Abstract
Normal linear growth is an integrated process driven by multiple contributing factors involved in chondrogenesis and bone elongation. Prenatal growth is usually assessed by weight gain with gestational age, while postnatal growth is assessed with World Health Organization, Centers for Disease Control, or country-specific growth charts that provide linear growth trajectories with age for weight and height. These references provide insight to better understand human growth and aid clinicians with both evaluating an individual’s growth and recognizing abnormal growth. The mechanisms regulating prenatal and postnatal growth are thought to be distinct; therefore, they optimize the speed of growth during fetal life and prevent the overgrowth of infants during postnatal life. Previous studies showed that many fetal growth-promoting signals may have reduced expression (1) and/or transition to other mechanisms to adjust the speed of linear growth after birth. Consequently, growth velocity during postnatal life significantly slows immediately after birth in mammals. However, some sets of genes are reported to modulate both prenatal and postnatal linear growth. For example, altered methylations affecting IGF2 expression can cause Silver-Russell syndrome (small for gestational age [SGA] and reduced postnatal growth) or Beckwith-Wiedemann syndrome (large for gestational age [LGA] and overgrowth), depending on the degree of IGF2 expression (2). However, to date, very few genetic factors that regulate both prenatal and postnatal linear growth have been identified.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have