Department of Pediatrics, School of Medicine, Emory University, Atlanta, Georgia, USA.
Department of Pediatrics, School of Medicine, University of Colorado Denver, Aurora, Colorado, USA.
J Clin Invest. 2021 Dec 15;131(24). doi: 10.1172/JCI150996.
BACKGROUNDHepatic de novo lipogenesis (DNL) is elevated in nonalcoholic fatty liver disease (NAFLD). Improvements in hepatic fat by dietary sugar reduction may be mediated by reduced DNL, but data are limited, especially in children. We examined the effects of 8 weeks of dietary sugar restriction on hepatic DNL in adolescents with NAFLD and correlations between DNL and other metabolic outcomes.METHODSAdolescent boys with NAFLD (n = 29) participated in an 8-week, randomized controlled trial comparing a diet low in free sugars versus their usual diet. Hepatic DNL was measured as percentage contribution to plasma triglyceride palmitate using a 7-day metabolic labeling protocol with heavy water. Hepatic fat was measured by magnetic resonance imaging-proton density fat fraction.RESULTSHepatic DNL was significantly decreased in the treatment group (from 34.6% to 24.1%) versus the control group (33.9% to 34.6%) (adjusted week 8 mean difference: -10.6% [95% CI: -19.1%, -2.0%]), which was paralleled by greater decreases in hepatic fat (25.5% to 17.9% vs. 19.5% to 18.8%) and fasting insulin (44.3 to 34.7 vs. 35.5 to 37.0 μIU/mL). Percentage change in DNL during the intervention correlated significantly with changes in free-sugar intake (r = 0.48, P = 0.011), insulin (r = 0.40, P = 0.047), and alanine aminotransferase (ALT) (r = 0.39, P = 0.049), but not hepatic fat (r = 0.13, P = 0.532).CONCLUSIONOur results suggest that dietary sugar restriction reduces hepatic DNL and fasting insulin, in addition to reductions in hepatic fat and ALT, among adolescents with NAFLD. These results are consistent with the hypothesis that hepatic DNL is a critical metabolic abnormality linking dietary sugar and NAFLD.TRIAL REGISTRYClinicalTrials.gov NCT02513121.FUNDINGThe Nutrition Science Initiative (made possible by gifts from the Laura and John Arnold Foundation, Ambrose Monell Foundation, and individual donors), the UCSD Altman Clinical and Translational Research Institute, the NIH, Children's Healthcare of Atlanta and Emory University's Children's Clinical and Translational Discovery Core, Children's Healthcare of Atlanta and Emory University Pediatric Biostatistical Core, the Georgia Clinical and Translational Science Alliance, and the NIH National Institute of Diabetes, Digestive, and Kidney Disease.
非酒精性脂肪性肝病 (NAFLD) 患者的肝从头合成 (DNL) 增加。通过减少饮食中的糖来改善肝脂肪可能与 DNL 减少有关,但数据有限,尤其是在儿童中。我们研究了 8 周饮食中减少糖对青少年 NAFLD 患者肝 DNL 的影响,以及 DNL 与其他代谢结果之间的相关性。
29 名患有 NAFLD 的青少年男性参与了一项为期 8 周的随机对照试验,比较低糖饮食与他们的常规饮食。使用重水 7 天代谢标记方案测量血浆甘油三酯棕榈酸的肝 DNL 百分比贡献。通过磁共振成像质子密度脂肪分数测量肝脂肪。
与对照组(33.9%至 34.6%)相比,治疗组(34.6%至 24.1%)的肝 DNL 显著降低(调整后的第 8 周平均差异:-10.6% [95%CI:-19.1%,-2.0%]),肝脂肪(25.5%至 17.9%对 19.5%至 18.8%)和空腹胰岛素(44.3 至 34.7 对 35.5 至 37.0 μIU/mL)的下降幅度更大。干预期间 DNL 的变化百分比与游离糖摄入量(r = 0.48,P = 0.011)、胰岛素(r = 0.40,P = 0.047)和丙氨酸氨基转移酶(ALT)(r = 0.39,P = 0.049)显著相关,但与肝脂肪(r = 0.13,P = 0.532)无关。
我们的结果表明,饮食中减少糖可降低青少年 NAFLD 患者的肝 DNL 和空腹胰岛素,同时降低肝脂肪和 ALT。这些结果与 DNL 是连接饮食糖和 NAFLD 的关键代谢异常的假设一致。
ClinicalTrials.gov NCT02513121。
营养科学倡议(由 Laura 和 John Arnold 基金会、Ambrose Monell 基金会和个人捐赠者提供)、加州大学圣地亚哥分校阿尔特曼临床和转化研究研究所、NIH、亚特兰大儿童保健和埃默里大学儿童临床和转化发现核心、亚特兰大儿童保健和埃默里大学儿科生物统计学核心、格鲁吉亚临床和转化科学联盟以及 NIH 国家糖尿病、消化和肾脏疾病研究所。