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Modulation of inflammatory pathway in insulin sensitive tissues of normo and hyperphagic obese animals.
Author(s) -
Quadros Caren Dal'Mora,
Alves Eduardo Silva,
Haidar Andre Abou,
Morgan Daniela,
Rocha Marlene Santos,
Carpinelli Angelo Rafael,
Hirata Aparecida Emiko
Publication year - 2010
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.24.1_supplement.1035.6
Subject(s) - adipose tissue , endocrinology , medicine , proinflammatory cytokine , insulin resistance , inflammation , kinase , phosphorylation , mapk/erk pathway , insulin , obesity , insulin receptor , signal transduction , chemistry , biochemistry
Obesity is characterized by the activation of an inflammatory process in metabolically active sites such as adipose tissue and liver. The consequence of this response is an increase proinflammatory markers. This activation response in obesity is mediated by some specific signaling pathways including kinase families such as JNK, MAPK and IKKb. It is known that these molecules can lead to impairment of insulin signaling and result in the development of insulin resistance. The aim of this study was to evaluate the expression of these molecules in different models of obesity. Liver, muscle and adipose tissue from MSG‐obese rats (normophagic) and High‐fat induced obesity‐HF (hyperphagic) were evaluated. MSG‐obese rats showed significant increase in phosphorylation of ERK1/2 in liver and adipose tissue while HF‐rats showed a decreased in phosphorylation of this kinase in adipose tissue. Preliminary data also showed a differential modulation of p38MAPK, JNK and IKKb of these models. It is possible that the different energy load condition may have an important role in the signaling pathways of these molecules associated with the development of obesity‐induced inflammation.