Nutritional Signaling Pathway Activities in Obesity and Diabetes
Chapter 2: Maternal Nutrition and the Risk of Obesity and Diabetes in the Offspring
Published:24 Aug 2020
C. M. Reynolds, P. E. Bridge-Comer, and M. H. Vickers, in Nutritional Signaling Pathway Activities in Obesity and Diabetes, ed. Z. Cheng, The Royal Society of Chemistry, 2020, ch. 2, pp. 24-47.
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Epidemiological observations and work in experimental models in animals have highlighted the link between the nutritional environment in early life and an increased risk for offspring to develop a range of cardiometabolic and reproductive disorders in later life. This framework falls under the “Developmental Origins of Health and Disease” (DOHaD) hypothesis via a process termed developmental programming. Altered maternal nutrition, including undernutrition, overnutrition and specific micronutrient deficiencies during critical early windows of developmental plasticity, results in adaptive processes that confer short-term survival advantages but can lead to lifelong adverse impacts on the health of offspring. These effects are amplified postnatally via an obesogenic diet and sedentary behaviour and can also be passed on to future generations. The mechanistic basis of early-life programming remains largely undefined. However, involvement of epigenetic mechanisms, such as altered DNA methylation, histone modifications and miRNAs, has been implicated in addition to permanent structural changes during organ development. Further, at least in animal models, aberrant developmental programming can be reversed via targeted nutritional supplementation during early life, albeit in a sex-specific manner. A better understanding of early nutritional programming and how disease traits are transmitted across future generations is essential for the development of preventative strategies aimed at addressing the current health crisis around obesity and related metabolic disorders.