Department of Nutrition and Dietetics, School of Health Science and Education, Harokopio University of Athens, 70 El Venizelou Ave, 17671, Athens, Greece.
First Department of Propaedeutic Medicine, School of Medicine, National and Kapodistrian University of Athens, Laiko General Hospital, 11527, Athens, Greece.
Eur J Nutr. 2019 Jun;58(4):1463-1473. doi: 10.1007/s00394-018-1675-4. Epub 2018 Mar 24.
Non-alcoholic fatty liver disease (NAFLD) is a complex disease, resulting from a variety of genetic and environmental factors. The aim of this case-control study was to evaluate the effect of selected genetic polymorphisms, nutrition aspects and their interaction on the risk of NAFLD.
The sample consisted of 134 patients with NAFLD and 217 controls. Disease was diagnosed by liver ultrasound and volunteers were clinically and nutritionally assessed. Food groups were extracted from a 172 food-item FFQ questionnaire. Three genetic polymorphisms were assessed: PNPLA3 rs738409, TM6SF2 rs58542926 and GCKR rs780094.
We replicated the effect of previously reported risk factors for NAFLD, such as elevated liver enzymes, obesity and metabolic syndrome. Food groups rich in simple sugars, fat and especially saturated fat were positively associated with NAFLD risk, whereas food groups rich in polyunsaturated fatty acids were reversely associated with the possibility of developing the disease (p < 0.05). Only the PNPLA3 genetic variant was statistically significantly associated with the disease (p = 0.015). However, it was found that a one-portion increase in fish intake increased the risk of NAFLD in carriers of the risk allele of TM6SF2 rs58542926 polymorphism compared to non-carriers, after adjusting for age, gender, energy intake, pack-years, PAL, TM6SF2 genotype and fish consumption (OR = 1.503, 95% CI 1.094-2.064).
Fish intake exerts an additive effect on NAFLD risk for carriers of the TM6SF2 polymorphism. This novel finding provides further rationale on the need for personalized nutritional advice, based on the genetic background of NAFLD patients.
非酒精性脂肪性肝病（NAFLD）是一种复杂的疾病，由多种遗传和环境因素导致。本病例对照研究旨在评估特定遗传多态性、营养方面及其相互作用对 NAFLD 风险的影响。
该样本包括 134 名 NAFLD 患者和 217 名对照。通过肝脏超声诊断疾病，志愿者进行临床和营养评估。从包含 172 种食物的 FFQ 问卷中提取食物组。评估了三种遗传多态性：PNPLA3 rs738409、TM6SF2 rs58542926 和 GCKR rs780094。
我们复制了先前报道的 NAFLD 风险因素的影响，如升高的肝酶、肥胖和代谢综合征。富含单糖、脂肪特别是饱和脂肪的食物组与 NAFLD 风险呈正相关，而富含多不饱和脂肪酸的食物组与患该病的可能性呈负相关（p<0.05）。只有 PNPLA3 遗传变异与该疾病具有统计学显著相关性（p=0.015）。然而，发现与非携带者相比，携带 TM6SF2 rs58542926 多态性风险等位基因的个体中，鱼类摄入量每增加一份，NAFLD 的风险就会增加，调整年龄、性别、能量摄入、吸烟包年数、PAL、TM6SF2 基因型和鱼类摄入量后（OR=1.503，95%CI 1.094-2.064）。
对于携带 TM6SF2 多态性的个体，鱼类摄入对 NAFLD 风险具有附加效应。这一新发现为基于 NAFLD 患者的遗传背景提供了个性化营养建议的必要性提供了更多依据。
