Insulin resistance during puberty: results from clamp studies in 357 children.

Abstract

Insulin resistance may be an important cause of a constellation of cardiovascular risk factors in adults, and onset of this syndrome may occur in childhood. However, children normally experience transient insulin resistance at puberty. There were 357 normal children (159 girls, 198 boys) age 10-14 years who underwent euglycemic clamp studies to assess the effects of Tanner stage (T), sex, ethnicity, and BMI on insulin resistance. Insulin resistance increased immediately at the onset of puberty (T2), but returned to near prepubertal levels by the end of puberty (T5). Its peak occurred at T3 in both sexes, and girls were more insulin resistant than boys at all T stages. White boys appeared to be more insulin resistant than black boys; no difference was seen between white and black girls. Insulin resistance was strongly related to BMI, triceps skinfold thickness, and waist circumference, and this relationship was independent of Tanner stage or sex. Differences in BMI and adiposity did not, however, entirely explain the insulin resistance of puberty. These results demonstrate that 1) significant differences in insulin resistance are present between boys and girls; 2) insulin resistance increases significantly at T2, T3, and T4, but decreases to near prepubertal levels at T5; and 3) while insulin resistance is related to BMI and anthropometric measures of fatness, these factors do not completely explain the insulin resistance that occurs during the Tanner stages of puberty.

Insulin sensitivity, insulin secretion and β-cell function during puberty in overweight Hispanic children with a family history of type 2 diabetes

“…Gender was included as a fixed factor along with Tanner stage since previous research has shown that girls may have lower SI than boys. 3,22 Subsequently, adjusted 5 Â 2 GLM for log fasting insulin, fasting glucose, log 2-h glucose, log SI, log AIRg, and log DI were run after covarying age, fat mass, and soft lean tissue mass; SI was also included as a covariate when AIRg was entered as the dependent variable. Unadjusted and adjusted models were followed up with pair-wise contrasts using a Bonferroni correction for multiple comparisons.…”

“…[1][2][3][4] In Caucasian children, decreased SI during puberty is accompanied by increased insulin secretion that normalizes as insulin resistance improves near the end of puberty. 5 Cross-sectionally, Moran et al 3 showed that SI (measured using the euglycemic-hyperinsulinemic clamp) was highest in Tanner stage I, lowest in Tanner stage III (B20% lower than stage I), and near prepubertal levels in Tanner stage V. Using a longitudinal design, Goran and Gower 2 observed that the pubertal transition from Tanner stage I to III was associated with a 32% reduction in SI (measured by the intravenous glucose tolerance test and minimal modeling) in Caucasian and African-Americans which was consistent across a range of body fatness. Our research group has previously demonstrated that Hispanic and African-American children have lower SI in relation to Caucasians, and while Hispanics compensate for their lower SI by increasing insulin secretion, African-Americans exhibit reduced insulin clearance to help maintain normoglycemia.…”

The gender insulin hypothesis: why girls are born lighter than boys, and the implications for insulin resistance

“…The higher prevalence might in principle be explained by gender differences in anthropometry or physical activity, although such explanations are unnecessary. As noted above, girls are more insulin resistant than boys even after taking anthropometry into account, 15,18,24 and significant differences in physical activity are unable to explain the sex difference in insulin resistance. 24 Diabetes is commoner among male subjects once they enter adulthood, 53 perhaps because they acquire more central fat.…”

“…[15][16][17][18][19][20][21][22][23] This sex difference in insulin resistance has usually been attributed to differences in adiposity or pubertal stage, but in studies which have adjusted for these factors 15,18 a residual difference remains which has not been explained. We have shown that girls are substantially (B33%) more insulin resistant than boys at 5 years 24 and in the years leading up to puberty.…”

IMMULITE® 2000 age and sex-specific reference intervals for alpha fetoprotein, homocysteine, insulin, insulin-like growth factor-1, insulin-like growth factor binding protein-3, C-peptide, immunoglobulin E and intact parathyroid hormone

“…Hypoglycemia and insulin resistance can be detected and managed by testing insulin concentrations [12]. IGF-1, also known as Somatomedin C, is structurally similar to insulin and its production is stimulated by growth hormone (GH).…”