Reyna Rodríguez-Mortera1, Russell Caccavello2, Ma Eugenia Garay-Sevilla3, Alejandro Gugliucci4. 1. Department of Medical Science, University of Guanajuato, Mexico; Glycation, Oxidation and Disease Laboratory, Dept. of Research, College of Osteopathic Medicine, Touro University California, United States. 2. Glycation, Oxidation and Disease Laboratory, Dept. of Research, College of Osteopathic Medicine, Touro University California, United States. 3. Department of Medical Science, University of Guanajuato, Mexico. 4. Glycation, Oxidation and Disease Laboratory, Dept. of Research, College of Osteopathic Medicine, Touro University California, United States. Electronic address: alejandro.gugliucci@tu.edu.
Abstract
BACKGROUND: We hypothesized that adolescents with obesity have higher remnant B48 concentrations associated with lipoprotein lipase dysregulation. METHODS: Cross-sectional study of 32 adolescents with obesity and 27 control subjects. RESULTS: As compared to lean controls, obese participants showed 35% higher concentrations of apoB48: 3.60 (2.93-4.30) vs 2.65 (1.64-3.68) ng/ml; 28% of apoC-III: (72.7 (58.6-89.7) vs 56.9 (44.8-79.8 ug/ml and 17% ANGPTL 3: (72.2 ± 20.2 vs 61.2 ± 19.2 ng/ml). This was accompanied by a 33% reduction in LPL: 13.1 ± 5.1 vs 18.9 ± 4.7 ng/ml. Obese participants had 25% lower adiponectin 2.9 (1.9-3.8) vs 4.4 (3.2.-5.2) μg/ml; 260% higher leptin 25.7 (11.2-44.8) vs 9.3 (2.8-20.7) ng/ml c and 83% higher Il-6: 2.2 (1.3-5.4) vs 1.2 (0.8-1.4) pg/ml. ApoC-III and ANGPTL3 correlated positively with VAI; ANGPTL3 negatively with HDL-C; LDL size and VLDL-C. ApoB48 correlated negatively with LDL-C. CONCLUSIONS: Adolescents with obesity show higher ANGPTL3 compounded with increased apoC-III associated with increased CR and lower LPL mass. This is associated with inflammation and visceral fat. The significance of these findings resides in that they shed light on a mechanism for TRL dyslipidemia in adolescents: increased LPL inhibition impairs VLDL and chylomicron catabolism leading to atherogenic remnants.
BACKGROUND: We hypothesized that adolescents with obesity have higher remnant B48 concentrations associated with lipoprotein lipase dysregulation. METHODS: Cross-sectional study of 32 adolescents with obesity and 27 control subjects. RESULTS: As compared to lean controls, obese participants showed 35% higher concentrations of apoB48: 3.60 (2.93-4.30) vs 2.65 (1.64-3.68) ng/ml; 28% of apoC-III: (72.7 (58.6-89.7) vs 56.9 (44.8-79.8 ug/ml and 17% ANGPTL 3: (72.2 ± 20.2 vs 61.2 ± 19.2 ng/ml). This was accompanied by a 33% reduction in LPL: 13.1 ± 5.1 vs 18.9 ± 4.7 ng/ml. Obese participants had 25% lower adiponectin 2.9 (1.9-3.8) vs 4.4 (3.2.-5.2) μg/ml; 260% higher leptin 25.7 (11.2-44.8) vs 9.3 (2.8-20.7) ng/ml c and 83% higher Il-6: 2.2 (1.3-5.4) vs 1.2 (0.8-1.4) pg/ml. ApoC-III and ANGPTL3 correlated positively with VAI; ANGPTL3 negatively with HDL-C; LDL size and VLDL-C. ApoB48 correlated negatively with LDL-C. CONCLUSIONS: Adolescents with obesity show higher ANGPTL3 compounded with increased apoC-III associated with increased CR and lower LPL mass. This is associated with inflammation and visceral fat. The significance of these findings resides in that they shed light on a mechanism for TRL dyslipidemia in adolescents: increased LPL inhibition impairs VLDL and chylomicron catabolism leading to atherogenic remnants.