Ethanol inhibits LPS stimulation of ¹⁸FDG uptake in mice

Objectives LPS alters glucose metabolism, in part by activating tissues rich in macrophages. This response to LPS is part of the inflammatory reaction which helps protect against infections. Ethanol is known to increase the susceptibility to infections by mechanism(s) that are not fully understood. In the present study we evaluated the effect of ethanol pretreatment on LPS stimulation of ¹⁸FDG uptake.

Methods Male mice (28-30 grams) were fasted overnight. The mice were injected intraperitonealy with ethanol (5mg/kg,20% vol/vol, in saline) or saline alone. 30 minutes later the mice were injected intravenously with LPS (33 mg/kg). One hour later the mice were injected with ¹⁸FDG, 50μCi/kg via tail vein. One hour after that, the mice were sacrificed by carbon dioxide overdose and subjected to complete necroscopy. Tissues were weighed and radioactivity was measured with a Wizard 1480 gamma counter. Results were expressed as %ID/gram tissue, mean ± SD. There were six mice in each group.

Results LPS injection resulted in significant increases in ¹⁸FDG uptake in spleen and heart (p<0.01). Ethanol pretreatment appeared to stimulate ¹⁸FDG uptake in the heart, while decreasing uptake in the brain (p<0.01). The combination of ethanol and LPS resulted in a greater increase in ¹⁸FDG uptake by the heart than either treatment alone. By contrast, the combination of ethanol and LPS resulted in a greater decrease in uptake of ¹⁸FDG in the brain than either treatment alone (p<0.01), and blunted the LPS stimulation of ¹⁸FDG uptake in the spleen compared to LPS alone.

Conclusions Ethanol pretreatment can alter the inflammatory responses in glucose metabolism produced by LPS injection, in some cases ameliorating while in other cases, increasing the effects.

Research Support Shriners Hospital for Children, Bosto

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*p<0.01 compared to sham