@Article{ecn.2006.0039,
AUTHOR = {Lei Zhou, Yixing Li, Tao Xia, Shengqiu Feng, Xiaodong Chen, Zaiqing Yang},
TITLE = {Resistin overexpression impaired glucose tolerance in hepatocytes},
JOURNAL = {European Cytokine Network},
VOLUME = {17},
YEAR = {2006},
NUMBER = {3},
PAGES = {189--195},
URL = {http://www.techscience.com/ECN/v17n3/66149},
ISSN = {1952-4005},
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.},
DOI = {10.1684/ecn.2006.0039}
}