Biosynthesis of protein relative to the accumulation of fat in the liver of EFA deficient rats

Abstract

Effect of an essential fatty acid (EFA) deficiency in the rat on the incorporation of leucine‐14C and glucosamine‐14C into serum and liver protein are reported. Weanling male rats of the Sprague‐Dawley strain were raised on a fat‐free diet for 10–12 weeks and then switched to diets supplemented with 10% corn oil or 10% hydrogenated coconut oil. Leucine‐14C or glucosamine‐14C was injected into the tail veins of the animals of each group. At selected intervals up to 120 min after the injections, the animals were sacrificed and the radioactivity of the liver and serum proteins was measured. The levels of triglyceride (TG) in the serum and the liver were also determined. Less radio‐activity was incorporated into the serum β‐lipoprotein (β‐LP) fraction of the hydrogenated coconut oil than the corn oil fed animals injected with leucine‐14C, but no differences were observed in the incorporation of radioactivity into the liver protein and both albumin and globulin fractions of the serum of these groups of animals. In the similar experiments with glucosamine‐14C less radioactivity was incorporated into the β‐LP fraction of the serum and into the smooth endoplasmic reticulum of the liver in the hydrogenated coconut oil (EFA deficient) than the corn oil fed animals. Time course studies also indicated that less radioactivity was incorporated into the β‐LP fraction than into the albumin and globulin fractions of the serum of the hydrogenated coconut oil group. These findings suggest that an EFA deficiency results in an impairment of the synthesis or release of lipoprotein.

Fatty liver diseases in the domestic fowl — A review

“…The removal of lipids from the liver in the form of lipoproteins depends on the availability of the protein moiety and also the phospholipid components which are essential for the complete assembly of the lipoproteins. Thus a build-up of lipid occurs in the liver if the protein content of the diet does not supply adequate amounts of the amino acids required for the synthesis of the apolipoproteins (Marion and Edwards, 1962;Flores et al, 1970) or the synthesis is inhibited by an essential fatty acid deficiency (Fukazawa and Privett, 1972) or a toxic substance such as phosphorus. Aflatoxin may inhibit the transport of lipids in this way (Carnaghan etal, 1966;Tung etal, 1972).…”