Studies on the role of phospholipids in the triglyceride cycle. 3. Liver and plasma phospholipid exchange in depancreatized dogs.

Abstract

AbstractLipid mobilization from the liver to extrahepatic sites of utilization and to adipose tissue for storage and recycling via the triglyceride cycle requires de novo synthesis of liver lecithins. The role of liver phospholipid (PL) synthesis and plasma phospholipid turnover has been studied under a number of conditions which appear to relate liver lipoprotein formation and release to liver PL synthesis and transport. Conditions which enhance nonesterified fatty acid (NEFA) release from adipose tissue or which inhibit liver PL synthesis prompt liver lipid accumulation. Lipid accumulates in the liver principally as triglyceride when any one of a number of factors required for liver lipoprotein comple formation is blocked, such as by ethionine, or when NEFA release to plasma is increased, such as in cold acclimatization. The relationship of liver PL to liver lipid transport is shown also following recovery from these conditions. Recovery from liver triglyceride (TG) accumulation is accompanied by increased PL synthesis, remobilization of liver PL, and increased turnover of plasma phospholipids. The relative specific activity (RSA) of phospholipid phosphorus (SA of plasma to liver PLP) is increased in depancreatized dogs during liver lipid accumulation. Following the initial depression in liver PL synthesis and transport caused by ethionine administration the RSA increased in all animals studied, indicating a remobilization of the accumulated TG. This remobilization of liver lipid occurs to a greater extent in depancreatized dogs than in normal dogs under the same conditions.