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Gestational high saturated fat diet alters C57BL/6 mouse perinatal skeletal formation.

Research paper by Chengya C Liang, Megan E ME Oest, Jeryl C JC Jones, M Renee MR Prater

Indexed on: 15 Sep '09Published on: 15 Sep '09Published in: Birth Defects Research Part B: Developmental and Reproductive Toxicology



Abstract

Our present work joins growing evidence that gestational environment (maternal nutrition, health, and chemical exposures) strongly influences prenatal development (www.thebarkertheory.org). The present study suggests that maternal consumption of a diet high in saturated fats (HFD), which approximates the macronutrient content of fast food, impairs perinatal skeletal development.In this study, administration of HFD (32% saturated fat) for one month prior to conception and throughout gestation in C57BL/6J mice was associated with a marked reduction in late-gestation fetal skeletal developmental delay that included shorter long bone lengths, decreased average bone mineral density (ABMD; 20%), lower total bone volume (TBV; 45%), and shorter crown-to-rump length (C-R; 12%), as compared to controls.A putative mechanism linking prenatal HFD to dysregulated fetal osteogenesis is HFD-induced oxidative stress (OS), which has been shown in our laboratory to cause placental labyrinthine vascular damage and impaired fetal signaling pathways associated with osteogenesis (Liang et al., unpublished data).The theory of HFD-associated, OS-mediated placental damage and skeletal pathogenesis was supported by demonstrating a protective effect of the dietary antioxidant quercetin (Q) against HFD-associated fetal skeletal developmental delay. Improved understanding of the role of HFD and elevated OS in fetal skeletal development will help to more completely elucidate the importance of the prenatal environment to fetal formation, and will be applied to better understand the contribution of the fetal environment to long-term risk of adult-onset disease.