Metabolic Imprinting by Prenatal, Perinatal, and Postnatal Overnutrition: A Review

Abstract

Epidemiological studies have suggested that metabolic programming is one of the critical factors contributing to the etiology of obesity as well as concurrent increase in related chronic diseases (e.g., type 2 diabetes and cardiovascular disease). Metabolic programming is the phenomenon whereby a nutritional stress/stimulus applied during critical periods of early development permanently alters an organism's physiology and metabolism, the consequences of which are often observed much later in life. The idea of metabolic programming originated from the fetal origins hypothesis proposed by Barker in which he suggested that disproportionate size at birth of the newborn due to an adverse intrauterine environment correlated well with an increased risk of adult-onset ill health outcomes (type 2 diabetes, hypertension, and cardiovascular disease). The fetal origins hypothesis, proposed by Barker, suggests that adequate nutrition during fetal development is critical. Overnutrition is a form of malnutrition that has increased in the United States over the past several decades in which nutrients are oversupplied relative to the amounts required for normal growth, development, and metabolism. Evidence for the effects of maternal obesity and overnutrition on metabolic programming is reviewed during critical prenatal, perinatal, and postnatal periods.

Pediatric Type 2 Diabetes: Prevention and Treatment Through a Life Course Health Development Framework

“…Over the last 20 years, a significant body of evidence from epidemiological and animal studies has established a strong link between the intrauterine environment and long-term health (Dyer and Rosenfeld 2011;Gluckman et al 2008;McMillen and Robinson 2005;Sebert et al 2011;Sinclair et al 2007). The notion of biological embedding is now widely accepted, even though the mechanisms are not completely understood (Tarry-Adkins and Ozanne 2011).…”

“…These factors are briefly reviewed below. Several excellent papers review the underlying mechanisms of these relationships in greater depth (Dyer and Rosenfeld 2011;Armitage et al 2004;Berends and Ozanne 2012;Martin-Gronert and Ozanne 2012;Thayer et al 2012;Prince et al 2014). …”

“…GDM has been shown to alter pancreatic development and insulin sensitivity in the fetus (Warner and Ozanne 2010). Fetal growth is often affected, resulting in macrosomia or large-for-gestational-age infants (Dyer and Rosenfeld 2011). The Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study found a strong linear relation between fasting glucose and post challenge glucose with macrosomia and neonatal adiposity (Metzger et al 2008).…”

Pregnancy, Exercise and Late Effects in the Offspring until Adult Age

“…Fetal origin hypothesis of morbidity [4,5,7,8,9] and metabolic imprinting by prenatal, perinatal and postnatal factors [6][7][8][9][10] concern also PA and Ex. Their impact can be transferred during pregnancy on the fetus due to physical activity régimes and reactive changes to them of the pregnant mother, and could manifest significantly in the offspring during its own postnatal period up to the adult age.…”

Advanced aging phenotype is revealed by epigenetic modifications in rat liver after in utero malnutrition

“…The myriad of intrauterine conditions leading to low birthweight or intrauterine growth restriction show increased risk for obesity, type 2 diabetes, hypertension, and cardiovascular heart disease in adulthood (Barker & Osmond, 1986; Barker et al ., 1989; Ravelli et al ., 1998). Interestingly, at the other extreme of fetal growth, infants born large for gestational age, used as an indicator of exposure to excess nutrients, are also at greater risk for these chronic age‐related diseases in addition to some cancers (Lahmann et al ., 2004; Dyer & Rosenfeld, 2011). …”