Abstract
The incidence of obesity and comorbidities has increased to epidemic levels in recent years, with important changes in the sociodemographic profile of the disease. At present, a high prevalence of the disease is not only found in developed countries but also in developing areas like India, Brazil, China, and Middle East countries. Concomitantly, the highest prevalence has moved from mature individuals to infant, young, and middle-aged populations. There is currently strong evidence supporting that these changes are related to modifications in nutritional patterns and lifestyle of women in childbearing age that affects prenatal and early postnatal environment, and therefore, modifies the developmental programming of their offspring. The present chapter outlines, based on the results of translational animal research and epidemiological human studies, the processes of developmental programming involved in the onset of obesity at infancy and adulthood.
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Abbreviations
- AGRP:
-
Agouti related protein
- DNA:
-
Deoxyribonucleic acid
- DOHaD:
-
Developmental Origins of Health and Disease
- IUGR:
-
Intrauterine Growth Restriction or Retardation
- LEP:
-
Leptin
- LEPR:
-
Leptin receptor
- LGA:
-
Large-for-gestational-age
- MC3R:
-
Melanocortin 3 receptor
- MC4R:
-
Melanocortin 4 receptor
- NPY:
-
Neuropeptide Y
- POMC:
-
Propiomelanocortin
- RNA:
-
Ribonucleic acid
- SGA:
-
Small-for-gestational-age
- α-MSH:
-
Alpha-melanocyte stimulating hormone
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Gonzalez-Bulnes, A., Astiz, S. (2019). Prenatal Programming and Epigenetics of Obesity Metabolic Phenotype: Pre- and Postnatal Metabolic Phenotypes and Molecular Mechanisms. In: Patel, V., Preedy, V. (eds) Handbook of Nutrition, Diet, and Epigenetics. Springer, Cham. https://doi.org/10.1007/978-3-319-55530-0_109
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