Interleukin-1 induced increases in glucose utilization are insulin mediated.

Interleukin-1 (IL-1) is known to modulate a variety of the acute-phase responses to infection. Since an enhanced rate of whole-body glucose utilization is a consistent feature of the hypermetabolic phase of infection, the purpose of the present study was to determine whether IL-1 could increase glucose uptake and whether that increase was dependent on the concomitant elevation in plasma insulin. Glucose utilization (Rg) of different tissues was investigated in vivo by the 2-deoxyglucose tracer technique. Human purified IL-1 was administered to chronically, catheterized conscious rats and increased the plasma insulin levels and the Rg in macrophage-rich tissues, including the lung, spleen, liver and skin. IL-1 also increased Rg in skeletal muscle and diaphragm. To eliminate the insulin-stimulated increase in Rg, somatostatin (SRIF) was infused 1 h prior to IL-1. SRIF prevented the IL-1 induced increase in insulin and tissue glucose utilization. IL-1 administration to streptozotocin-induced diabetic rats also failed to increase Rg in any tissue examined. These data suggest that the administration of IL-1 increases organ glucose utilization by insulin-dependent mechanisms.