Plasma advanced glycation end products are decreased in obese children compared with lean controls.
OBJECTIVE
In obesity, the combined effects of enhanced food consumption, enhanced oxidative stress and microinflammation could augment the advanced glycation end products (AGEs) accumulation in plasma. We compared the plasma concentrations of AGEs and the soluble receptor for AGEs (sRAGE) in relation to markers of oxidative stress, microinflammation and renal function in obese and lean children/adolescents.


METHODS
In 18 apparently healthy obese children/adolescents (7 females/11 males; age: 5-18 years; body mass index, BMI: 27.3+/-3.3 kg/m2) and 18 healthy lean controls (10 females/8 males; age: 4-17 years, BMI: 22.4+/-2.1 kg/m2) the plasma concentration of N(epsilon)-carboxymethyllysine (CML), fructoselysine (FL), AGE-associated fluorescence, sRAGE, high sensitive-C-reactive protein (hsCRP), interleukin-6 (IL-6) and urinary 8-hydroxy-2-deoxyguanosine (U-8-OHdG) excretion, plasma advanced oxidation protein products (AOPPs), renal function, and the HOMA index of insulin resistance were determined.


RESULTS
Obese children/adolescents had significantly lower concentrations of plasma FL (6.8+/-0.3 mmol/mol lysine vs. 7.7+/-0.3, p<0.02), CML (0.14+/-0.03 mmol/mol lysine vs. 0.22+/-0.04, p<0.001), and fluorescent AGEs (223+/-37 arbitrary units (AU) vs. 318+/-64, p<0.01) than their lean counterparts. Plasma sRAGE concentration did not differ (2.3+/-0.6 ng/ml vs. 2.6+/-0.6). Obese children/adolescents were more insulin-resistant (HOMA index: p<0.01), exhibited higher levels of markers of inflammation (hs-CRP: p<0.03; IL-6: p<0.02), of oxidative stress (AOPPs: p<0.05; 8-OHdG: p<0.04) and had a higher creatinine clearance (p<0.01) and proteinuria (p<0.01).


CONCLUSIONS
We present the first evidence that childhood/adolescent obesity is characterized by lower plasma AGE levels, despite lower insulin sensitivity, enhanced oxidative stress and microinflammation. An enhanced removal of AGE peptides via hyperfiltration may partially contribute to the lower plasma AGE levels.
Sebeková
Katarĺna
K
Department of Clinical and Experimental Pharmacotherapy, Slovak Medical University, Limbová 14, Bratislava 833 03, Slovakia. katarina.sebekova@szu.sk
Somoza
Veronika
V
Jarcusková
Monika
M
Heidland
August
A
Podracká
Ludmila
L
D000080242:8-Hydroxy-2'-Deoxyguanosine; D000293:Adolescent; D015415:Biomarkers / Q000097:blood / Q000652:urine; D001786:Blood Glucose / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000652:urine; D005260:Female; D005453:Fluorescence; D017127:Glycation End Products, Advanced / Q000097:blood*; D006801:Humans; D007249:Inflammation / Q000097:blood*; D007328:Insulin / Q000097:blood; D007668:Kidney / Q000502:physiology; D008239:Lysine / Q000031:analogs & derivatives / Q000097:blood; D008297:Male; D050177:Overweight / Q000097:blood*; D018384:Oxidative Stress; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000097:blood*
D015415:Biomarkers; D001786:Blood Glucose; D017127:Glycation End Products, Advanced; D007328:Insulin; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic; C033186:fructosyl-lysine; D000080242:8-Hydroxy-2'-Deoxyguanosine; D002097:C-Reactive Protein; D003849:Deoxyguanosine; D008239:Lysine