Objective To observe the effects of aspirin and tumor necrosis factor-α (TNF-α) on glucose metabolism and
insulin sensitivity
in
3T3-L1 adipocytes. Methods The amount of glucose disappearance from the culture medium after incubation with aspirin and TNF-α for 48 h was determined as glucose consumption of the cells. Theuptakeof2-deoxy-〔 3H〕-D-glucosewasusedtoobserveglucosetransport. The mRNA levels of genes related signal transduction of insulin were evaluated by semi-quantitative RT-PCR. Results Glucose con-sumption test revealed that 5 mmol/L aspirin and 5 μg/L TNF-α significantly increased glucose consumption in 3T3-L1 adipocytes by 25% and 46% respectively. In the presence of 100 nmol/L insulin, aspirin increased glucose consumption by 10%, while TNF-α decreased glucose consumption; but the combination of TNF-α and aspirin potentiated glucose consumption. Glucose transport testrevealedthat3T3-L1adipocytestreated with 5 μg/L TNF-α for 72 h exhibited a significant decrease in insulin-sensitive glucose uptake (P<0.01) , but TNF-α increased basal glucose transport (P<0.05). In the presence of TNF-α, aspirin potentiated insulin-sensitive glucose uptake by 85% (P<0.01). Aspirin also significantly increased basal glucose transport and insulin-stimulated glucose transport (P<0.01 or P<0.05). Using semiquantitative RT-PCR techniques, it was found that TNF-α inhibited glucose transporter 4 (GLUT4) and c-cbl-associated protein (CAP) gene expression. Aspirin did not influence GLUT4 and CAP gene expression, but alleviated the inhibiting effect of TNF-α on GLUT4 and CAP expression. Conclusion Aspirin increases
insulin sensitivity and partly antagonises TNF-α-induced insulin resistance in 3T3-L1 adipocytes.