1Institute for Innovation and Sustainable Development in Food Chain (IS-FOOD),Public University of Navarra,31006 Pamplona,Spain.
2Nutrition and Metabolism Section,International Agency for Research on Cancer,World Health Organization,69008 Lyon,France.
Br J Nutr. 2019 May;121(10):1158-1165. doi: 10.1017/S0007114519000436. Epub 2019 Mar 5.
Paediatric non-alcoholic fatty liver disease has increased in parallel with childhood obesity. Dietary habits, particularly products rich in sugars, may influence both hepatic fat and insulin resistance (homeostatic model assessment for insulin resistance (HOMA-IR)). The aim of the study was to examine the association of the consumption of foods and food components, dairy desserts and substitutes (DDS), sugar-sweetened beverages (SSB), as well as total and added sugars, with hepatic fat and HOMA-IR. Dietary intake (two non-consecutive 24 h-recalls), hepatic fat (MRI) and HOMA-IR were assessed in 110 overweight/obese children (10·6 (sd 1·1) years old). Linear regression analyses were used to examine the association of dietary intake with hepatic fat and HOMA-IR adjusted for potential confounders (sex, age, energy intake, maternal educational level, total and abdominal adiposity and sugar intake). The results showed that there was a negative association between cereal intake and hepatic fat (β=-0·197, P<0·05). In contrast, both SSB consumption (β=0·217; P=0·028) and sugar in SSB (β=0·210, P=0·035), but not DDS or sugar in DDS or other dietary components, were positively associated with hepatic fat regardless of potential confounders including total sugar intake. In conclusion, cereal intake might decrease hepatic fat, whereas SSB consumption and its sugar content may increase the likelihood of having hepatic steatosis. Although these observations need to be confirmed using experimental evidence, these results suggest that healthy lifestyle intervention programs are needed to improve dietary habits as well as to increase the awareness of the detrimental effects of SSB consumption early in life.
儿科非酒精性脂肪性肝病的发病率与儿童肥胖率呈平行增长。饮食习惯,尤其是富含糖的产品,可能会影响肝脏脂肪和胰岛素抵抗(稳态模型评估胰岛素抵抗(HOMA-IR))。本研究旨在研究消耗食物和食物成分、乳制甜点和替代品(DDS)、含糖饮料(SSB)以及总糖和添加糖与肝脂肪和 HOMA-IR 的关系。在 110 名超重/肥胖儿童(10.6(sd 1.1)岁)中评估了饮食摄入(两次非连续 24 小时回忆)、肝脂肪(MRI)和 HOMA-IR。线性回归分析用于检查饮食摄入与肝脂肪和 HOMA-IR 的关系,调整了潜在混杂因素(性别、年龄、能量摄入、母亲教育水平、总脂肪和腹部肥胖以及糖摄入)。结果表明,谷物摄入量与肝脂肪呈负相关(β=-0.197,P<0.05)。相反,SSB 摄入量(β=0.217;P=0.028)和 SSB 中的糖(β=0.210,P=0.035),而不是 DDS 或 DDS 中的糖或其他饮食成分,与肝脂肪呈正相关,无论潜在的混杂因素包括总糖摄入量如何。总之,谷物摄入可能会降低肝脂肪,而 SSB 的摄入及其糖含量可能会增加发生肝脂肪变性的可能性。尽管这些观察结果需要使用实验证据来证实,但这些结果表明需要开展健康生活方式干预计划,以改善饮食习惯,并提高人们对生命早期 SSB 摄入有害影响的认识。