Effect of fructose on markers of non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of controlled feeding trials.

Effect of fructose on markers of non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of controlled feeding trials.
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DOI:
10.1038/ejcn.2014.8
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发表时间:
2014-04
影响因子:
4.7
通讯作者:
--
中科院分区:
医学3区
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--
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在缺乏一致的临床证据的情况下,有人担心果糖会导致非酒精性脂肪肝(NAFLD)。为了确定果糖对NAFLD标志物的影响,我们对控制喂养试验进行了系统回顾和荟萃分析。我们检索了MEDLINE、EMBASE、CINAHL和科克伦图书馆(截至2013年9月3日)。我们纳入了随访时间为107天的相关试验。两名评审员独立提取相关数据。使用随机效应模型,通过通用逆方差法合并数据,并表示为肝细胞内脂质(IHCL)的标准化平均差异(SMD)和丙氨酸氨基转移酶(ALT)的平均差异(MD)。对研究间异质性进行评估(Cochran Q统计)和定量(I2统计)。8份报告符合资格标准,其中包含260名健康参与者的13项试验:7项等热量试验,其中果糖等热量地交换为其他碳水化合物,以及6项高热量试验,其中饮食补充有来自高剂量果糖(+104 - 220 g/天)的过量能量(+21 - 35%能量)。虽然在等热量试验中果糖没有影响,但在高热量试验中果糖增加了IHCL(SMD=0.45(95%置信区间(CI):0.18,0.72))和ALT(MD=4.94 U/l(95% CI:0.03,9.85))。很少有试验可供纳入,其中大多数是小,短(约4周),质量差。果糖与其他碳水化合物的等热量交换不会引起健康参与者的NAFLD变化。然而,在极端剂量下提供过量能量的果糖确实会提高IHCL和ALT,这种效应可能更多地归因于过量能量而不是果糖。需要更大,更长和更高质量的果糖对组织病理学NAFLD变化的影响试验。
In the absence of consistent clinical evidence, there are concerns that fructose contributes to non-alcoholic fatty liver disease (NAFLD). To determine the effect of fructose on markers of NAFLD, we conducted a systematic review and meta-analysis of controlled feeding trials. We searched MEDLINE, EMBASE, CINAHL and the Cochrane Library (through 3 September 2013). We included relevant trials that involved a follow-up of ⩾7 days. Two reviewers independently extracted relevant data. Data were pooled by the generic inverse variance method using random effects models and expressed as standardized mean difference (SMD) for intrahepatocellular lipids (IHCL) and mean difference (MD) for alanine aminotransferase (ALT). Inter-study heterogeneity was assessed (Cochran Q statistic) and quantified (I2 statistic). Eligibility criteria were met by eight reports containing 13 trials in 260 healthy participants: seven isocaloric trials, in which fructose was exchanged isocalorically for other carbohydrates, and six hypercaloric trials, in which the diet was supplemented with excess energy (+21–35% energy) from high-dose fructose (+104–220 g/day). Although there was no effect of fructose in isocaloric trials, fructose in hypercaloric trials increased both IHCL (SMD=0.45 (95% confidence interval (CI): 0.18, 0.72)) and ALT (MD=4.94 U/l (95% CI: 0.03, 9.85)). Few trials were available for inclusion, most of which were small, short (⩽4 weeks), and of poor quality. Isocaloric exchange of fructose for other carbohydrates does not induce NAFLD changes in healthy participants. Fructose providing excess energy at extreme doses, however, does raise IHCL and ALT, an effect that may be more attributable to excess energy than fructose. Larger, longer and higher-quality trials of the effect of fructose on histopathological NAFLD changes are required.
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