Interleukin-1 induced impairment in pancreatic islet oxidative metabolism of glucose is potentiated by tumor necrosis factor

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Abstract
Recent observations suggest that human interleukin-1 (IL-1) causes functional impairment and death of pancreatic B-cells. This action seems to be potentiated by another cytokine, tumor necrosis factor (TNF). In the present investigation, the effects of recombinant human (r) IL-1 (10, 30 and 150 pmol/l), and a combination of rIL-1 and human rTNF (as .mu.g/l), on islet glucose metabolism were examined in the presence of D-[5-3H] and D[6-14C] glucose. The utilization of glucose was not affected by rIL-1 or rIL-1 plus rTNF. However rIL-1 induced a 40% decrease in glucose oxidation, which was further potentiated by the addition of rTNF. rTNF alone did not impair islet glucose utilization or oxidation. It is concluded that rIL-1 induces a perturbation of islet glucose handling, mainly at the mitochondrial level. This impairment in the oxidative metabolism of glucose is further increased by the addition of rTNF.