and type II diabetes in the offspring. However, little is known about whether maternal diet causes developmental programming of bone mass acquisition and/or of the skeletal response to postnatal diet.

Devlin et al. tested the effects of maternal HF diet on body composition, hormone levels, and cortical and trabecular bone properties in male and female mice. Maternal HF diet during gestation and lactation alters offspring skeletal phenotype at 3–6 months of age, even when pups are raised on a normal postnatal diet. A maternal HF diet may impair postnatal cortical bone acquisition in pups but also slow age-related trabecular bone loss. Their data supports the hypothesis that maternal diet alters postnatal skeletal homeostasis.

Read the full article in Devlin et al (2013) Journal of Endocrinology 217 69-81 DOI: 10.1530/JOE-12-0403