Brief Article
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World J Gastroenterol. Jun 14, 2013; 19(22): 3487-3493
Published online Jun 14, 2013. doi: 10.3748/wjg.v19.i22.3487
Role of nesfatin-1 in a rat model of visceral hypersensitivity
Fang-Yuan Jia, Xue-Liang Li, Tian-Nv Li, Jing Wu, Bi-Yun Xie, Lin Lin
Fang-Yuan Jia, Xue-Liang Li, Jing Wu, Bi-Yun Xie, Lin Lin, Department of Gastroenterology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, Jiangsu Province, China
Tian-Nv Li, Department of PET/CT, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, Jiangsu Province, China
Author contributions: Jia FY, Wu J and Xie BY performed the experiments; Jia FY was involved in acquisition and analysis of data, and wrote the manuscript; Li XL and Li TN designed the study and revised the manuscript; Lin L provided vital guidance to the study.
Supported by Natural Science Foundation of China, No. 81070308/H0308
Correspondence to: Xue-Liang Li, MD, PhD, Professor, Department of Gastroenterology, the First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing 210029, Jiangsu Province, China. ligakur@yahoo.com.cn
Telephone: +86-25-83718836 Fax: +86-25-83780711
Received: January 13, 2013
Revised: May 15, 2013
Accepted: May 22, 2013
Published online: June 14, 2013
Core Tip

Core tip: This is a well conducted experimental study on the possible effect of nesfatin-1 in visceral hypersensitivity. Currently no reports have been published concerning the role of nesfatin-1 in irritable bowel syndrome (IBS). In a well-established visceral hypersensitivity animal model, we found an elevated nesfatin-1 level in the serum, and there was a reduction in evoked abdominal electromyography and abdominal withdrawal reflex scores after treatment with nesfatin-1 antibody, a non-selective corticotropin releasing factor (CRF) receptor antagonist, or a selective CRF1 receptor antagonist. These results suggest that nesfatin-1 may be associated with visceral hypersensitivity in model rats and implicated in brain CRF/CRF1 signaling pathways, which contribute to the visceral hypersensitivity of IBS.