Abstract

Associations between body mass index (BMI)- standard deviation score (SDS)/waist-to-height ratio (WHtR) were studied with (i) serum uric acid (sUA)/gamma-glutamyl-transferase (GGT) and (ii) cardiometabolic risk markers in children with obesity, considering sex, pubertal development, and degree of weight loss/type of patient care. 102 936 children from the Adiposity-Follow-up registry (APV; 47% boys) were included. Associations were analysed between sUA/GGT and anthropometrics, transaminases, lipids, fasting insulin (FI), homeostasis model assessment of insulin resistance (HOMA-IR), triglycerides to HDL-cholesterol (TG/HDL)-ratio. Follow-up analyses (3-24 months after baseline) considered a BMI-SDS reduction ≥0.2 (n= 11 096) or ≥0.5 (n= 3728). Partialized correlation analyses for sex and BMI-SDS were performed, taking pubertal development into consideration. At baseline, BMI-SDS showed the strongest correlations to sUA (r= 0.35; n= 26 529), HOMA-IR/FI (r= 0.30; n= 5513 /n= 5880), TG/HDL-ratio (r= 0.23; n= 24 501), and WHtR to sUA (r= 0.32; n= 10 805), GGT (r= 0.34; n= 11 862) and Alanine-aminotransferase (ALAT) (r= 0.33; n= 11 821), with stronger correlations in boys (WHtR and GGT: r= 0.36, n= 5793) and prepubertal children (r= 0.36; n= 2216). GGT and sUA (after partializing effects of age, sex, BMI-SDS) showed a correlation to TG/HDL-ratio (r= 0.27; n= 24 501). Following a BMI-SDS reduction ≥0.2 or ≥0.5, GGT was most strongly related to Aspartate-aminotransferase (ASAT)/ ALAT, most evident in prepuberty and with increasing weight loss, and also to TG/HDL-ratio (r= 0.22; n= 1528). Prepubertal children showed strongest correlations between BMI-SDS/WHtR and GGT. ΔBMI-SDS was strongly correlated to ΔsUA (r= 0.30; n= 4160) and ΔGGT (r= 0.28; n= 3562), and ΔWHtR to ΔGGT (r= 0.28; n= 3562) (all p < 0.0001). Abdominal obesity may trigger hyperuricemia and hepatic involvement already in prepuberty. This may be stronger in infancy than anticipated to date. Even moderate weight loss has favourable effects on cardiometabolic risk profile and glucose homeostasis.

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