Open Access

ARTICLE

Resistin overexpression impaired glucose tolerance in hepatocytes

Lei Zhou, Yixing Li, Tao Xia, Shengqiu Feng, Xiaodong Chen, Zaiqing Yang

Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, College of Life Science and Technology, Huazhong Agricultural University, Wuhan 430070, P.R.China
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* Corresponding Author: Z. Yang,

European Cytokine Network 2006, 17(3), 189-195. https://doi.org/10.1684/ecn.2006.0039

Accepted 07 September 2006;

Abstract

Resistin is a 12.5-kDa cysteine-rich protein secreted from adipose tissue and is an important factorlinking obesity with insulin resistance. Here, we investigated the effect of resistin on glucose tolerance in adulthuman hepatocytes (L-02 cells). In this study, resistin cDNA was transfected into L-02 cells, and glucoseconcentration and glucokinase activity were determined subsequently. The data indicated resistin impaired,insulin-stimulated glucose utilization, which implied liver was a target tissue of resistin. To understand itsmolecular mechanism, mRNA levels of key genes in glucose metabolism and insulin signaling pathway wereanalyzed. The results demonstrated resistin-stimulated expression of glucose-6-phosphatase (G6Pase), sterolregulatory element-binding protein 1c (SREBP1c) and suppressor of cytokine signaling 3 (SOCS-3), repressedexpression of peroxisome proliferator-activated receptor γ (PPARγ) as well as insulin receptor substrate 2 (IRS-2).Given that glucokinase (GK) activity and glucose transporter 2 (GLUT2) expression were not altered, wepresumed that resistin did not effect them. Moreover, resistin lowered mRNA levels of IRS-2 while stimulatingSOCS-3 expression, which suggests it impairs glucose tolerance by blocking the insulin signal transductionpathway.

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Keywords

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