Insulin resistance is not due to persistently elevated serum tumor necrosis-α levels in small for gestational age, premature, or twin children

: Background: In pregnancies with small for gestational age (SGA) fetuses, elevated amniotic fluid tumor necrosis factor‐α (TNF‐α) levels have been reported. TNF‐α has been shown to induce insulin resistance in rodents and humans. We hypothesized that an adverse fetal or early neonatal environment for SGA, twin, and premature children leads to persistently elevated TNF‐α levels that induce insulin resistance in each of these groups. Methods: The study group consisted of 16 SGA, 14 premature, 53 twin subjects, and the control group of 40 normal subjects (10 short‐stature and 30 normal‐stature). All subjects were prepubertal and non‐obese. Insulin sensitivity (SI) was measured in all but the normal‐statured control subjects. Fasting plasma TNF‐α and cortisol levels were measured in all subjects. Results: The study group had reduced SI[SGA 18.5 ± 3, premature 17.8 ± 2, twin 12.7 ± 0.7 (×10−4/min/µU/mL)] compared to the short normal control subjects (43 ± 8 × 10−4/min/µU/mL, p