Influence of copper deficiency on liver morphology, aortic integrity, plasma lipoprotein and hepatic lipid profiles, and hepatic fatty acid synthesis in vivo.

Abstract

Three studies were designed to investigate the influence of dietary copper (Cu) on liver morphology, aortic integrity, lipid composition of lipoproteins, fatty acid profile of hepatic lipids, as well as in vivo hepatic fatty acid synthesis. Animals were randomly assigned to two dietary Cu treatments (deficient and adequate). Reductions in body weight, liver Cu content, and hematocrit, as well as elevations in liver weight and plasma volume were observed in animals fed Cu-deficient diet. Electron micrographs suggest that the Cu-deficient liver parenchymal cells contain a higher number of mitochondria, a more extensive network of rough endoplasmic reticulum and an increased quantity of chromatin in nucleus. Female hamsters fed the low Cu diet demonstrated a disruption and folding of collagen fibrils in the aorta. The percentage of total plasma cholesterol carried by LDL was increased from 20 to 24% but was reduced from 71 to 68% for HDL as a result of Cu deficiency. In LDL the percent composition of triglycerides and phospholipids were increased by 25% but that of cholesterol was reduced by 13%. With exception of smaller increases in VLDL protein (52%) and phospholipid (60%) pool size, as well as the more than 3-fold increases in LDL triglyceride and phospholipid plasma pool size, the plasma pool size for the rest of the lipoprotein components were increased about 2-fold in Cu-deficient hamsters. Furthermore, Cu deficiency altered the fatty acid composition of hepatic triglycerides, cholesteryl esters and phospholipids. The percent composition of palmitoleic (16:1 n-7) was reduced and arachidonic acid was elevated for all lipids in hamsters fed Cu-deficient diet. The percentage of stearic acid (18:0) was increased, and that of oleic (18:1 n-9) acid was decreased in the hepatic phospholipids and triglycerides of Cu-deficient animals. In study III, incorporation of [1-¹⁴C]acetate into fatty acids was used to determine the capacity of hepatic tissue to synthesize fatty acids. As a result of Cu deficiency, a 2.1-fold increase in hepatic total fatty acid synthesis was demonstrated.