Literature DB >> 34850317

Clinical investigation of lipopolysaccharide in the persistence of metabolic syndrome (MS) through the activation of GRP78-IRE1α-ASK1 signaling pathway.

Xiangyu Wang1, Huaping Zhang2, Pengfu Zhang1, Shulan Hao1, Xi Yang3, Xin Zhou4.   

Abstract

OBJECTIVE: Endoplasmic reticulum stress (ERS) might play a pivotal role in the persistence of metabolic syndrome (MS). Lipopolysaccharide (LPS) derived from various gram-negative bacteria could result in the ERS. Therefore, we aimed to investigate the association between LPS and ERS in MS.
METHOD: We enrolled 86 patients with MS and 42 healthy people aged 35-65 years. Body weight, waist circumference, blood pressure were measured. LPS, LBP and inflammation factors, fasting plasma glucose (FPG), insulin, total cholesterol (TC), triglyceride, high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), free fatty acid (FFA) were analyzed in blood plasma of patient's cohort. Body mass index (BMI) and HOMA-IR were calculated. The mRNA and protein expression of ERS GRP78, IRE1α, ASK1 and IKKβ, JNK1 were measured in blood plasma of patient's cohort by RT-PCR and Elisa. MS was defined by the updated National Cholesterol Education Program Adult Treatment Panel III criterion for Asian Americans.
RESULTS: BMI, waist circumference, blood pressure, FPG, insulin, HOMA-IR, TC, triglyceride, HDL-C, LDL-C, FFA and LPS, LBP, TNF-α, CRP, IL-1, IL-6, MCP-1 were significantly higher in patients with MS than healthy people (P < 0.001). The correlation analysis suggested that LPS were associated with TNF-α, IL-1, IL-6, MCP-1, LBP, FFA, HOMA-IR potently (P < 0.05). The marker gene and protein expressions of ERS (GRP78, IRE1α, ASK1, IKKβ and JNK) were significantly overexpressed in patients with MS and were positive correlation with LPS (P < 0.05).
CONCLUSION: LPS may play an important role in mediating chronic low-grade inflammation by activating the ERS GRP78-IRE1α-ASK1 signaling pathway, contributing to the persistence of MS.
© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

Entities:  

Keywords:  Endoplasmic reticulum (ER) stress; Inflammation; Insulin resistance; Lipopolysaccharide (LPS)

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Year:  2021        PMID: 34850317     DOI: 10.1007/s11010-021-04302-2

Source DB:  PubMed          Journal:  Mol Cell Biochem        ISSN: 0300-8177            Impact factor:   3.396


  2 in total

1.  Hepatotoxicity Induced by Isoniazid-Lipopolysaccharide through Endoplasmic Reticulum Stress, Autophagy, and Apoptosis Pathways in Zebrafish.

Authors:  Yun Zhang; Juan Cen; Zhili Jia; Chung-Der Hsiao; Qing Xia; Xue Wang; Xiqiang Chen; Rongchun Wang; Zhenzhou Jiang; Luyong Zhang; Kechun Liu
Journal:  Antimicrob Agents Chemother       Date:  2019-04-25       Impact factor: 5.191

2.  Mechanisms of impaired pancreatic β‑cell function in high‑fat diet‑induced obese mice: The role of endoplasmic reticulum stress.

Authors:  Xiaoqing Yi; Xuan Cai; Sisi Wang; Yanfeng Xiao
Journal:  Mol Med Rep       Date:  2020-03-05       Impact factor: 2.952

  2 in total

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