Catch-up growth and catch-up fat in children born small for gestational age

Abstract

Infants born small for gestational age (SGA) are at increased risk of perinatal morbidity, persistent short stature, and metabolic alterations in later life. Recent studies have focused on the association between birth weight (BW) and later body composition. Some reports suggest that fetal nutrition, as reflected by BW, may have an inverse programing effect on abdominal adiposity later in life. This inverse association between BW and abdominal adiposity in adults may contribute to insulin resistance. Rapid weight gain during infancy in SGA children seemed to be associated with increased fat mass rather than lean mass. Early catch-up growth after SGA birth rather than SGA itself has been noted as a cardiovascular risk factor in later life. Children who are born SGA also have a predisposition to accumulation of fat mass, particularly intra-abdominal fat. It is not yet clear whether this predisposition is due to low BW itself, rapid postnatal catch-up growth, or a combination of both. In this report, we review the published literature on central fat accumulation and metabolic consequences of being SGA, as well as the currently popular research area of SGA, including growth aspects.

Maternal and early‐life area‐level characteristics and childhood adiposity: A systematic review

“…Only one study included measures of paternal smoking or weight, which is a limitation because paternal genetics, attitudes, and behaviours likely also affect childhood adiposity, and their exclusion from models overemphasizes the effect of maternal factors . The exclusion of preterm and low birthweight babies in some studies may have affected the estimates as these outcomes may be on the causal pathway between the environment and childhood adiposity, given evidence of links between the environment, birth outcomes, and infancy catch‐up growth for preterm and small babies . Residual confounding may also occur at the area‐level, where certain environments experience multiple forms of disadvantage in terms of suitability for healthy weight gain, for example, areas with limited park access tend to have fewer outlets selling healthy foods .…”

“…66 The exclusion of preterm and low birthweight babies in some studies 47,48,51 may have affected the estimates as these outcomes may be on the causal pathway between the environment and childhood adiposity, given evidence of links between the environment, birth outcomes, 42 and infancy catch-up growth for preterm and small babies. 44,67 Residual confounding may also occur at the area-level, where certain environments experience multiple forms of disadvantage in terms of suitability for healthy weight gain, for example, areas with limited park access tend to have fewer outlets selling healthy foods. 68 The results of these studies may have been All of the studies in this review used data from recruited prospective cohorts.…”

Early-Life Nutritional Programming of Type 2 Diabetes: Experimental and Quasi-Experimental Evidence

“…Such preferential catch-up fat is partly driven by mechanisms of energy conservation operating through suppression of thermogenesis and resulting in the development of thrifty ‘catch-up fat’ phenotype generally characterized by insulin and leptin resistance. Abnormalities in the growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis, known to play a central role in promoting human growth and development, have been repeatedly reported in children born small for gestational age (SGA) [19]. Such long-lasting abnormalities of IGF-1 in SGA children with catch-up growth are believed to be critically implicated in the association with metabolic disorders, including T2D, later in life.…”

The Impact of Prenatal Exposure to Dexamethasone on Gastrointestinal Function in Rats

“…On the other hand, TGF has no impact in small intestine size in adult animals [56]. At 8 months old, iuGC rats did not show differences in the small intestine size, which could reflect that the catch-up phenomenon seen in some preterm babies [57] may be delayed in the gut. Our results are in agreement with other studies, which show that iuGC delays puberty onset and neurodevelopment [10, 58].…”