Obesity-Associated Inflammatory Cytokines and Prostaglandin E2 Stimulate Glucose Transporter mRNA Expression and Glucose Uptake in Primary Human Adipose Stromal Cells.
Academic Article
Overview
abstract
Obesity is associated with chronic low-grade inflammation. This occurs largely as a result of the infiltration of immune cells within the obese adipose, which produce a number of inflammatory factors, including interleukin-6 (IL-6), IL-1β, tumor necrosis factor-α (TNFα), and prostaglandin E(2) (PGE(2)). These factors have previously been shown to affect insulin-mediated glucose uptake in differentiated adipocytes. However, the insulin-independent effect of inflammation on adipocyte precursors, the adipose stromal cells, has not been explored. This study therefore aimed to examine the effect of obesity-associated inflammatory factors on the expression of insulin-independent glucose transporters (GLUT1 and GLUT3) and on the uptake of glucose within adipose stromal cells. Primary human subcutaneous adipose stromal cells were isolated from abdominoplasty, and the effect of inflammatory cytokines (IL-6, IL-1β, and TNFα) and PGE(2) on GLUT mRNA expression and glucose transport was assessed using real-time polymerase chain reaction and radiolabeled deoxyglucose uptake assays, respectively. Results demonstrate that all four inflammatory mediators caused a dose-dependent increase in GLUT1 mRNA expression and glucose uptake. GLUT3 mRNA expression was also upregulated by IL-6 (0.5 ng/mL), TNFα (0.1 and 10 ng/mL), and PGE(2) (0.1 μM). Overall, these results demonstrate that obesity-associated inflammation increases insulin-independent glucose transporter expression and glucose uptake in undifferentiated adipose stromal cells.
