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Adiponectin enhances murine colitis via adiponectine receptor 1 pathway
Author(s) -
Peng Yu-Ju,
Liu Bing-Hsien,
Mersmann Harry John,
Ding Shin-Torng
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1108.3
Subject(s) - colitis , proinflammatory cytokine , adiponectin , inflammation , adipokine , inflammatory bowel disease , medicine , immunology , endocrinology , diabetes mellitus , disease , insulin resistance
Adiponectin (ADN) is an adipokine derived from adipocytes. It binds to adiponectin recetor1 and 2 (AdipoR1 and 2) to exert into function regulating in whole‐body energy homeostasis, anti‐cardiovascular disease and inflammatory response. The role of ADN in inflammation response is likely multifaceted. It may play an anti‐inflammatory (e.g. diabetes, atherosclerosis and obesity) or proinflammatory (reheumatic disease and emphysema) role in different diseases. As the effect of ADN on colitis is still controversial, the goal of this study was to determine the inflammatory role of AdipoR1 in murine colitis. We generated AdipoR1‐transgenic mice to increase the effect of ADN and treated dextran sulfate sodium (DSS) to induce colitis. After administration of 2% DSS in drinking water for 7 days, AdipoR1‐transgenic mice developed more severe colitis than wild‐type mice, the symptoms including weight loss, bloody‐diarrhea, short coloength, crypt disruption and immunity cell infiltration. Our data show that ADN plays a proinflammatory role in colitis. Therefore, treatment of reducing ADN function during colitis may help the animal to cope with the inflammation.