(P06-19-26) Dietary Sugar Intake Is Associated With Hepatic Steatosis in Prepubertal Hispanic/Latino Children

Objectives: To examine associations between dietary risk factors and hepatic steatosis (HS) in prepubertal Hispanic/Latino children.

Methods: Cross-sectional study of 128 prepubertal Hispanic/Latino children aged 6-9 y. Hepatic steatosis was measured using MRI-proton density fat fraction (MRI-PDFF), and metabolic-associated steatotic liver disease (MASLD) was defined as HS ≥5% with ≥1 cardiometabolic risk factor. Dietary intake was assessed using 24-hour recalls and analyzed using the Nutrition Data System for Research (NDSR). Seven exposures were examined, including added sugars, free sugars, ultra-processed food (UPF), diet quality, saturated fat, fiber, and vitamin E, using sequential linear regression models adjusting for age and sex (Model 1), body mass index (BMI) z-score (Model 2), and patatin-like phospholipase domain-containing 3 (PNPLA3) genotype (Model 3; primary model). Secondary analyses included logistic regression for MASLD status, sensitivity analyses adjusting for physical activity, and gene-diet interaction testing.

Results: Participants had a mean age of 8.0 ± 1.1 y; 58% were male, 59.4% had obesity, and 35.9% met MASLD criteria. In the fully adjusted primary model, added sugars (β=0.28 per % kcal; 95% CI: 0.05, 0.50; p=0.016) and free sugars (β=0.19 per % kcal; 95% CI: 0.02, 0.35; p=0.027) were positively associated with HS, independent of BMI z-score and PNPLA3 genotype. Both associations remained significant after adjusting for physical activity. In a joint model, added sugars remained independently associated with HS (β=0.29; 95% CI: 0.07, 0.52; p=0.012), while UPF intake was not (p=0.354). No significant dietary exposure by PNPLA3 interaction was detected. Logistic analyses for MASLD were directionally consistent but not statistically significant.

Conclusions: Dietary sugar intake was positively associated with HS in prepubertal Hispanic/Latino children, independent of adiposity and genetic risk. These findings highlight dietary sugar intake as a potential modifiable target to reduce MASLD risk in this high-risk population and warrant longitudinal investigation.

Funding Sources: This work was supported by the NIH and the Georgia Clinical and Translational Science Alliance.