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Insulin resistance is not due to persistently elevated serum tumor necrosis‐α levels in small for gestational age, premature, or twin children
Author(s) -
Jefferies Craig A.,
Hofman Paul L.,
Keelan Jeffrey A.,
Robinson Elizabeth M.,
Cutfield Wayne S.
Publication year - 2004
Publication title -
pediatric diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.678
H-Index - 75
eISSN - 1399-5448
pISSN - 1399-543X
DOI - 10.1111/j.1399-543x.2004.00038.x
Subject(s) - medicine , insulin resistance , gestational age , insulin , alpha (finance) , necrosis , gestation , obstetrics , endocrinology , pregnancy , surgery , biology , genetics , construct validity , patient satisfaction
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 ( S I ) 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 S I [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 < 0.001). Plasma TNF‐α levels were lower in the insulin‐resistant study group when compared to the control group (2.9 ± 0.1 vs. 5.0 ± 0.2 pg/mL, p < 0.001). An association was present between reduced S I and low plasma TNF‐α levels in the study group (p = 0.01, r = 0.4). Fasting plasma cortisol was lower in the study compared to the control group (266 ± 16 vs. 341 ± 28 nmol/L, p < 0.01) due to the influence of the twin study subgroup. There was no relationship between plasma cortisol and TNF‐α levels (p = 0.3). Conclusion: SGA, premature, and twin children are insulin resistant and have low plasma TNF‐α and cortisol levels. We speculate that the mechanism leading to insulin resistance in these subjects is also suppressing plasma TNF‐α and cortisol concentrations.