Abstract P080: Fructose Acutely Increases Size of Very Low Density Lipoprotein In Adolescents With Hepatic Steatosis

Abstract

Introduction: Cardiovascular complications are a leading cause of mortality in nonalcoholic fatty liver disease (NAFLD). Fructose has been reported to be associated with dyslipidemia and increased cardiovascular risk in adults but its impact on adolescents with NAFLD is not well understood. We previously demonstrated that fructose disproportionately increased postprandial hypertriglyceridemia in pediatric NAFLD as compared to healthy children. However, the mechanism remains unclear.

Hypothesis: We hypothesized that fructose would contribute to hypertriglyceridemia in pediatric NAFLD by increasing the size of VLDL particles.

Methods: We examined the acute response to a single dose of fructose beverage in 50 Hispanic-American obese adolescents with varying degrees of hepatic steatosis. Those with hepatic fat >5% on MRI imaging were designated as presumed NAFLD. Subjects consumed a 12oz drink containing 33g of fructose and plasma samples were collected at baseline and 30, 60, and 90 minutes afterwards. Plasma lipoproteins were measured using NMR (Liposcience, Raleigh, NC).

Results: In response to acute fructose load, subjects without NAFLD increased the total number of TG rich lipoprotein particles (p = 0.047). However, this increase was not observed in subjects with NAFLD; instead, they increased the subpopulation of large VLDL particles (p = 0.008) and the mean size of VLDL particles (p = 0.004) (Figure 1). In line with this finding, TG-to-apoB ratio significantly increased in subjects with NAFLD (2.25 ± 0.26 to 2.37 ± 0.25, p = 0.031) but not in non-NAFLD.

Conclusions: These findings demonstrate that adolescents with NAFLD have more atherogenic, large VLDL in response to fructose compared to obese adolescents without NAFLD. Dietary fructose restriction may be a critical component in the treatment of NAFLD associated cardiovascular disease and should be tested further.