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A B S T R A C T Several aspects of the effects of dietary fat on plasma lipids and lipoproteins were investigated in 12 subjects during the long-term feeding of formulas containing 40% of their calories as either saturated or unsaturated fats. The changes in fatty acid composition of plasma lipids, shown previously to occur after prolonged feedings of a dietary fat, required 10-14 days to be complete and were synchronous with the effect of the fat on plasma lipid concentrations. The change in lipid concentration occurred in low but not in high density lipoproteins. The effects on lipid levels of the low density lipoproteins were found to occur with little or no effect on the concentration of the protein moiety of these lipoproteins; as a result, cholesterol-and phospholipid to protein ratios in low density lipoproteins fell during unsaturated fat feeding. The effects of dietary fat on plasma phospholipids were studied in detail: the relative amounts of phosphatidylcholine, phosphatidylethanolamine, sphingomyelin, and lysophosphatidylcholine were unaffected by the type of dietary fat. However, the molecular species of phosphatidylcholine were markedly affected. More than 90% of the fatty acids at the a-position were saturated during both saturated and unsaturated feedings. In contrast, during unsaturated feedings, linoleate at the ,8-position outnumbered oleate by approximately 4: 1, whereas during saturated feedings these two types of fatty acids were present in nearly equal amounts.This work was presented in part at the Council on Atherosclerosis of the American Heart Association, San Francisco, Calif., 1967, and has been published in abstract form (1).

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Although the hypocholesteremic effect of unsaturated dietary fats has been repeatedly demonstrated, the mechanism underlying this effect is by no means clear. Four possibilities exist: 1) decreased cholesterol synthesis, 2) increased excretion of cholesterol or its metabolites, or both, 3) shift of plasma cholesterol to some other tissue(s), or 4) some combination of these factors.In a previous study of a single patient in this hospital (2) significantly increased excretion of neutral but not acidic fecal sterols was demonstrated when unsaturated fat replaced saturated fat in the diet. The present study extends that single experience to five studies in four other patients and utilizes a different and more generally useful methodology.An adequate evaluation of steroid 1 excretion depends first on devising a satisfactory procedure for quantitative isolation of fecal neutral steroids and simultaneously of other metabolic end products, notably the fecal bile acids; and second, on measuring accurately these excretion products by means that take into account the numerous chemical forms of these excretion products, some of which are still not identified.

Abstract. Replacement of dietary triglycerides containing long-chain fatty acids (LCFA) by triglycerides containing medium-chain fatty acids (MCFA) markedly reduced the capacity of alcohol to produce fatty liver in rats. After 24 days of ethanol and MCFA, the increase in hepatic triglycerides was only 3 times that of controls, whereas an 8-fold rise was observed after ethanol and LCFA. The triglyceride fatty acids that accumulated in the liver after feeding of ethanol with MCFA contained only a small percentage of the MCFA; their composition also differed strikingly from that of adipose lipids.To study the mechanism of the reduction in steatosis, we compared oxidation to CO2 and incorporation into esterified lipids of 14C-labeled chylomicrons or palmitate-14C (representing LCFA), and of octanoate-14C (as MCFA) in liver slices and isolated perfused livers, in the presence or absence of ethanol. Ethanol depressed the oxidation of all substrates to CO2; MCFA, however, was much more oxidized and reciprocally much less esterified than LCFA, with a 100-fold difference in the ratio of esterified lipid-14C to 14CO2. Furthermore, in hepatic microsomal fractions incubated with a-glycerophosphate, octanoate was much less esterified than palmitate. This propensity of MCFA to oxidation rather than esterification represents a likely explanation for the reduction in alcoholic steatosis upon replacement of dietary LCFA by MCFA.