Abstract
In normal alimentary lipemia in humans, following the ingestion of a fat meal, the serum triglyceride concentration rises to a peak level approximately four hours after the meal and falls to the original fasting level within eight hours (1, 2). Excessive and prolonged alimentary lipemia occurs in several types of familial hyperlipemia (3) and frequently in various pathological conditions such as atherosclerosis (4), coronary heart disease (5), diabetes (6), alcoholism (7, 8), pancreatitis (9), nephrotic syndrome (3), and hypothyroidism (3). An important variable in hyperlipemia is that it may be due largely to excessive amounts of exogenous triglyceride, of endogenous triglyceride , or a combination of both. | Following the metabolic pathways of ingested triglyceride is complicated by the ubiquitous presence of endogenous triglyceride and a heterogeneous series of serum lipoprotein complexes. Chylomicron fat particles which are formed in the intestinal mucosa after a fat meal and move into the thoracic duct lymph have been referred to as exogenous (10). However lymph chylomicrons have been found to contain endogenous as well as dietary lipid (11-14). Chylomicrons separateci from serum contain even larger amounts of endogenous lipid (15, 16). Of the soluble 1iproproteins produced largely by the liver and considered to be endogenous, the pre-beta or very low density fraction contain significant quantities of dietary lipid during the late phases of alimentary lipemia (10). Beta-1ipoprotein (low- density) and alpha-1 ipoprotein (high density) show only a minor tendency to incorporate dietary lipid. | The goal of this study was twofold: 1) to estimate the quantitative relationships between the endogenous and dietary contributions to normal alimentary triglyceridemia in humans, and 2) to evaluate the changes in endogenous serum lipid levels which we believe play an important role in determining the degree of alimentary lipemia.