Prenatal Stress or High Fat Diet increases Susceptibility to Diet-Induced Obesity in Rat Offspring

Abstract

Objective Perturbations to the prenatal environment has been associated with the development of adult chronic disease, findings that gave rise to the “Barker Hypothesis” or the “developmental origins of adult disease” concept. In this study we used an animal model to determine the metabolic consequences of maternal prenatal stress and high fat feeding on the developing offspring.

Research Design and Methods Pregnant female Sprague-Dawley rats were maintained on standard chow (CHOW) or 60% high fat (HF) diet throughout gestation and lactation. Half of each group were exposed to a novel variable stress paradigm (STRESS) during the third week of gestation while control dams were left undisturbed (CON). Body weight, body composition, glucose tolerance and endocrine parameters were measured in offspring through early adulthood.

Results Male and female pups from dams that experienced prenatal stress and/or were on HF diet weighed more beginning on postnatal day 7 compared to CHOW-CON. Access to HF diet at weaning enhanced increased the body weight effect through early adulthood and was attributable to greater adiposity. Pups weaned onto CHOW diet showed no significant difference in glucose clearance or insulin secretion. However, pups weaned onto HF diet had impaired glucose tolerance if their dams were on HF diet, experienced prenatal stress, or both.

Conclusions Our data demonstrate that prenatal stress and/or high fat diet during the intrauterine or postnatal environment affects offspring in a manner that increases their susceptibility to diet-induced obesity and leads to secondary adverse metabolic consequences.