4.3 Article

Pubertal changes in HOMA and QUICKI: relationship to hepatic and peripheral insulin sensitivity

Journal

PEDIATRIC DIABETES
Volume 5, Issue 3, Pages 122-125

Publisher

BLACKWELL MUNKSGAARD
DOI: 10.1111/j.1399-543X.2004.00050.x

Keywords

glucose; insulin resistance; insulin; models biological; puberty

Funding

  1. NIBIB NIH HHS [P41 EB-01975] Funding Source: Medline

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Background: Homeostasis model assessment (HOMA) and quantitative insulin-sensitivity check index (QUICKI) are measures of insulin resistance and insulin sensitivity derived from fasting glucose (FG) and insulin levels. They thus should reflect, in principle, insulin action on both the liver and the periphery. Methods: Twenty-three prepubertal and early pubertal adolescents were studied at baseline and after 6 months, using the frequently sampled intravenous glucose tolerance test (IVGTT) with labeled glucose. Total body insulin sensitivity (S-I) was calculated using the minimal model and total glucose concentrations. Peripheral insulin sensitivity (S-I*) was calculated from labeled glucose concentrations. Hepatic insulin resistance (HIR) was calculated by multiplying glucose production over the last hour by the average insulin level. HOMA and QUICKI were calculated from the fasting glucose and insulin values. Results: HOMA, QUICKI fasting insulin, and glucose to insulin ratio were all significantly related to S-I (p < 0.05) but were not independently related to S-I* or HIR. Multiple linear regression analysis revealed that both S-I* and HIR independently predicted HOMA and fasting glucose (p < 0.1). QUICKI, fasting insulin, and glucose to insulin ratio were not independently related to S-I, S-I*, or HIR. Conclusions: HOMA and fasting insulin reflect total body insulin sensitivity and HIR but not peripheral insulin sensitivity in prepubertal and early pubertal adolescents.

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