Adiposity in children born small for gestational age

Area of Science:

• Developmental biology
• Metabolic disorders
• Public health

Background:

• Epidemiological studies link small for gestational age (SGA) birth to increased adult metabolic and cardiovascular disease risk.
• The thrifty phenotype hypothesis suggests fetal undernutrition causes permanent metabolic changes, predisposing individuals to disease later in life.
• This association extends beyond fetal undernutrition to include premature birth and high birth weight, with postnatal nutrition and catch-up growth also playing a role.

Purpose of the Study:

• To explore the long-term metabolic and cardiovascular consequences of early life growth patterns.
• To investigate the mechanisms underlying metabolic alterations in individuals born SGA.
• To understand how fetal and early postnatal nutrition influence later health.

Main Methods:

• Review of epidemiological studies on SGA and adult health outcomes.
• Examination of animal models of intrauterine growth retardation (IUGR) to study glucose homeostasis.
• Analysis of human studies assessing insulin resistance, glucose metabolism, and body composition in SGA individuals.

Main Results:

• Animal models of IUGR exhibit altered glucose homeostasis, including reduced beta-cell mass and insulin secretion.
• Human studies confirm insulin resistance in adolescents and young adults born SGA.
• SGA children show early pubertal alterations in glucose homeostasis, increased lipid oxidation, altered stature, and increased fat mass, contributing to insulin resistance.

Conclusions:

• Fetal and early neonatal nutrition ('metabolic imprinting') can induce permanent metabolic changes.
• Mechanisms may involve gene expression modulation (e.g., DNA methylation), organ structure alterations, or long-lasting changes in hormonal axes.
• These early-life events establish a 'thrifty phenotype' that increases susceptibility to metabolic and cardiovascular disorders in adulthood.