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Cytokine Production by Insulin Resistant Adipocytes
Author(s) -
Levenberg Kate Robbins,
LaakkoTrain Tonya
Publication year - 2017
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.31.1_supplement.lb222
Subject(s) - insulin resistance , insulin , endocrinology , medicine , cytokine , inflammation , downregulation and upregulation , 3t3 l1 , interleukin 6 , diabetes mellitus , proinflammatory cytokine , lipid droplet , fgf21 , adipocyte , insulin receptor , chemistry , fibroblast , type 2 diabetes , biology , adipose tissue , fibroblast growth factor , in vitro , receptor , biochemistry , gene
The pathogenesis of type II diabetes is associated with obesity‐induced chronic inflammation. This association is thought to be mediated by pro‐inflammatory cytokines that inhibit insulins' signaling pathways. This study aimed to further the knowledge on the development of type II diabetes by identifying the cytokines that are expressed by adipocytes in an insulin resistant state. In order to do this, the 3T3‐L1 fibroblast cell line was first differentiated into adipocytes by exposure to dexamethasone (0.25 pM) and methylisobutylxanthine (0.5 mM) for two days, followed by exposure to insulin (2 pg/ml) for two days. Differentiation was evaluated by lipid droplet accumulation. The differentiated adipocytes were estimated to contain an average of 40 lipid droplets with a diameter of 7–15 μm each, as compared to an average of 4 droplets, with a diameter of 2–3 μm, in each fibroblast cell. Insulin resistance was induced by exposure to insulin for a minimum of 8 hours at a concentration of 10 nM. The secretion of 32 different cytokines by insulin resistant and non‐insulin resistant adipocytes was then evaluated by a membrane‐based antibody array. It was found that RANTES, TNF‐r1, TIMP‐1, and MCP1 were significantly upregulated in an insulin resistant state (p<.05). This work indicates that these specific cytokines may interfere with insulins' signaling pathway. Future research should study the interaction between these cytokines and the insulin signaling pathway, to further understand the link between inflammation and type II diabetes.