High-fructose diet induced changes in gut microbiota structure and function, which have been linked to inflammatory response. However, the effect of small or appropriate doses of fructose on gut microbiota and inflammatory cytokines is not fully understood. Hence, the abundance changes of gut microbiota in fructose-treated Sprague-Dawley rats were analyzed by 16S rRNA sequencing. The effects of fructose diet on metabolic disorders were evaluated by blood biochemical parameter test, histological analysis, short-chain fatty acid (SCFA) analysis, ELISA analysis, and Western blot. Rats were intragastrically administered with pure fructose at the dose of 0 (Con), 2.6 (Fru-L), 5.3 (Fru-M), and 10.5 g/kg/day (Fru-H) for 20 weeks. The results showed that there were 36.5% increase of uric acid level in the Fru-H group when compared with the Con group. The serum proinflammatory cytokines (IL-6, TNF-α, and MIP-2) were significantly increased (), and the anti-inflammatory cytokine IL-10 was significantly decreased () with fructose treatment. A higher fructose intake induced lipid accumulation in the liver and inflammatory cell infiltration in the pancreas and colon and increased the abundances of Lachnospira, Parasutterella, Marvinbryantia, and Blantia in colonic contents. Fructose intake increased the expressions of lipid accumulation proteins including perilipin-1, ADRP, and Tip-47 in the colon. Moreover, the higher level intake of fructose impaired intestinal barrier function due to the decrease of the expression of tight junction proteins (ZO-1 and occludin). In summary, there were no negative effects on body weight, fasting blood glucose, gut microbiota, and SCFAs in colonic contents of rats when fructose intake is in small or appropriate doses. High intake of fructose can increase uric acid, proinflammatory cytokines, intestinal permeability, and lipid accumulation in the liver and induce inflammatory response in the pancreas and colon.

中文翻译：

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高果糖饮食会增加大鼠的炎症细胞因子并改变肠道微生物群的组成

高果糖饮食引起肠道微生物群结构和功能的变化，这与炎症反应有关。然而，小剂量或适当剂量的果糖对肠道微生物群和炎症细胞因子的影响尚不完全清楚。因此，通过 16S rRNA 测序分析了果糖处理的 Sprague-Dawley 大鼠肠道微生物群的丰度变化。通过血液生化参数测试、组织学分析、短链脂肪酸（SCFA）分析、ELISA分析和蛋白质印迹评估果糖饮食对代谢紊乱的影响。大鼠以 0 (Con)、2.6 (Fru-L)、5.3 (Fru-M) 和 10.5 g/kg/天 (Fru-H) 的剂量与纯果糖一起灌胃给药 20 周。结果显示，与Con组相比，Fru-H组的尿酸水平升高了36.5%。α和 MIP-2) 显着增加 ()，并且抗炎细胞因子 IL-10 显着降低 ()果糖处理。较高的果糖摄入量会导致肝脏中的脂质积累和胰腺和结肠中的炎性细胞浸润，并增加毛螺菌属、 Parasutterella、 Marvinbryantia和Blantia的丰度。在结肠内容物中。果糖摄入增加了脂质积累蛋白的表达，包括结肠中的 perilipin-1、ADRP 和 Tip-47。此外，由于紧密连接蛋白（ZO-1 和 occludin）的表达降低，较高水平的果糖摄入会损害肠道屏障功能。总之，当果糖摄入量较小或适当时，对大鼠的体重、空腹血糖、肠道微生物群和结肠内容物中的 SCFA 没有负面影响。大量摄入果糖会增加尿酸、促炎细胞因子、肠道通透性和肝脏中的脂质积累，并诱发胰腺和结肠的炎症反应。