Intrauterine Growth Retardation, Insulin Resistance, and Nonalcoholic Fatty Liver Disease in Children

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Abstract
Intrauterine growth retardation is associated with the development of abnormalities in glucose tolerance in adulthood (1,2). Studies in adults and children born small for gestational age (SGA) (3–7) indicate that insulin resistance is the earliest component associated with low birth weight, irrespective of confounding factors, including obesity (8) and a family history of type 2 diabetes. In SGA children, the typical central fat accumulation may actively contribute to insulin resistance (9). Visceral fat and fatty liver represent special depots of ectopic fat, independently associated with insulin resistance (10–12). In the liver, hepatic triglyceride accumulation characterizes nonalcoholic fatty liver disease (NAFLD), a highly prevalent and potentially progressive condition in adults, now considered the hepatic expression of the metabolic syndrome (13). In the pediatric population, the prevalence of NAFLD is only 2–3% but increases to 53% in the presence of obesity (14,15). We studied the association of low birth weight with histologically assessed pediatric NAFLD to test the hypothesis that intrauterine growth retardation might be an additional factor responsible for metabolic liver disease in children via insulin resistance. We studied 90 children with NAFLD, consecutively observed in the Liver Unit, Bambino Gesù Children's Hospital, Rome, Italy, from June 2001 to April 2003. Part of this cohort group was reported elsewhere (16). All had a complete anthropometric …