Triglyceride Transport in Protein-depleted Rats

Abstract

The hypothesis that fatty liver in protein malnutrition is produced mainly by a deficit in the availability of the protein moiety of low density lipoproteins was investigated in rats. The animals were made protein-depleted by feeding a protein-free diet. They developed fatty livers as well as several other symptoms characteristic of infantile protein malnutrition. The injection of a plasma protein fraction containing the apoprotein of low density lipoproteins as compared to albumin-injected controls produced an increase of 80% in the fasting plasma triglyceride levels and a significantly higher incorporation of ¹³¹I-oleic acid into triglycerides of d < 1.020 plasma lipoprotein. These effects were not observed in normal, well-nourished animals. The results of these experiments strongly suggest that in protein malnutrition the protein moiety of low density lipoproteins is the limiting factor for their synthesis. The impaired rate of synthesis of the lipoprotein would cause triglycerides to accumulate in the liver.