Excess dietary fructose does not alter gut microbiota or permeability in humans: A pilot randomized controlled study.
Excess dietary fructose does not alter gut microbiota or permeability in humans: A pilot randomized controlled study.
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DOI：
10.1017/cts.2021.801
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发表时间：
2021
影响因子：
2.6
通讯作者：
Holt PR
中科院分区：
文献类型：
--
作者：
Alemán JO;Henderson WA;Walker JM;Ronning A;Jones DR;Walter PJ;Daniel SG;Bittinger K;Vaughan R;MacArthur R;Chen K;Breslow JL;Holt PR
非酒精性脂肪肝病 (NAFLD) 是伴随肥胖和代谢综合征而来的慢性肝病的一个日益增长的原因。过量果糖摄入可能引发或加剧 NAFLD，部分原因是肝脏果糖代谢受损。临床前数据强调，果糖引起的肠道微生物组改变、肠道通透性增加和内毒素血症在 NAFLD 中发挥着重要作用，但人类研究很少。本研究旨在确定两周过量果糖摄入是否会显着改变人类肠道微生物群或通透性。我们对 10 名肥胖受试者（体重指数 [BMI] 30–40 mg/kg/m2）进行了一项试点双盲、交叉代谢单位研究。每组在受试者的个人饮食中添加 75 克果糖或葡萄糖，持续 14 天，以等热量替代复杂碳水化合物，两组之间有 19 天的清除期。该研究的果糖组提供的总果糖摄入量平均占卡路里的 20.1%。结果指标包括粪便微生物群分布、粪便代谢物、肠道通透性、内毒素血症标志物和血浆代谢物。常规血液、尿酸、肝功能和血脂测量结果不受果糖干预的影响。粪便微生物群（包括阿克曼氏菌）、粪便代谢物、肠道通透性、内毒素血症指数、肠道损伤或炎症以及血浆代谢物在两种干预措施中基本没有变化。与啮齿类动物临床前研究结果相反，肥胖人群连续 14 天喂食已知会增强 NAFLD 的果糖，过量果糖不会引起肠道微生物组、代谢组、渗透性以及内毒素血症的变化。
Non-alcoholic fatty liver disease (NAFLD) is an increasing cause of chronic liver disease that accompanies obesity and the metabolic syndrome. Excess fructose consumption can initiate or exacerbate NAFLD in part due to a consequence of impaired hepatic fructose metabolism. Preclinical data emphasized that fructose-induced altered gut microbiome, increased gut permeability, and endotoxemia play an important role in NAFLD, but human studies are sparse. The present study aimed to determine if two weeks of excess fructose consumption significantly alters gut microbiota or permeability in humans. We performed a pilot double-blind, cross-over, metabolic unit study in 10 subjects with obesity (body mass index [BMI] 30–40 mg/kg/m2). Each arm provided 75 grams of either fructose or glucose added to subjects’ individual diets for 14 days, substituted isocalorically for complex carbohydrates, with a 19-day wash-out period between arms. Total fructose intake provided in the fructose arm of the study totaled a mean of 20.1% of calories. Outcome measures included fecal microbiota distribution, fecal metabolites, intestinal permeability, markers of endotoxemia, and plasma metabolites. Routine blood, uric acid, liver function, and lipid measurements were unaffected by the fructose intervention. The fecal microbiome (including Akkermansia muciniphilia), fecal metabolites, gut permeability, indices of endotoxemia, gut damage or inflammation, and plasma metabolites were essentially unchanged by either intervention. In contrast to rodent preclinical findings, excess fructose did not cause changes in the gut microbiome, metabolome, and permeability as well as endotoxemia in humans with obesity fed fructose for 14 days in amounts known to enhance NAFLD.
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影响因子：
14.8
作者：
Pacold ME;Brimacombe KR;Chan SH;Rohde JM;Lewis CA;Swier LJ;Possemato R;Chen WW;Sullivan LB;Fiske BP;Cho S;Freinkman E;Birsoy K;Abu-Remaileh M;Shaul YD;Liu CM;Zhou M;Koh MJ;Chung H;Davidson SM;Luengo A;Wang AQ;Xu X;Yasgar A;Liu L;Rai G;Westover KD;Vander Heiden MG;Shen M;Gray NS;Boxer MB;Sabatini DM
通讯作者：
Sabatini DM
影响因子：
3.7
作者：
Di Luccia B;Crescenzo R;Mazzoli A;Cigliano L;Venditti P;Walser JC;Widmer A;Baccigalupi L;Ricca E;Iossa S
通讯作者：
Iossa S
DOI：
10.1016/j.jcmgh.2015.01.001
发表时间：
2015-03
影响因子：
7.2
作者：
Luther J;Garber JJ;Khalili H;Dave M;Bale SS;Jindal R;Motola DL;Luther S;Bohr S;Jeoung SW;Deshpande V;Singh G;Turner JR;Yarmush ML;Chung RT;Patel SJ
通讯作者：
Patel SJ
影响因子：
5.4
作者：
Kawabata, Katsuto;Kanmura, Shuji;Ido, Akio
通讯作者：
Ido, Akio
影响因子：
5.8
作者：
Hudgins, Lisa C.;Parker, Thomas S.;Hellerstein, Marc K.
通讯作者：
Hellerstein, Marc K.