Studies on aminoacetonitrile and its related compounds. IV. Effect of aminoacetonitrile on experimental fatty liver

Abstract

Effect of aminoacetonitrile on hepatic injuries by treatment of rats with carbon tetrachloride was tested. The possible participation of the sympathetic nervous system in the development of fatty liver was also examined. A long-lasting elevation of free fatty acids was observed in plasma of rats after an administration of CCl4. The increase of plasma fatty acids and liver lipid by CCl4 was partially prevented by dibenzyline, propranolol, and trimethidium. The fatty liver produced by CCl4 was markedly potentiated by phenelzine but not by pyrogallol. When 50 to 100 mg/kg of aminoacetonitrile was injected before poisoning with CCl4, the liver dysfunction was clearly prevented. The lipid accumulation in the liver produced by CCl4 was partially prevented by the administration of 50 mg/kg of aminoacetonitrile, which also inhibited the elevation of plasma fatty acids induced by the administrations of CCl4 and morphine or by exposing the rats to cold, but not that induced by norepinephrine, etc. The protective effect of aminoacetonitrile on the mobilization of free fatty acids and lipid accumulation procuced by CCl4 was not observed in reserpinized rats. It is concluded from these results that CCl4 increases the mobilization of free fatty acids by stimulating the sympathetic nervous system. Furthermore, it is considered that the effect of aminoacetonitrile on the lipid accumulation induced by CCl4 is due to inhibition of the mobilization of fatty acids.