Maternal nutrition is critically involved in the growth and development of the fetus. Suboptimal nutrition during pregnancy cannot only cause maternal health problems (such as gestational diabetes and preeclampsia) and complications during pregnancy, but also adverse fetal outcomes. It has already been shown that genetic and environmental alterations can induce changes in the regulation of fetal growth and development, but there is growing evidence that the susceptibility to a number of chronic diseases (e.g. metabolic and cardiovascular diseases) in adulthood can be increased due to poor perinatal nutrition. This has been called the ‘Developmental Origins of Health and Disease’ hypothesis (DOHaD), which postulates that the development of the oocyte, embryo and fetus is particularly responsive to inadequate nutrition and other environmental influences (e.g. endocrine-disrupting chemicals) leading to permanent changes in physiology and metabolism and thereby increasing the predisposition to metabolic, endocrine, and cardiovascular diseases further in life. Several factors are involved both directly and indirectly in the association between maternal nutrition and short- and long-term maternal/offspring outcomes. Epigenetic modifications are among the most suitable molecular explanation linking maternal nutrition and adult diseases. Indeed, maternal nutrition can affect both fetal and placental epigenetic modification, leading to possible long lasting consequences for the child and the adult. “Nutritional epigenetics” has therefore been viewed as an attractive tool to prevent future adult diseases as well as to delay aging-associated processes.

Keynote lecture: Nutrition during the first 1000 days of life and the programming of adults’ health / C. Mando'. ((Intervento presentato al 47. convegno Annual meeting of the Fetal and Neonatal Physiological Society tenutosi a virtual nel 2021.

Keynote lecture: Nutrition during the first 1000 days of life and the programming of adults’ health

C. Mando'
2021-10-04

Abstract

Maternal nutrition is critically involved in the growth and development of the fetus. Suboptimal nutrition during pregnancy cannot only cause maternal health problems (such as gestational diabetes and preeclampsia) and complications during pregnancy, but also adverse fetal outcomes. It has already been shown that genetic and environmental alterations can induce changes in the regulation of fetal growth and development, but there is growing evidence that the susceptibility to a number of chronic diseases (e.g. metabolic and cardiovascular diseases) in adulthood can be increased due to poor perinatal nutrition. This has been called the ‘Developmental Origins of Health and Disease’ hypothesis (DOHaD), which postulates that the development of the oocyte, embryo and fetus is particularly responsive to inadequate nutrition and other environmental influences (e.g. endocrine-disrupting chemicals) leading to permanent changes in physiology and metabolism and thereby increasing the predisposition to metabolic, endocrine, and cardiovascular diseases further in life. Several factors are involved both directly and indirectly in the association between maternal nutrition and short- and long-term maternal/offspring outcomes. Epigenetic modifications are among the most suitable molecular explanation linking maternal nutrition and adult diseases. Indeed, maternal nutrition can affect both fetal and placental epigenetic modification, leading to possible long lasting consequences for the child and the adult. “Nutritional epigenetics” has therefore been viewed as an attractive tool to prevent future adult diseases as well as to delay aging-associated processes.
Settore MED/49 - Scienze Tecniche Dietetiche Applicate
Keynote lecture: Nutrition during the first 1000 days of life and the programming of adults’ health / C. Mando'. ((Intervento presentato al 47. convegno Annual meeting of the Fetal and Neonatal Physiological Society tenutosi a virtual nel 2021.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2434/874489
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