Chromium (VI) induces insulin resistance in 3T3-L1 adipocytes through elevated reactive oxygen species generation

Xuemei Ge; Zhen Liu; Wei Qi; Xianglin Shi; Qiwei Zhai

doi:10.1080/10715760802155113

Chromium (VI) induces insulin resistance in 3T3-L1 adipocytes through elevated reactive oxygen species generation

Xuemei Ge
, Zhen Liu
, Wei Qi
, Xianglin Shi
, Qiwei Zhai

Toxicology and Cancer Biology

Research output: Contribution to journal › Article › peer-review

12 Scopus citations

Abstract

Reactive oxygen species (ROS) have been proposed to be involved in the development of insulin resistance, although the exact molecular link between ROS and insulin resistance remains to be determined. Chromium (Cr(VI)) is known as an inducer of ROS. Therefore, this study examined whether Cr(VI) could induce insulin resistance. It demonstrated that Cr(VI) treatment significantly inhibited insulin-stimulated glucose uptake and attenuated insulin signalling. Moreover, Cr(VI) treatment markedly increased the intracellular levels of superoxide anion, hydrogen peroxide and hydroxyl radical. N-acetylcysteine, superoxide dismutase and catalase can block the ROS generation and alleviate the insulin resistance induced by Cr(VI) treatment. In addition, Cr(VI) treatment induced endoplasmic reticulum (ER) stress and JNK activation and these effects were diminished by N-acetylcysteine. These results suggested that ROS generation through Cr(VI) treatment cause ER stress, JNK activation and insulin resistance in adipocytes. Therefore, the oxidative stress could be a potential interventional target for insulin-resistance related diseases.

Original language	English
Pages (from-to)	554-563
Number of pages	10
Journal	Free Radical Research
Volume	42
Issue number	6
DOIs	https://doi.org/10.1080/10715760802155113
State	Published - Jun 2008

Bibliographical note

Funding Information:
This study was supported by grants from National Natural Science Foundation of China (30570558, 30671775 and 30271124) and PLA (02M003), the Chinese Academy of Sciences (KSCX2-YW-N-034 and KSCX1-YW-02), National Basic Research Program of China (973 Program, 2006CB503900 and 2007CB914501), the Science and Technology Commission of Shanghai Municipality (06DZ19021) and the Knowledge Innovation Program of Shanghai Institutes for Biological Sciences (2007KIP103). Q. Zhai is a scholar of the Hundred Talents Program from Chinese Academy of Sciences.

Funding

This study was supported by grants from National Natural Science Foundation of China (30570558, 30671775 and 30271124) and PLA (02M003), the Chinese Academy of Sciences (KSCX2-YW-N-034 and KSCX1-YW-02), National Basic Research Program of China (973 Program, 2006CB503900 and 2007CB914501), the Science and Technology Commission of Shanghai Municipality (06DZ19021) and the Knowledge Innovation Program of Shanghai Institutes for Biological Sciences (2007KIP103). Q. Zhai is a scholar of the Hundred Talents Program from Chinese Academy of Sciences.

Funders	Funder number
National Natural Science Foundation of China (NSFC)	30570558, 30271124, 02M003, 30671775
Chinese Academy of Sciences	KSCX1-YW-02, KSCX2-YW-N-034
Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences	2007KIP103
Science and Technology Commission of Shanghai Municipality	06DZ19021
National Key Research and Development Program of China	2007CB914501, 2006CB503900

Keywords

Cr(VI)
ER stress
Insulin resistance
JNK
ROS

ASJC Scopus subject areas

Biochemistry

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10.1080/10715760802155113

Cite this

@article{51a6bd073ef04dbfb87df15fa1ab73d1,

title = "Chromium (VI) induces insulin resistance in 3T3-L1 adipocytes through elevated reactive oxygen species generation",

abstract = "Reactive oxygen species (ROS) have been proposed to be involved in the development of insulin resistance, although the exact molecular link between ROS and insulin resistance remains to be determined. Chromium (Cr(VI)) is known as an inducer of ROS. Therefore, this study examined whether Cr(VI) could induce insulin resistance. It demonstrated that Cr(VI) treatment significantly inhibited insulin-stimulated glucose uptake and attenuated insulin signalling. Moreover, Cr(VI) treatment markedly increased the intracellular levels of superoxide anion, hydrogen peroxide and hydroxyl radical. N-acetylcysteine, superoxide dismutase and catalase can block the ROS generation and alleviate the insulin resistance induced by Cr(VI) treatment. In addition, Cr(VI) treatment induced endoplasmic reticulum (ER) stress and JNK activation and these effects were diminished by N-acetylcysteine. These results suggested that ROS generation through Cr(VI) treatment cause ER stress, JNK activation and insulin resistance in adipocytes. Therefore, the oxidative stress could be a potential interventional target for insulin-resistance related diseases.",

keywords = "Cr(VI), ER stress, Insulin resistance, JNK, ROS",

author = "Xuemei Ge and Zhen Liu and Wei Qi and Xianglin Shi and Qiwei Zhai",

note = "Funding Information: This study was supported by grants from National Natural Science Foundation of China (30570558, 30671775 and 30271124) and PLA (02M003), the Chinese Academy of Sciences (KSCX2-YW-N-034 and KSCX1-YW-02), National Basic Research Program of China (973 Program, 2006CB503900 and 2007CB914501), the Science and Technology Commission of Shanghai Municipality (06DZ19021) and the Knowledge Innovation Program of Shanghai Institutes for Biological Sciences (2007KIP103). Q. Zhai is a scholar of the Hundred Talents Program from Chinese Academy of Sciences.",

year = "2008",

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doi = "10.1080/10715760802155113",

language = "English",

volume = "42",

pages = "554--563",

number = "6",

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TY - JOUR

T1 - Chromium (VI) induces insulin resistance in 3T3-L1 adipocytes through elevated reactive oxygen species generation

AU - Ge, Xuemei

AU - Liu, Zhen

AU - Qi, Wei

AU - Shi, Xianglin

AU - Zhai, Qiwei

N1 - Funding Information: This study was supported by grants from National Natural Science Foundation of China (30570558, 30671775 and 30271124) and PLA (02M003), the Chinese Academy of Sciences (KSCX2-YW-N-034 and KSCX1-YW-02), National Basic Research Program of China (973 Program, 2006CB503900 and 2007CB914501), the Science and Technology Commission of Shanghai Municipality (06DZ19021) and the Knowledge Innovation Program of Shanghai Institutes for Biological Sciences (2007KIP103). Q. Zhai is a scholar of the Hundred Talents Program from Chinese Academy of Sciences.

PY - 2008/6

Y1 - 2008/6

N2 - Reactive oxygen species (ROS) have been proposed to be involved in the development of insulin resistance, although the exact molecular link between ROS and insulin resistance remains to be determined. Chromium (Cr(VI)) is known as an inducer of ROS. Therefore, this study examined whether Cr(VI) could induce insulin resistance. It demonstrated that Cr(VI) treatment significantly inhibited insulin-stimulated glucose uptake and attenuated insulin signalling. Moreover, Cr(VI) treatment markedly increased the intracellular levels of superoxide anion, hydrogen peroxide and hydroxyl radical. N-acetylcysteine, superoxide dismutase and catalase can block the ROS generation and alleviate the insulin resistance induced by Cr(VI) treatment. In addition, Cr(VI) treatment induced endoplasmic reticulum (ER) stress and JNK activation and these effects were diminished by N-acetylcysteine. These results suggested that ROS generation through Cr(VI) treatment cause ER stress, JNK activation and insulin resistance in adipocytes. Therefore, the oxidative stress could be a potential interventional target for insulin-resistance related diseases.

AB - Reactive oxygen species (ROS) have been proposed to be involved in the development of insulin resistance, although the exact molecular link between ROS and insulin resistance remains to be determined. Chromium (Cr(VI)) is known as an inducer of ROS. Therefore, this study examined whether Cr(VI) could induce insulin resistance. It demonstrated that Cr(VI) treatment significantly inhibited insulin-stimulated glucose uptake and attenuated insulin signalling. Moreover, Cr(VI) treatment markedly increased the intracellular levels of superoxide anion, hydrogen peroxide and hydroxyl radical. N-acetylcysteine, superoxide dismutase and catalase can block the ROS generation and alleviate the insulin resistance induced by Cr(VI) treatment. In addition, Cr(VI) treatment induced endoplasmic reticulum (ER) stress and JNK activation and these effects were diminished by N-acetylcysteine. These results suggested that ROS generation through Cr(VI) treatment cause ER stress, JNK activation and insulin resistance in adipocytes. Therefore, the oxidative stress could be a potential interventional target for insulin-resistance related diseases.

KW - Cr(VI)

KW - ER stress

KW - Insulin resistance

KW - JNK

KW - ROS

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ER -

Chromium (VI) induces insulin resistance in 3T3-L1 adipocytes through elevated reactive oxygen species generation

Abstract

Bibliographical note

Funding

Keywords

ASJC Scopus subject areas

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