Background and Aims

The role of triglyceride-rich lipoprotein remnants (IDL and chylomicron remnants) in atherosclerosis residual risk is uncontroversial. Albeit, data on adolescents is scarce especially with regards to apoB48 lipoproteins such as chylomicron remnants. We hypothesized that obese adolescents have higher remnant B48 levels associated with lipoprotein lipase dysregulation.

Methods

Cross-sectional study of 29 obese adolescents and 30 controls subjects.

Results

As compared to lean controls, obese participants showed 35% higher levels of apoB48: 3.6 (2.9-4.3) vs 2.6 (1.6-3.6) ug/ml^b; 16% of apoCIII: 72.7 (58.6-89.7) vs 56.9 (44.8-79.8) ug/ml^a and 17% ANGPTL 3: 72 ± 20 vs 61.9 ± 19 ng/ml^a. This was accompanied by a 33% reduction in LPL: 14.4 ± 6.2 vs 21.4 ± 5.5 pg/ml^b. Obese participants had 25% lower adiponectin 2.9 (1.9.2-3. 8.7) vs 4.4 (3.2.9-5.2) ug ml^c; 260% higer leptin 2.5 (1.1.7-4.4.1) vs 9.3 (2.8.1-20.1) ng/ml^d and 83% higher Il-6: 2.2 (1.3-5.4) vs 1.2 (0.8-1.4) pg/ml ^d. Apo CIII and ANGPTL3 correlated with VAI r=0.42^b VAI r=0.40^b respectively. APO CIII correlated negatively with HDL-C r= -0.35^a. ANGPTL3 correlated withVLDL-C,r=0.40^a. ApoB48 correlated with LDL size r=-0.35^b.

Conclusions

Adolescents with obesity show higher fasting chylomicron remnants associated with inflammation, visceral fat and lower LPL and its dysregulation. The latter is evidenced by the increases in its main inhibitor, ANGPTL3, compounded with increased apoCIII which also impairs hepatocyte uptake of remnants. These changes point to a key role of the inhibition of LPL in defective TRL catabolism leading to atherogenic chylomicron remnant accumulation which is already present early in life.

^ap<0.05; ^bp<0.01, ^cp<0.001 ^dp<0.0001