Author
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CHEN, JIN-RAN - Arkansas Children'S Nutrition Research Center (ACNC) |
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Submitted to: Book Chapter
Publication Type: Book / Chapter Publication Acceptance Date: 9/21/2017 Publication Date: 9/21/2017 Citation: Chen, J. 2017. High-fat diet and maternal obesity-associated epigenetic regulation of bone development. In: Patel, V., Preedy, V., editors. Handbook of Nutrition, Diet, and Epigenetics. Cham, Swizterland: Springer International Publishing. p. 1-17. https://doi.org/10.1007/978-3-319-31143-2_113-1. DOI: https://doi.org/10.1007/978-3-319-31143-2_113-1 Interpretive Summary: The aim of this study was to determine the relationship between weight gain and energy intake during infancy and childhood adiposity at 5 years of age. Growth, body composition, and dietary intake were monitored during the first year of life and at age 5 years in 152 healthy formula-fed infants. Results suggested that body weight gain during the first year of life are important determinant of body mass index (BMI) at 5 years of age even after considering other important variables such as maternal BMI and infancy energy intake. These findings suggests that other factors such as energy expenditure and/or the efficiency of nutrient utilization may be different in these children. Technical Abstract: Due to the worldwide epidemic in obesity, maternal obesity has recently seen an explosion in investigations in both animal models and humans on its effects on offspring phenotype and pathologies including diabetes, hyperlipidemia, cardiovascular disease, and cancer. Epigenetic mechanisms presumably explain how metabolic or nutritional status during intrauterine and early postnatal life impacts the risk of chronic diseases. Developmental programming and epigenetic regulation of the fetal skeletal development associated with maternal obesity and diet is understudied. The fetal and neonatal bone cells represent potential targets for developmental programming. Maternal obesity-associated epigenetically regulated events in utero contributes toward changes in the ability to attain peak bone mass and increases in risk of the adult onset of degenerative bone disorders. Recent studies in rodents showed that the embryonic/neonatal skeletal phenotype can be programmed by maternal high fat/high sugar obesity-promoting diets prior to and during pregnancy. Importantly, evidence from a human study suggested that umbilical cord mesenchymal stem cells (UC-MSCs) from obese mothers have less potential to differentiate toward osteoblast, and more potential for adipogenesis. Further research on the mechanisms connecting maternal obesity, fetal bone development, and postnatal bone formation are required. |
