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Changes in signaling pathways through NOD2 in high fat diet‐induced obesity is associated with inflammatory response in immune cells (1037.8)
Author(s) -
Kim Min Soo,
Kim HyeKyeong,
Park Chan Yoon,
Park Jeong Min,
Han Sung Nim
Publication year - 2014
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.28.1_supplement.1037.8
Subject(s) - nod2 , endocrinology , immune system , medicine , inflammation , chemistry , mapk/erk pathway , signal transduction , innate immune system , immunology , biochemistry
Previously, we observed higher production of inflammatory cytokines and higher expression of nucleotide‐binding oligomerization domain 2 (NOD2) by immune cells from obese mice. The changes in signaling pathways through NOD2 protein were investigated to understand the mechanisms involved in inflammatory response associated with obesity. Four‐wk‐old C57BL mice were fed diets containing 10% energy from fat (Control) or 45% energy from fat (HFD) for 18 wks. HFD group gained significantly more weight than the Control. Splenocytes (1 x 10 7 cells) were stimulated with 10 µg/mL peptidoglycan for 6 or 24 hrs. Production of pro‐inflammatory cytokines, IL‐1β and IL‐6, were significantly higher in HFD compared with Control. The mRNA levels of Nod2, Nlrp3 and IL‐18 were significantly higher in HFD compared with Control (49%, 89%, and 76% higher in HFD than Control, respectively). The protein expression of NOD2, pIκB/IκB, and caspase‐1 p10 (cleavage form) were higher in HFD compared with Control, but, there was no difference in the expression of pERK/ERK. Increased expression of NOD2 and NLRP3 with obesity might have contributed to higher caspase‐1 activation, leading to higher IL‐18 expression and IL‐1 β production. In conclusion, increased NOD2 expression with obesity seemed to lead to NF‐κB and Caspase‐1 activations, but, not ERK activation. Grant Funding Source : Supported by the grant from the National Research Foundation (NRF) of Korea, (NRF‐2010‐0024878).