Abstract
Placental insufficiency, maternal malnutrition, and other causes of intrauterine growth restriction (IUGR) can significantly affect short-term growth and long-term health. Following IUGR, there is an increased risk for cardiovascular disease and Type 2 Diabetes. The etiology of these diseases is beginning to be elucidated, and premature aging or cellular senescence through increased oxidative stress and DNA damage to telomeric ends may be initiators of these disease processes. This paper will explore the areas where telomere and telomerase biology can have significant effects on various tissues in the body in IUGR outcomes.
Highlights
Placental insufficiency, maternal malnutrition, and other causes of intrauterine growth restriction (IUGR) can significantly affect short-term growth and long-term health
This redistribution of nutritional supplies leads to a decrease in muscularity and an increase in the percentage of body fat in these infants that persists throughout childhood and adult life [15, 16] and is commonly associated with changes in insulin sensitivity and other markers of the metabolic syndrome [17, 18]
Through the work of David Barker and colleagues, the concept that there further Journal of Pregnancy exists a relationship between birth weight and an increased risk for developing diseases including coronary heart disease, Type 2 Diabetes, and hypertension in later life has been generally accepted as a secondary concern for low birth weight (LBW) infants [20, 21]
Summary
The World Health Organization (WHO) estimates that the incidence of infants born low birth weight (LBW) in North America is approximately 7% [1] and is commonly characterized as a birth weight under 2500 g. Due to the lack of oxygen and altered nutrient balance, the fetus redirects these scarce resources to the brain, heart, and adrenal glands, leaving other tissues in the body more severely growth restricted, resulting in asymmetric IUGR [13, 14]. This redistribution of nutritional supplies leads to a decrease in muscularity and an increase in the percentage of body fat in these infants that persists throughout childhood and adult life [15, 16] and is commonly associated with changes in insulin sensitivity and other markers of the metabolic syndrome [17, 18]. These observations and others set the stage for the idea that changes in growth during in utero life may predispose offspring to increased risk of disease in later life, or the concept of the developmental origins of health and disease (DOHaD)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
