食品科学 ›› 2018, Vol. 39 ›› Issue (1): 165-171.doi: 10.7506/spkx1002-6630-201801025

• 营养卫生 • 上一篇    下一篇

新琼四糖通过改善肠道微环境对力竭运动小鼠脂质代谢的影响

李 晶,张 娜,宋 佳,毛相朝,薛长湖,唐庆娟*   

  1. 中国海洋大学食品科学与工程学院,山东 青岛 266003
  • 出版日期:2018-01-15 发布日期:2018-01-05
  • 基金资助:
    国家自然科学基金面上项目(31271923);国家自然科学基金联合基金项目(U1406402)

Neoagarotetraose Protects Mice against Exhaustive Exercise-Induced Dyslipidemia by Modulating Gut Microbial Composition and Function

LI Jing, ZHANG Na, SONG Jia, MAO Xiangzhao, XUE Changhu, TANG Qingjuan*   

  1. College of Food Science and Engineering, Ocean University of China, Qingdao 266003, China
  • Online:2018-01-15 Published:2018-01-05

摘要: 目的:研究新琼四糖对力竭运动所致脂质代谢紊乱的调节作用。方法:采用BALB/C雄性小鼠,并将其随 机分为3 组,即正常组、力竭运动组和新琼四糖干预组。本研究采用小鼠转轮式疲劳仪力竭运动模型,力竭运动组 和新琼四糖组小鼠给予力竭运动干预,而正常组保持正常活动。连续喂养16 d后,测定血清血脂指标并无菌收集小 鼠粪便,进行肠道菌群的宏基因组分析。结果显示:力竭运动导致小鼠脂质代谢紊乱,血清总胆固醇、低密度脂蛋 白胆固醇和高密度脂蛋白胆固醇水平显著升高(P<0.05),而甘油三酯水平显著降低(P<0.05)。同时,新琼四 糖能显著改变力竭运动小鼠肠道菌群结构以及菌群功能。总之,新琼四糖可靶向调节肠道菌群结构,改善肠道菌群 脂质代谢通路,调控脂肪酸氧化和脂质合成相关酶,进而缓解力竭运动导致的脂质代谢紊乱。

关键词: 新琼四糖, 力竭运动, 脂质代谢紊乱, 肠道菌群, 宏基因组

Abstract: Purpose: To investigate the possible mechanism of neoagarotetraose (NAT) in regulating lipid metabolism. Methods: Male BALB/C mice were randomly divided into three groups: control group, exhaustive exercise group and NAT intervention group. A wheel-track treadmill was used in this study to propose an exhaustive exercise protocol. The animals in both the exhaustive exercise and NAT groups were subjected to exhaustive exercise, while those in the control group maintained normal physical activity. After sixteen consecutive days of treatment, serum lipid parameters were measured and fecal samples were collected to investigate gut microbiota changes by metagenome sequencing. Our results showed that the concentrations of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) in serum increased sharply (P < 0.05) after exhaustive exercise, while serum triglycerides (TG) concentration decreased significantly (P < 0.05) indicating that exhaustive exercise could be an important cause of lipid metabolism disorder. Our data also showed that NAT treatment resulted in a profound change in the gut microbiome structure, which subsequently led to widespread shifts in its function. Meanwhile, our findings suggested that NAT may protects mice against dyslipidemia induced by exhaustive exercise through modulating the gut microbial composition, improving the lipid metabolism signal pathway of the microbiota, and regulating enzymes activities involved in fatty acid oxidation and lipid synthesis.

Key words: neoagarotetraose, exhaustive exercise, dyslipidemia, gut microbiota, metagenome

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