Interleukin-1 induced increases in glucose utilization are insulin mediated

Charles H. Lang, Cornel Dobrescu

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35 Scopus citations


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 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.

Original languageEnglish (US)
Pages (from-to)2127-2134
Number of pages8
JournalLife Sciences
Issue number22
StatePublished - 1989

All Science Journal Classification (ASJC) codes

  • General Pharmacology, Toxicology and Pharmaceutics
  • General Biochemistry, Genetics and Molecular Biology


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