*School of Exercise and Health Science, Edith Cowan University, Joondalup †Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia, West Perth ‡School of Population Health, University of Western Australia, Crawley §School of Public Health ||School of Medicine and Pharmacology, University of Western Australia, Fremantle ¶Department of Gastroenterology, Fremantle Hospital, Fremantle, Australia.
J Pediatr Gastroenterol Nutr. 2014 May;58(5):624-31. doi: 10.1097/MPG.0000000000000267.
Although obesity is a major risk factor for nonalcoholic fatty liver (NAFL), not all individuals with obesity develop the condition, suggesting that other factors such as diet may also contribute to NAFL development. We evaluated associations between fructose and total sugar intake and subsequent diagnosis of NAFL in adolescents with obesity and without obesity in a population-based cohort.
Adolescents participating in the Western Australian Pregnancy Cohort (Raine) Study completed 3-day food records and body mass index measurement at age 14 years. At age 17 years, participants underwent abdominal ultrasound to determine NAFL status. Multivariable logistic regression models were used to analyse associations between energy-adjusted fructose and total sugar intake and NAFL status. Food diaries and liver assessments were completed for 592 adolescents.
The prevalence of NAFL at age 17 was 12.8% for the total group and 50% for adolescents with obesity. Fructose intake did not significantly differ between adolescents with or without NAFL in our cohort as a whole. Among adolescents with obesity, those without NAFL had significantly lower energy-adjusted fructose intake at age 14 years compared with those with NAFL (mean ± standard deviation [SD] 38.8 ± 19.8 g/day, vs 55.7 ± 14.4 g/day, P = 0.02). Energy-adjusted fructose intake was independently associated with NAFL in adolescents with obesity (OR [odds ratio] 1.09, 95% CI 1.01-1.19, P = 0.03) after the adjustment for confounding factors. Energy-adjusted total sugar intake showed less significance (OR 1.03, 95% CI 0.999-1.07, P = 0.06). No significant associations were observed in other body mass index categories.
Lower fructose consumption in adolescents with obesity at 14 years is associated with a decreased risk of NAFL at 17 years. Fructose rather than overall sugar intake may be more physiologically relevant in this association.
尽管肥胖是导致非酒精性脂肪肝(NAFL)的一个主要危险因素,但并非所有肥胖者都会出现这种情况,这表明其他因素,如饮食,也可能导致 NAFL 的发生。我们在一个基于人群的队列中,评估了肥胖和非肥胖青少年果糖和总糖摄入量与随后 NAFL 诊断之间的关系。
参加西澳大利亚妊娠队列(Raine)研究的青少年在 14 岁时完成了 3 天的食物记录和体重指数测量。在 17 岁时,参与者接受了腹部超声检查以确定 NAFL 状态。多变量逻辑回归模型用于分析能量校正后的果糖和总糖摄入量与 NAFL 状态之间的关系。完成了 592 名青少年的饮食日记和肝脏评估。
整个队列中,17 岁时 NAFL 的患病率为 12.8%,肥胖青少年为 50%。在我们的整个队列中,患有或不患有 NAFL 的青少年之间的果糖摄入量没有显著差异。在肥胖的青少年中,与患有 NAFL 的青少年相比,不患有 NAFL 的青少年在 14 岁时的能量校正果糖摄入量显著较低(平均值±标准差[SD]38.8±19.8 g/天,vs. 55.7±14.4 g/天,P=0.02)。在校正混杂因素后,能量校正的果糖摄入量与肥胖青少年的 NAFL 独立相关(比值比[OR]1.09,95%可信区间[CI]1.01-1.19,P=0.03)。能量校正的总糖摄入量的相关性较小(OR 1.03,95%CI 0.999-1.07,P=0.06)。在其他体重指数类别中未观察到显著相关性。
14 岁肥胖青少年的果糖摄入量较低与 17 岁时 NAFL 的风险降低有关。在这种关联中,果糖而不是总糖摄入量可能与生理更相关。