AMINO-ACID-COMPOSITION OF DIETARY PROTEINS AFFECTS PLASMA-CHOLESTEROLCONCENTRATION THROUGH ALTERATION OF HEPATIC PHOSPHOLIPID-METABOLISM IN RATS FED A CHOLESTEROL-FREE DIET

This study was designed to investigate the relationship between the am ino acid composition of dietary proteins and the plasma cholesterol co ncentration and to examine whether the alteration of hepatic phospholi pid metabolism participates in the effect of dietary proteins in rats fed a cholesterol-free diet. There was a significant positive correlat ion between the plasma total cholesterol concentration and the plasma concentration of methionine and valine and the hepatic concentration o f valine and alanine in mts fed seven types of proteins, In contrast, the plasma cholesterol concentration exhibited a significant negative correlation with the hepatic-free ethanolamine concentration. As far a s methionine and ethanolamine, their positive and negative correlation with the plasma cholesterol concentration was consistent with their k nown hyper- and hypocholesterolemic effects, respectively. The phospho lipid profile as represented by the ratio of phosphatidylcholine (PC) to phosphatidyl-ethanolamine (PE) in liver microsomes, but not in othe r tissues tested, was largely influenced by die type of dietary protei ns; the PC/PE ratio exhibited a significant positive con elation with the plasma total cholesterol concentration. There was a significant co rrelation between the methionine content of dietary proteins and sever al biochemical variables including plasma cholesterol and liver micros omal PC/PE ratio. A significantly lower concentration of hepatic S-ade nosylmethionine was observed with soybean protein diet than with casei n diet suggesting a decrease in the PC biosynthesis via the PE N-methy lation pathway in rats fed soybean protein. From these results, it is suggested that the plasma cholesterol concentration might be influence d by the methionine content of dietary proteins at least in part throu gh an alteration of hepatic phospholipid metabolism.