Yu Renqiang, Yin Yongxiang, Cao Minkai, Ye Danni, Zhang Yinghui, Zhou Qin, Mei Yingzi
Department of Neonatology, The Affiliated Wuxi Maternity and Child Health Care Hospital of Nanjing Medical University, Wuxi, China.
Department of Pathology, The Affiliated Wuxi Maternity and Child Health Care Hospital of Nanjing Medical University, Wuxi, China.
J Int Med Res. 2020 Apr;48(4):300060519896714. doi: 10.1177/0300060519896714. Epub 2019 Dec 31.
This study aimed to investigate the effects of fructo-oligosaccharides (FOS) on serum lipid levels and to determine the mechanisms underlying these effects and the potential role of inflammation.
Male C57BL/6 mice received a normal diet, a high-fat/high-sugar (HFS) diet, or an HFS diet supplemented with 10% FOS for 10 weeks. intestinal and serum short-chain fatty acid (SCFA) levels were measured by gas chromatography. serum levels of alanine transaminase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL), low-density lipoprotein (LDL), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), 8-hydroxy-2'-deoxyguanosine (8-OHdG), and malonaldehyde (MDA) were also measured. Lipid accumulation was visualized. Reactive oxygen species (ROS) generation was evaluated and apoptosis was quantified.
FOS reversed HFS-induced lipid accumulation in the liver. An HFS diet increased ALT, AST, TC, TG, and LDL serum levels, decreased HDL serum levels, and increased IL-6, TNF-α, 8-OHdG, and MDA levels. These changes were reduced by FOS. FOS also increased intestinal and serum levels of short chain fatty acids (SCFAs). , SCFAs ameliorated palmitic acid-induced ROS production and apoptosis of HepG2 cells.
FOS supplementation lowers serum lipid levels and ameliorates HFS-induced inflammation by upregulating SCFAs.
本研究旨在探讨低聚果糖(FOS)对血清脂质水平的影响,确定这些影响的潜在机制以及炎症的潜在作用。
雄性C57BL/6小鼠分别接受正常饮食、高脂/高糖(HFS)饮食或补充10% FOS的HFS饮食,持续10周。通过气相色谱法测量肠道和血清短链脂肪酸(SCFA)水平。还测量了血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白(HDL)、低密度脂蛋白(LDL)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、8-羟基-2'-脱氧鸟苷(8-OHdG)和丙二醛(MDA)水平。观察脂质积累情况。评估活性氧(ROS)生成并定量细胞凋亡。
FOS逆转了HFS诱导的肝脏脂质积累。HFS饮食增加了ALT、AST、TC、TG和LDL血清水平,降低了HDL血清水平,并增加了IL-6、TNF-α、8-OHdG和MDA水平。FOS减少了这些变化。FOS还增加了肠道和血清中的短链脂肪酸(SCFA)水平。SCFA改善了棕榈酸诱导的HepG2细胞ROS产生和细胞凋亡。
补充FOS可通过上调SCFA降低血清脂质水平并改善HFS诱导的炎症。