Chan Ruth, Wong Vincent Wai-Sun, Chu Winnie Chiu-Wing, Wong Grace Lai-Hung, Li Liz Sin, Leung Jason, Chim Angel Mei-Ling, Yeung David Ka-Wai, Sea Mandy Man-Mei, Woo Jean, Chan Francis Ka-Leung, Chan Henry Lik-Yuen
Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong, China; Centre for Nutritional Studies, The Chinese University of Hong Kong, Hong Kong, China.
Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong, China; Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, China.
PLoS One. 2015 Apr 23;10(4):e0122406. doi: 10.1371/journal.pone.0122406. eCollection 2015.
Nonalcoholic fatty liver disease (NAFLD) has been associated with reduced growth hormone levels and signaling. Such hormonal changes also occur in metabolic acidosis. Since mild metabolic acidosis can be diet induced, diet-induced acid load may constitute a nutritional factor with possible influence on NAFLD development. This study explored whether a higher diet-induced acid load is associated with an increased likelihood of NAFLD. Apparently healthy Chinese adults (330 male, 463 female) aged 19-72 years were recruited through population screening between 2008 and 2010 in a cross-sectional population-based study in Hong Kong. Estimated net endogenous acid production (NEAP) was calculated using Frassetto's method and potential renal acid load (PRAL) was calculated using Remer's method based on dietary data from a food frequency questionnaire. NAFLD was defined as intrahepatic triglyceride content at >5% by proton-magnetic resonance spectroscopy. Possible advanced fibrosis was defined as liver stiffness at >7.9 kPa by transient elastography. Multivariate logistic regression models were used to examine the association between each measure of dietary acid load and prevalent NAFLD or possible advanced fibrosis with adjustment for potential anthropometric and lifestyle factors. 220 subjects (27.7%) were diagnosed with NAFLD. Estimated NEAP was positively associated with the likelihood of having NAFLD after adjustment for age, sex, body mass index, current drinker status and the presence of metabolic syndrome [OR (95% CI) = 1.25 (1.02-1.52), p = 0.022]. The association was slightly attenuated but remained significant when the model was further adjusted for other dietary variables. No association between PRAL and NAFLD prevalence was observed. Both estimated NEAP and PRAL were not associated with the presence of possible advance fibrosis. Our findings suggest that there may be a modest association between diet-induced acid load and NAFLD. More studies are needed to ascertain the link between diet-induced acid load and NAFLD and to investigate the underlying mechanisms.
非酒精性脂肪性肝病（NAFLD）与生长激素水平降低及信号传导减少有关。这种激素变化在代谢性酸中毒中也会出现。由于轻度代谢性酸中毒可能由饮食引起，饮食诱导的酸负荷可能构成一个对NAFLD发展有潜在影响的营养因素。本研究探讨了较高的饮食诱导酸负荷是否与NAFLD发生可能性增加相关。在2008年至2010年期间，通过人群筛查在香港进行的一项基于人群的横断面研究中，招募了年龄在19至72岁之间、表面健康的中国成年人（330名男性，463名女性）。使用弗拉塞托方法计算估计的内源性净酸产生量（NEAP），并根据食物频率问卷中的饮食数据，使用雷默方法计算潜在肾酸负荷（PRAL）。NAFLD定义为质子磁共振波谱显示肝内甘油三酯含量>5%。可能的晚期纤维化定义为瞬时弹性成像显示肝脏硬度>7.9 kPa。使用多变量逻辑回归模型来检验饮食酸负荷的各项指标与现患NAFLD或可能的晚期纤维化之间的关联，并对潜在的人体测量和生活方式因素进行调整。220名受试者（27.7%）被诊断为NAFLD。在对年龄、性别、体重指数、当前饮酒状况和代谢综合征的存在进行调整后，估计的NEAP与患NAFLD的可能性呈正相关[比值比（95%置信区间）= 1.25（1.02 - 1.52），p = 0.022]。当模型进一步针对其他饮食变量进行调整时，这种关联略有减弱但仍具有显著性。未观察到PRAL与NAFLD患病率之间的关联。估计的NEAP和PRAL均与可能的晚期纤维化的存在无关。我们的研究结果表明，饮食诱导的酸负荷与NAFLD之间可能存在适度关联。需要更多研究来确定饮食诱导的酸负荷与NAFLD之间的联系，并研究其潜在机制。
