Interleukin‐1β inhibits glucokinase activity in clonal HIT‐T15 β‐cells

Interleukin-1β (IL-1β) has been implicated in the pathogenesis of insulin-dependent diabetes mellitus. In the present study we have investigated the effects of IL-1β on glucose metabolism in clonal HIT-T15 β cells. In the short-term (1 h), 25 IL-1β significantly increased the rates of insulin release and glucose utilisation, but not glucose oxidation. In contrast, after 48 h, IL-1β inhibited insulin release and glucose utilisation and oxidation. By assaying enzymes (hexokinase, glucokinase, pyruvate dehydrogenase, glucose 6-phosphatase) and nucleotides (ATP, ADP) associated with the regulation of glycolysis and glucose oxidation, we conclude that the inhibitory effects of IL-1β may be due to impaired glucokinase activity.