[Experimental and clinical studies on the mechanism of alcoholic fatty liver (author's transl)].

In order to clarify the mechanism of alcoholic fatty liver, rats were reared with alcohol diet from adult, foetal or weanling periods. When rats were fed with the diet from adult for 4 weeks, these livers showed apparent fatty deposition histologically and biochemically. Low density lipoprotein (LDL) in serums of these rats lowered in level significantly than control, which indicate decreased production of secretion of very low density lipoprotein (VLDL) in the liver from which converted to LDL in peripheral tissues. When rats were reared with the diet from their foetal life, their livers deposited little of fat at any time examined after birth up to 13 weeks in spite of good diet uptake. The same phenomenon was observed in rats reared from their weanling period with the diet. In situ liver perfusion was performed to clarify the anti-fatty liver mechanism. Ketone body (KB) production rates from palmitate infused constantly at physiological concentration and bile production rates were not different among control, weanling and foetal groups. Oxygen consumption rate in control decreased after infusion of palmitate-albumin complex solution. However the rates in weanling and foetal alcohol rats increased significantly after infusion of the solution. The latter group showed more increase in rate than the former. When theoretical oxygen consumption for production of KB was compared with actual one, livers from control rats seemed to use the whole oxygen for KB production. On the other hand only 59.7% of whole oxygen in foetal alcohol group and 85.9% in weanling group used for KB production respectively. It is surmized that the increased non ketone oxygen in these groups, especially in foetal alcohol group, indicate the anti-fatty liver mechanism in these groups, probably augmented FFA oxidation. Electrophoretic analysis of lipoproteins in chronic alcoholisms showed decreased beta and pre-beta band and increased alpha band. These changes returned to normal after 1 week of admission. These experimental and clinical data indicate that impaired oxidation of FFA is an important factor for the formation of alcoholic fatty liver and impaired transport of fat from liver might enhance the change in the liver.