Background: Adipocyte fatty acid binding protein (aFABP) regulates intracellular transport of fatty acids and seems to be involved in the pathogenesis of the Metabolic Syndrome. aFABP overproduction leads to increased cholesterol and triglyceride accumulation and to higher expression of pro-inflammatory genes. In adults aFABP seems to promote insulin resistance and atherosclerosis, and aFABP levels are significantly higher in obese compared to lean subjects. Fat mass, lipid markers and inflammatory markers are also associated with aFABP levels. However, metabolism of aFABP in children/adolescents is poorly understood.
Objective and hypotheses: We investigated the correlation between circulating aFABP and several markers of weight status and of metabolic risk in a well characterized cohort of overweight or obese adolescents.
Method: 28 adolescents aged 13.518.5 years with a BMI≧90th percentile according to national reference values were included. Weight, height, waist and hip circumferences were measured following standardized procedures, and a fasting blood sample was taken to measure insulin, glucose, transaminases, lipids, free fatty acids, uric acid and aFABP. Pearsons correlation and linear models were determined using the R package.
Results: aFABP was correlated with BMI-SDS (0.48 (0.13, 0.72); P=0.0095) and waist-to-height ratio (WHtR) (0.63 (0.33, 0.81), P=0.00036). A correlation was also observed with HOMA-IR (0.52 (0.19, 0.75), P=0.0044) and the dependence remained significant after correcting for sex and pubertal stage. Some markers of metabolic risk were significantly correlated (γGT 0.48 (0.13, 0.73), P=0.0091; uric acid 0.46 (0.11, 0.71) P=0.013; HDL-C −0.39 (−0.66, −0.01) P=0.043; triglycerides 0.38 (0.01, 0.66), P=0.047), whereas others were not (cholesterol P=0.32; LDL-C P=0.12; free fatty acids P=0.68). aFABP did not depend on gender, age or pubertal stage in obese adolescents.
Conclusion: Our data provide evidence that aFABP in obese adolescents as in adults is associated with weight status as well as insulin resistance and metabolic risk markers.
Funding: This work was supported by the Federal Ministry of Education and Research, Germany (Integrated Research and Treatment Center IFB AdiposityDiseases, FKZ: 01EO1001).
01 - 03 Oct 2015
European Society for Paediatric Endocrinology