The clearance of chylomicron remnants was assessed in normolipaemic, dyslipidaemic and obese male subjects by monitoring the plasma kinetics of apolipoprotein (apo) B48, retinyl palmitate and triglyceride after a lipid meal. Regression analysis of fasting plasma apo B48 with the area under the post-prandial curves of apo B48, retinyl ester and triglyceride was carried out in order to determine whether the post-prandial response could be predicted by the fasting concentration of this exclusive chylomicron marker. Fasted subjects were given an oral fat load supplemented with retinyl palmitate, and blood samples were drawn over a 10-h period. Apolipoprotein B48 was determined by Western blotting in the plasma density fraction less than 1.063 g mL-1. Plasma retinyl palmitate and triglyceride were determined by high-performance liquid chromatography (HPLC) and colorimetric procedures respectively. The areas under the apo B48, retinyl ester and triglyceride curves were determined by integration. Relationships between the post-prandial response and the fasting concentration of apolipoprotein B48 were assessed using least-squares regression analysis. We found a strong positive relationship between the fasting plasma concentration of apo B48 and the post-prandial kinetics of apo B48. Similarly, there was a positive relationship of fasting apo B48 with the retinyl ester area under the curve. Collectively, the data suggested that chylomicron remnant kinetics can be predicted based on the fasting level of apo B48. There was also a significant but weaker relationship of fasting apo B48 with post-prandial triglyceride kinetics, consistent with removal of this lipid by hydrolytic mechanisms in addition to particle uptake. The fasting plasma concentration of apo B48 appeared to be a good surrogate marker for the degree of post-prandial lipidaemia and may circumvent the need for oral fat challenges. Moreover, in the fasting state apo B48 concentration is a marker of chylomicron remnants, which are considered to be the proatherogenic form of these intestinally derived lipoproteins.