Obesity in women of reproductive years is now an epidemic. As a result, there is considerable interest in developmental programming of offspring (F1) as a consequence of maternal obesity. 1 Developmental programming can be defined as responses to challenges during critical time windows that alter development with persistent effects on phenotype that may not emerge until later life. Maternal obesity is associated with multiple maternal complications, including preeclampsia, gestational diabetes, thromboembolic complications, infection, poor progress in labor, increased incidence of cesarean section, postpartum hemorrhage difficulties in delivery, and hypertension. 2,3 In addition, F1 of obese pregnant women experience more neonatal morbidity and mortality. 4,5 Recently, much interest has focused on the predisposition of F1 born to obese mothers to multiple chronic life course adverse health conditions, such as diabetes, hypertension, and themselves becoming obese. 4,6-11 In animal models, maternal obesity has been shown to result in offspring hypertension, glucose metabolism dysregulation, and altered endocrine and reproductive function. 12 Many rodent models have been extensively studied in multiple laboratories, 13-16 but to date, only two non-human primate models of maternal obesity have been reported: the Japanese macaque (Macaca fuscata) 17 and baboon (Papio species). 18 While data on maternal changes in pregnancy and F1 function in fetal life and postnatally have been published, 19-21 the fetal and early life growth phenotype programmed by maternal obesity have not been established. To characterize early life programming Abstract Background: Non-human primate models of developmental programming by maternal obesity (MO) are needed for translation to human programming outcomes.We present baboon offspring (F1) morphometry, blood cortisol, and adrenocorticotropic hormone (ACTH) from 0.9 gestation to 0-2 years.Methods: Control mothers ate chow; MO mothers ate high-fat high-energy diet prepregnancy through lactation.Results: Maternal obesity mothers weighed more than controls pre-pregnancy.Maternal obesity gestational weight gain was lower with no correlation with fetal or placenta weights. At 0.9 gestation, MO and control F1 morphometry and ACTH were similar. MO-F1 0.9 gestation male cortisol was lower, rising slower from 0-2 years vs control-F1. At birth, male MO-F1 and control-F1 weights were similar, but growth from 0-2 years was steeper in MO-F1; newborn female MO-F1 weighed more than control-F1 but growth from 0-2 years was similar. ACTH did not change in either sex.
Conclusions:Maternal obesity produced sexually dimorphic fetal and postnatal growth and hormonal phenotypes.
K E Y W O R D SACTH, baboon, cortisol, developmental programming, fructose, high-energy diet, high-fat diet, maternal nutrition, non-human primates