Effects of triglyceride on ER stress and insulin resistance

Do Sung Kim; Seul Ki Jeong; Hyung Ryong Kim; Dal Sik Kim; Soo Wan Chae; Han Jung Chae

doi:10.1016/j.bbrc.2007.08.151

Effects of triglyceride on ER stress and insulin resistance

Do Sung Kim
, Seul Ki Jeong
, Hyung Ryong Kim
, Dal Sik Kim
, Soo Wan Chae
, Han Jung Chae^*

^*Corresponding author for this work

Department of Dentistry

School of Medicine
Jeonbuk National University
School of Dentistry

Research output: Contribution to journal › Journal article › peer-review

48 Scopus citations

Abstract

This study was conducted to examine the mechanism by which triglyceride induces insulin resistance and ER stress in HepG2 cells. Using in vitro study models, we show that triglyceride causes insulin resistance through serine phosphorylation of insulin receptor substrate-1 (IRS-1). In addition, triglyceride induces the expression of endogenous endoplasmic reticulum (ER) stress markers, including GRP 78, IRE-1alpha, XBP-1, p-eIF2alpha, CHOP, and p-JNK. ER stress, in turn, leads to the suppression of insulin receptor signaling through tyrosine dephosphorylation of IRS-1. The results of this study show that triglyceride is a central feature of peripheral insulin resistance, and also suggest that triglyceride-induced ER stress influences insulin resistance. These experiments may be used in the development of an in vitro acute obesity model.

Original language	English
Pages (from-to)	140-145
Number of pages	6
Journal	Biochemical and Biophysical Research Communications
Volume	363
Issue number	1
DOIs	https://doi.org/10.1016/j.bbrc.2007.08.151
State	Published - 2007.11.9

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

ER stress
Insuline resistance
IRS-1
JNK
Triglyceride

Quacquarelli Symonds(QS) Subject Topics

Biological Sciences

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10.1016/j.bbrc.2007.08.151

Cite this

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title = "Effects of triglyceride on ER stress and insulin resistance",

abstract = "This study was conducted to examine the mechanism by which triglyceride induces insulin resistance and ER stress in HepG2 cells. Using in vitro study models, we show that triglyceride causes insulin resistance through serine phosphorylation of insulin receptor substrate-1 (IRS-1). In addition, triglyceride induces the expression of endogenous endoplasmic reticulum (ER) stress markers, including GRP 78, IRE-1alpha, XBP-1, p-eIF2alpha, CHOP, and p-JNK. ER stress, in turn, leads to the suppression of insulin receptor signaling through tyrosine dephosphorylation of IRS-1. The results of this study show that triglyceride is a central feature of peripheral insulin resistance, and also suggest that triglyceride-induced ER stress influences insulin resistance. These experiments may be used in the development of an in vitro acute obesity model.",

keywords = "ER stress, Insuline resistance, IRS-1, JNK, Triglyceride",

author = "Kim, \{Do Sung\} and Jeong, \{Seul Ki\} and Kim, \{Hyung Ryong\} and Kim, \{Dal Sik\} and Chae, \{Soo Wan\} and Chae, \{Han Jung\}",

year = "2007",

month = nov,

day = "9",

doi = "10.1016/j.bbrc.2007.08.151",

language = "English",

volume = "363",

pages = "140--145",

journal = "Biochemical and Biophysical Research Communications",

issn = "0006-291X",

number = "1",

}

TY - JOUR

T1 - Effects of triglyceride on ER stress and insulin resistance

AU - Kim, Do Sung

AU - Jeong, Seul Ki

AU - Kim, Hyung Ryong

AU - Kim, Dal Sik

AU - Chae, Soo Wan

AU - Chae, Han Jung

PY - 2007/11/9

Y1 - 2007/11/9

N2 - This study was conducted to examine the mechanism by which triglyceride induces insulin resistance and ER stress in HepG2 cells. Using in vitro study models, we show that triglyceride causes insulin resistance through serine phosphorylation of insulin receptor substrate-1 (IRS-1). In addition, triglyceride induces the expression of endogenous endoplasmic reticulum (ER) stress markers, including GRP 78, IRE-1alpha, XBP-1, p-eIF2alpha, CHOP, and p-JNK. ER stress, in turn, leads to the suppression of insulin receptor signaling through tyrosine dephosphorylation of IRS-1. The results of this study show that triglyceride is a central feature of peripheral insulin resistance, and also suggest that triglyceride-induced ER stress influences insulin resistance. These experiments may be used in the development of an in vitro acute obesity model.

AB - This study was conducted to examine the mechanism by which triglyceride induces insulin resistance and ER stress in HepG2 cells. Using in vitro study models, we show that triglyceride causes insulin resistance through serine phosphorylation of insulin receptor substrate-1 (IRS-1). In addition, triglyceride induces the expression of endogenous endoplasmic reticulum (ER) stress markers, including GRP 78, IRE-1alpha, XBP-1, p-eIF2alpha, CHOP, and p-JNK. ER stress, in turn, leads to the suppression of insulin receptor signaling through tyrosine dephosphorylation of IRS-1. The results of this study show that triglyceride is a central feature of peripheral insulin resistance, and also suggest that triglyceride-induced ER stress influences insulin resistance. These experiments may be used in the development of an in vitro acute obesity model.

KW - ER stress

KW - Insuline resistance

KW - IRS-1

KW - JNK

KW - Triglyceride

UR - https://www.scopus.com/pages/publications/34548805821

U2 - 10.1016/j.bbrc.2007.08.151

DO - 10.1016/j.bbrc.2007.08.151

M3 - Journal article

C2 - 17868644

AN - SCOPUS:34548805821

SN - 0006-291X

VL - 363

SP - 140

EP - 145

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

IS - 1

ER -

Effects of triglyceride on ER stress and insulin resistance

Abstract

UN SDGs

Keywords

Quacquarelli Symonds(QS) Subject Topics

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