The possible mode of action of insulin, in terms of its sensitizing effect on dextran-induced anaphylactoid reaction was studied. In normal rats, the sensitizing effect was inhibited by actinomycin D and cycloheximide 1 h after the administration of the drugs. 24 h after actinomycin D or cycloheximide, the inflammatory response was considerably reduced. The inhibition could not be reversed by insulin. In contrast, insulin restored the decreased susceptibility of diabetic animals to dextran. This effect was not influenced by actinomycin D and cycloheximide. None of the drugs used influenced the blood-sugar-lowering activity of insulin. Cyclophosphamide, parallel to the profound lymphopenia produced, prevented the sensitizing effect of the hormone. Viable lymphoid cells prepared from young normal rats completely restored the suppressed insulin response. Liver cells had no such an effect. Lymph node cells incubated in the presence of insulin released a factor(s), capable of increasing dextran edema, to the incubation medium. Pretreatment with actinomycin D and cycloheximide of the lymphocyte-donor rats interfered with the ability of insulin to produce the pro-inflammatory factor(s). The possible significance of the findings is discussed.
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