ESPE Abstracts (2014) 82 FC12.4

ESPE2014 Free Communications Obesity (6 abstracts)

Pediatric Reference Values for Insulin from oGTT and Prevalence of Hyperinsulinemia in Obese Children

Antje Körner a, , Kathrin Scheuermann a , Madlen Neef a , Elena Sergeyev a , Mandy Vogel a , Jürgen Kratzsch b & Wieland Kiess a

aCenter for Pediatric Research, University Hospital for Children and Adolescents Leipzig, University of Leipzig, Leipzig, Germany; bLaboratory Medicine and Molecular Diagnostics, Institute of Clinical Chemistry, University of Leipzig, Leipzig, Germany; cMedical Center Adiposity Diseases (IFB), University of Leipzig, Leipzig, Germany

Background: Evaluation of glucose metabolism is currently based on 2 h glucose during an oral glucose tolerance test (oGTT) or fasting glucose and insulin or A1c, as these are the only parameters where cutoff values exist. This does, however, not adequately reflect the degree of hyperinsulinemia due to insulin resistance in obese children.

Objective and design: From frequent glucose and insulin levels during an oGTT of 64 healthy lean children (aged 7.7–18.8 years, BMI SDS −0.25±0.76) we aimed i) to established reference values for insulin secretion in normal children. ii) We compared insulin and glucose dynamics with data of 99 obese children (aged 6.1–17.9 years, BMI SDS 2.43±0.50). iii) We then applied these reference data to assess the prevalence of insulin resistance in an extended cohort of 1.085 obese children.

Results: i) From the healthy lean controls, we defined the maximal observed peak insulin (986 pmol/l) and minimal Matsuda ISI (3.154) as cutoffs. In lean children, pubertal status significantly affected fasting plasma (FPI) and Matsuda ISI. ii) In obese children, integral and 2 h glucose levels were significantly increased independent from age, gender and pubertal stage. However, particularly insulin parameters were markedly elevated, with peak and integral insulin levels doubled in obese compared to lean controls. The puberty effect seen in lean controls was overridden by BMI SDS when obese peers were included into multiple regression analyses, which explained 36.5% (peak insulin), 43.8% (FPI), 43.8% (Matsuda ISI) of variance. iii) Applying the obtained reference values to our extended obesity cohort, 47.3% of obese children had hyperinsulinemia and 49.2% were insulin resistant based on peak insulin and Matsuda ISI, respectively, while prevalence rates of impaired glucose tolerance (13.8%) and impaired fasting glucose (18.2%) were much lower.

Conclusion: We provide reference values for insulin secretion during an oGTT from healthy lean children. Compared to lean children, insulin secretion is doubled in obese children and almost 50% of obese children already present hyperinsulinemia as a sign of insulin resistance.

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