乳酸片球菌AS185调节高脂高糖饮食诱导的代谢综合征

doi:10.7506/spkx1002-6630-20191202-020

食品科学 ›› 2021, Vol. 42 ›› Issue (1): 215-221.doi: 10.7506/spkx1002-6630-20191202-020

乳酸片球菌AS185调节高脂高糖饮食诱导的代谢综合征

张麟，高磊，王超，赵子健，段翠翠，赵玉娟，杨舸，李盛钰

（1.吉林省农业科学院农产品加工研究所，吉林长春 130033；2.吉林农业大学食品科学与工程学院，吉林长春 130118）

发布日期:2021-01-18
基金资助:
吉林省农业科技创新工程重大项目（CXGC2017ZD011）；现代农业产业技术体系建设专项（CARS-36）；吉林省农业科技创新工程人才基金项目（C92070310）

Pediococcus acidilactici AS185 Improves Metabolic Syndrome Induced by a High-Fat and High-Fructose Diet

ZHANG Lin, GAO Lei, WANG Chao, ZHAO Zijian, DUAN Cuicui, ZHAO Yujuan, YANG Ge, LI Shengyu

(1. Institute of Agro-food Technology, Jilin Academy of Agricultural Sciences, Changchun 130033, China;2. College of Food Science and Engineering, Jilin Agricultural University, Changchun 130118, China)

Published:2021-01-18

摘要/Abstract

摘要： 目的：研究乳酸片球菌（Pediococcus acidilactici）AS185对代谢综合征小鼠的调节作用，并探讨其作用机制。方法：高脂高糖饮食诱导小鼠代谢综合征造模（6 周），灌胃乳酸片球菌AS185，每天1 次，连续8 周，通过测量体质量、血糖浓度、血脂和血清炎症因子水平并进行Western blot检测，评价乳酸片球菌AS185菌株改善代谢综合征的作用和机制。结果：灌胃乳酸片球菌AS185可降低高脂高糖饮食诱导的代谢综合征小鼠血清中总胆固醇、甘油三酯、低密度脂蛋白胆固醇、肿瘤坏死因子-α、白细胞介素-1β、白细胞介素-6、胰岛素、空腹血糖、游离脂肪酸、C-反应蛋白和脂多糖水平。Western blot分析结果表明，乳酸片球菌AS185抑制了高脂高糖诱导的核因子κB蛋白的活化、Toll样受体4（Toll-like receptor 4，TLR4）及髓样分化因子（myeloid differentiation factor 88，MyD88）蛋白的表达，抑制炎症通路和炎症因子的表达。乳酸片球菌AS185通过激活肝组织中肝激酶B1（liver kinase B1，LKB1）和腺苷酸活化蛋白激酶（adenylate activated protein kinase，AMPK）的表达，提高磷酸化AMPK和磷酸化乙酰辅酶A羧化酶蛋白表达，并抑制固醇调节元件结合蛋白1c蛋白的表达，调节脂类代谢通路。结论：乳酸片球菌AS185通过激活TLR4-MyD88-NF-κB通路，降低小鼠血清中的炎症因子的水平，并通过激活LKB1-AMPK信号通路，改善代谢综合征小鼠的血脂紊乱，调节高脂高糖饮食导致的代谢综合征。

关键词: 乳酸菌；乳酸片球菌；代谢综合征；胰岛素抵抗；核因子κB；腺苷酸活化蛋白激酶

Abstract: Objective: To study the regulatory effect and underlying mechanism of Pediococcus acidilactici AS185 on metabolic syndrome (MS) in mice. Methods: ICR mice were given a high-fat and high-fructose diet once a day for 6 consecutive weeks to establish an MS model, and AS185 was administered by gavage to the animals once a day from week 7 to 14. The body mass, blood glucose, blood lipid and serum inflammatory factors were determined and Western blot was performed to analyze the expression of relevant proteins. Results: The administration of P. acidilactici AS185 could reduce the serum levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, insulin (INS), fasting blood glucose (FBG), free fatty acid (FFA), C-reactive protein (CRP) and lipopolysaccharide (LPS) in the mouse model. Western blot analysis showed that P. acidilactici AS185 inhibited the activation of nuclear factor (NF)-κB, and the expression of Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88), suppressed inflammatory signaling pathways and the expression of inflammatory factors in the high-fat and high-fructose diet-fed mice. Moreover, it activated liver kinase B1 (LKB1) and the expression of adenylate activated protein kinase (AMPK), thereby enhancing the expression of phosphorylated AMPK (p-AMPK) and phosphorylated acetyl-CoA carboxylase (p-ACC), down-regulating the expression of sterol regulatory element-binding protein-1c (SREBP-1c) and finally regulating the lipid metabolism pathway. Conclusion: P. acidilactici AS185 can improve high-fat and high-fructose diet-induced metabolic syndrome in mice by activating the TLR4-MyD88-NF-κB pathway to regulate inflammatory factor levels, and activating the LKB1-AMPK signaling pathway to improve blood lipid disorders.

Key words: lactic acid bacteria; Pediococcus acidilactici; metabolic syndrome; insulin resistance; nuclear factor kappa-B; adenylate activated protein kinase

中图分类号:

TS201.3

张麟，高磊，王超，赵子健，段翠翠，赵玉娟，杨舸，李盛钰. 乳酸片球菌AS185调节高脂高糖饮食诱导的代谢综合征[J]. 食品科学, 2021, 42(1): 215-221.

ZHANG Lin, GAO Lei, WANG Chao, ZHAO Zijian, DUAN Cuicui, ZHAO Yujuan, YANG Ge, LI Shengyu. Pediococcus acidilactici AS185 Improves Metabolic Syndrome Induced by a High-Fat and High-Fructose Diet[J]. FOOD SCIENCE, 2021, 42(1): 215-221.

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乳酸片球菌AS185调节高脂高糖饮食诱导的代谢综合征

Pediococcus acidilactici AS185 Improves Metabolic Syndrome Induced by a High-Fat and High-Fructose Diet

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