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Introduction: The baboon is a well‐characterized model of human early stage atherosclerosis. However, histological and morphological changes involved in atherogenesis in baboons are not known. Previously, we challenged baboons with a high‐cholesterol, high‐fat diet for two years and observed fatty streak and plaque lesions in iliac arteries (RCIA). Methods: We evaluated histological and morphological changes of baboon arterial lesions and control arteries. In addition, we evaluated the vascular expression of CD68 and SMαA markers with progression of atherosclerosis. Results: We observed changes that correlated with extent of atherosclerosis, including increased maximum intimal thickness. We demonstrated at molecular level the infiltration of smooth muscle cells and macrophages into the intimal layer. Further, we observed histological and morphological discordancy between the affected and adjacent areas of the same RCIA. Conclusion: Atherogenesis in baboons is accompanied by histological, morphological, and molecular changes, as in humans, providing insights to evaluate the mechanisms underlying early stage atherosclerosis in target tissues. [ABSTRACT FROM AUTHOR]

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 pre‐pregnancy 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. [ABSTRACT FROM AUTHOR]

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 pre-pregnancy 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., (© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background: A sub-optimal intrauterine environment alters the trajectory of fetal development with profound effects on life-time health. Altered methylation, a proposed epigenetic mechanism responsible for these changes, has been studied in non-primate species but not nonhuman primates. We tested the hypotheses that global methylation in fetal baboon demonstrates organ specificity, gestational age specificity, and changes with maternal nutritional status., Methods: We measured global DNA methylation in fetuses of control fed (CTR) and nutrient restricted mothers fed 70% of controls (MNR) for brain, kidney, liver and heart at 0.5 and 0.9 gestation (G)., Results: We observed organ and gestation specific changes that were modified by maternal diet. Methylation in CTR fetuses was highest in frontal cortex and lowest in liver. MNR decreased methylation in 0.5G kidney and increased methylation in 0.9G kidney and frontal cortex., Conclusion: These results demonstrate a potential epigenetic mechanism whereby reduced maternal nutrition has long-term programming effects on fetal organ development.