OBJECTIVE -The study was to determine whether being the macrosomic offspring of a mother without detected glucose intolerance during pregnancy has an impact on lipid profile, glucose homeostasis, and blood pressure during childhood.RESEARCH DESIGN AND METHODS -Plasma total, HDL, and LDL cholesterol; triglycerides; apolipoprotein (Apo) A-1, -B, and -E; lipoprotein (a); fasting glucose and insulin; homeostasis model assessment of insulin resistance (HOMA-IR) index; blood pressure; BMI; and detailed anthropometry were evaluated in 85 children aged 3-10 years old, born appropriate for gestational age (AGA; n ϭ 48) and large for gestational age (LGA; n ϭ 37) of healthy mothers.RESULTS -At the time of the assessment, body weight, height, skinfold thickness, BMI, waist circumference, and blood pressure did not differ between the LGA and AGA groups with the exception of head circumference (P Ͻ 0.01). There were no significant differences in plasma total or LDL cholesterol; triglycerides; Apo A-1, -B, or -E; lipoprotein (a); Apo B-to-Apo A-1 ratio; or glucose levels between the groups. The LGA group had significantly higher HDL cholesterol levels (P Ͻ 0.01), fasting insulin levels (P Ͻ 0.01), and HOMA-IR index (P Ͻ 0.01) but lower values of the glucose-to-insulin ratio (P Ͻ 0.01) as compared with the AGA group.
CONCLUSIONS -Children bornLGA of mothers without confirmed impaired glucose tolerance during pregnancy show higher insulin concentrations than AGAs.
Diabetes Care 29:1197-1201, 2006F etal growth is a complex process involving the interaction of mother, placenta, and fetus (1). Growth and development of the fetus depends upon nutrients such as glucose, lipids, and amino acids (1). Genetic factors, in addition to the maternal and fetal status, are reported to play a role (1,2). Epidemiological, clinical, and experimental findings indicate that gestational diabetes mellitus (GDM), as well as maternal obesity or excessive weight gain during pregnancy, are significant risk factors for fetal overnutrition and macrosomia (1,2). Maternal hyperglycemia leads to fetal hyperglycemia, which in turn stimulates pancreatic islet cells and causes hyperinsulinemia (2,3). This intrauterine hyperinsulinemic state results in increased amounts of fat tissue, liver glycogen content, and total body size (2,3). Macrosomic infants of diabetic mothers are prone to glucose intolerance, obesity, and diabetes during childhood and adulthood (2,4 -6). Disturbances not only in the metabolism of carbohydrates but also in lipids observed at birth in newborns of diabetic mothers may influence the metabolic profile later in life (2,5,7-10).There is limited data regarding the metabolic profile of macrosomic offspring of healthy mothers. Moreover, these studies refer to neonatal or infantile agegroups and pay only restricted attention to childhood (8,11,12). It is important to determine whether being the macrosomic offspring of a mother without detected glucose intolerance during pregnancy has an impact on the lipid profile, insulin secretion, and glu...