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膳食果糖会导致肝脏中胰岛素信号传导缺陷和神经酰胺积累,而通过调节肠道微生物群可以逆转这种情况。

Dietary fructose causes defective insulin signalling and ceramide accumulation in the liver that can be reversed by gut microbiota modulation.

作者信息

Crescenzo Raffaella, Mazzoli Arianna, Di Luccia Blanda, Bianco Francesca, Cancelliere Rosa, Cigliano Luisa, Liverini Giovanna, Baccigalupi Loredana, Iossa Susanna

机构信息

Department of Biology, Federico II University of Naples, Naples, Italy.

出版信息

Food Nutr Res. 2017 Jun 9;61(1):1331657. doi: 10.1080/16546628.2017.1331657. eCollection 2017.

DOI:10.1080/16546628.2017.1331657
PMID:28659742
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5475320/
Abstract

: The link between metabolic derangement of the gut-2013liver-visceral white adipose tissue (v-WAT) axis and gut microbiota was investigated. : Rats were fed a fructose-rich diet and treated with an antibiotic mix. Inflammation was measured in portal plasma, ileum, liver, and v-WAT, while insulin signalling was analysed by measuring levels of phosphorylated kinase Akt. The function and oxidative status of hepatic mitochondria and caecal microbiota composition were also evaluated. : Ileal inflammation, increase in plasma transaminases, plasma peroxidised lipids, portal concentrations of tumour necrosis factor alpha, lipopolysaccharide, and non-esterified fatty acids, were induced by fructose and were reversed by antibiotic. The increased hepatic ceramide content, inflammation and decreased insulin signaling in liver and v-WAT induced by fructose was reversed by antibiotic. Antibiotic also blunted the increase in hepatic mitochondrial efficiency and oxidative damage of rats fed fructose-rich diet. Three genera, Coprococcus, Ruminococcus, and Clostridium, significantly increased, while the Clostridiaceae family significantly decreased in rats fed a fructose-rich diet, and antibiotic abolished these variations : When gut microbiota modulation by fructose is prevented by antibiotic, inflammatory flow from the gut to the liver and v-WAT are reversed.

摘要

研究了肠道 - 肝脏 - 内脏白色脂肪组织(v - WAT)轴的代谢紊乱与肠道微生物群之间的联系。给大鼠喂食富含果糖的饮食并用抗生素混合物进行处理。在门静脉血浆、回肠、肝脏和v - WAT中测量炎症,同时通过测量磷酸化激酶Akt的水平来分析胰岛素信号传导。还评估了肝脏线粒体的功能和氧化状态以及盲肠微生物群组成。果糖诱导了回肠炎症、血浆转氨酶升高、血浆过氧化脂质、门静脉中肿瘤坏死因子α、脂多糖和非酯化脂肪酸浓度升高,而抗生素可逆转这些变化。抗生素还逆转了果糖诱导的肝脏神经酰胺含量增加、炎症以及肝脏和v - WAT中胰岛素信号传导降低。抗生素还减弱了喂食富含果糖饮食的大鼠肝脏线粒体效率的增加和氧化损伤。在喂食富含果糖饮食的大鼠中,粪球菌属、瘤胃球菌属和梭菌属三个属显著增加,而梭菌科显著减少,抗生素消除了这些变化。当抗生素阻止果糖对肠道微生物群的调节时,从肠道到肝脏和v - WAT的炎症流会逆转。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1231/5475320/867d71841d3c/zfnr_a_1331657_f0005_c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1231/5475320/b67ef5032c1c/zfnr_a_1331657_f0001_b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1231/5475320/08594beb1e72/zfnr_a_1331657_f0002_c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1231/5475320/53d912d6e2ed/zfnr_a_1331657_f0004_b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1231/5475320/867d71841d3c/zfnr_a_1331657_f0005_c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1231/5475320/b67ef5032c1c/zfnr_a_1331657_f0001_b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1231/5475320/08594beb1e72/zfnr_a_1331657_f0002_c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1231/5475320/53d912d6e2ed/zfnr_a_1331657_f0004_b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1231/5475320/867d71841d3c/zfnr_a_1331657_f0005_c.jpg

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