Diets high in fat containing 4–5% casein with starch as the carbohydrate and supplemented with cystine and cholesterol proved most suitable for the production of choline deficiency liver necrosis and fibrosis in albino rats. Thiamine deficiency or restricted food consumption prevented the accumulation of excessive liver fat and also liver necrosis. N′-methylnicotinamide was found to exert no lipotropic activity alone or in combination with homocystine. Inclusion of excess nicotinamide in an 18% casein diet produced extensive fatty infiltration but only minimal necrosis of the liver. It is suggested that the hepatic necrosis and fibrosis of choline deficiency may be the result of chronic fatty infiltration. The ingestion of an adequate quantity of good protein protects the liver from the deleterious effects of chronic fatty infiltration but this protective capacity is not based upon lipotropic activity alone.