The occurrence of metabolic abnormalities related to insulin resistance syndrome in nondiabetic offspring of type 2 diabetic parents is known. However, information is lacking on the timing and the course of development of the components of this syndrome from childhood to adulthood in the offspring of parents with diabetes. This aspect was examined in a community-based cohort with (n = 303) and without (n = 1,136) a parental history of type 2 diabetes followed longitudinally since childhood (ages 4 to 17 years; mean follow-up period, 15 years) by repeated surveys. Offspring with parental diabetes versus those without such history had significantly excess generalized and truncal adiposity as measured by body mass index (BMI) and subscapular skinfold beginning in childhood, higher levels of fasting insulin and glucose and homeostasis model assessment index of insulin resistance (HOMA-IR) from adolescence, and higher levels of low-density lipoprotein (LDL) cholesterol and triglycerides and lower levels of high-density lipoprotein (HDL) cholesterol in adulthood. Many of these risk variables changed adversely at an increased rate in offspring of diabetic parents. In a multivariate analysis, parental diabetes was an independent predictor of longitudinal changes in adiposity, glucose, insulin, HOM-IR, systolic and diastolic blood pressure, and LDL cholesterol in the offspring, regardless of race and gender. As young adults, the offspring of diabetic parents had a higher prevalence of generalized (BMI > 30, 36% v 16%, P =.0001) and visceral (waist > 100 cm, 15% v 6%, P =.0001) obesity, hyperinsulinemia indicative of insulin resistance (insulin > 18 microU/mL, 15% v 8%, P =.0001), hyperglycemia (>or=110 mg/dL, 2% v 0.5%, P =.02), high LDL cholesterol (>or=160 mg/dL, 11% v 7%, P =.02), low HDL cholesterol (<40 mg/dL for males and <50 mg/dL for females, 40% v 31%, P =.004), high triglycerides (>or=150 mg/dL, 23% v 15%, P =.0001), and hypertension (>140/90 mm Hg, 11% v 6%, P =.004). Thus, the offspring of diabetic parents displayed excess body fatness beginning in childhood and accelerated progression of adverse risk profile characteristics of insulin resistance syndrome from childhood to young adulthood. These observations have important implications for early prevention and intervention.
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