Premium
Glucose Metabolism Influences MCP1 Expression in Adipocytes
Author(s) -
Grant Ryan,
Stephens Jacqueline
Publication year - 2015
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.29.1_supplement.258.3
Subject(s) - medicine , endocrinology , tumor necrosis factor alpha , glycolysis , adipose tissue , glucose uptake , inflammation , adiponectin , carbohydrate metabolism , gene expression , chemokine , adipocyte , biology , insulin resistance , lipopolysaccharide , chemistry , insulin , metabolism , gene , biochemistry
Adipose tissue inflammation is closely associated with obesity and insulin resistance. Adipocytes have the capacity to regulate the recruitment of immune cells through the secretion of chemokines. Here we investigated if glucose metabolism controls MCP1 expression in response to lipopolysaccharide (LPS) or tumor necrosis factor (TNF) in 3T3‐L1 adipocytes. TNF or LPS increased MCP1 expression at 20 hrs of treatment, and the glycolytic inhibitor 2‐deoxyglucose (2‐DOG) reduced TNF/LPS‐induced expression of MCP1, however adiponectin was unaffected. TNF induced MCP1 gene expression after 1 hr of treatment, and 30 min pre‐treatment with 2‐DOG prevented increased MCP1 gene expression. Adipocytes were more sensitive to TNF and LPS under conditions of 10 mM pyruvate and 0 mM glucose indicating that substrates produced from glycolysis prior to pyruvate are not driving MCP1 gene expression. However, 2‐DOG still decreased TNF induced MCP1 gene expression even when pyruvate alone was present. In conclusion, 2‐DOG decreases TNF and LPS induced MCP1 transcription in 3T3‐L1 adipocytes; however it does not appear that this effect is due to inhibition of glycolysis. Thus, other metabolic effects of 2‐DOG likely underlie the anti‐inflammatory response to this glycolytic inhibitor in adipocytes. This work was supported by NIH T32 DK064584 and Purdue University.