Alcohol and tobacco are frequently co-abused. Tobacco smoke increases alcoholic steatosis in apoE(−/−) mice. Tobacco smoke contains more than 4000 chemicals, but it is unknown which compounds in tobacco smoke play a major role in increasing alcoholic steatosis.
C57BL/J6 mice were intraperitoneally injected with nicotine at 1 mg/kg every day or saline at the same volume as a control and the mice were fed dextrose-control or ethanol Lieber–DeCarli liquid diets. Three weeks later the mice were sacrificed after overnight fasting.
Neither nicotine injection nor ethanol feeding alone increased serum levels of triglyceride, but the combination of nicotine and ethanol increased serum levels of triglyceride. Both nicotine injection alone and ethanol feeding alone increased hepatic collagen type I deposition, and nicotine injection and ethanol feeding combined further increased hepatic collagen type I deposition. The combination of nicotine and ethanol also activated hepatic stellate cells, a principal liver fibrogenic cell. Hepatic fat accumulation was induced by ethanol feeding, which was further enhanced by nicotine injection. Ethanol feeding caused an increase in serum ALT, but nicotine did not further increase serum ALT levels. Lipid droplets and inflammatory foci were observed in liver sections from ethanol-fed mice; nicotine treatment increased the number and size of lipid droplets, but not the number and size of inflammatory foci. Nicotine did not further increase ethanol-induced hepatic neutrophil infiltation.
These results suggest that nicotine enhances ethanol-induced steatosis and collagen deposition, but nicotine has no effect on ethanol-induced inflammation.
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