Abstract
The aim of this study was to compare the kinetics of apolipoprotein (apo)A-I during fed and fasted states in humans, and to determine to what extent the intestine contributes to apoA-I production. A stable isotope study was conducted to determine the kinetics of apoA-I in preβ1 high-density lipoprotein (HDL) and α-HDL. Six healthy male subjects received a constant intravenous infusion of 2H3-leucine for 14 h. Subjects in the fed group also received small hourly meals. Blood samples were collected hourly during tracer infusion and then daily for 4 days. Tracer enrichments were measured by mass spectrometry and then fitted to a compartmental model using asymptotic plateau of very-low-density lipoprotein (VLDL) apoB100 and triglyceride-rich lipoprotein (TRL) apoB48 as estimates of hepatic and intestinal precursor pools, respectively. The clearance rate of preβ1-HDL-apoA-I was lower in fed individuals compared with fasted subjects (p < 0.05). No other differences in apoA-I production or clearance rates were observed between the groups. No significant correlation was observed between plasma apoC-III concentrations and apoA-I kinetic data. In contrast, HDL-apoC-III was inversely correlated with the conversion of α-HDL to preβ1-HDL. Total apoA-I synthesis was not significantly increased in fed subjects. Hepatic production was not significantly different between the fed group (17.17 ± 2.75 mg/kg/day) and the fasted group (18.67 ± 1.69 mg/kg/day). Increase in intestinal apoA-I secretion in fed subjects was 2.20 ± 0.61 mg/kg/day. The HDL-apoA-I kinetics were similar in the fasted and fed groups, with 13% of the total apoA-I originating from the intestine with feeding.
Highlights
The aim of this study was to compare the kinetics of apolipoproteinA-I during fed and fasted states in humans, and to determine to what extent the intestine contributes to Apolipoprotein A-I (apoA-I) production
high-density lipoprotein (HDL) cholesterol (HDL-C), apolipoprotein B100 and apoA-I concentrations were kept constant with no difference between both experiments
We investigated preβ1-HDL-apoA-I and α-HDL-apoA-I human kinetics in fasted and fed states and estimated the relative intestinal contribution of apoA-I total synthesis
Summary
The aim of this study was to compare the kinetics of apolipoprotein (apo)A-I during fed and fasted states in humans, and to determine to what extent the intestine contributes to apoA-I production. Kinetic studies discriminating preβ1-HDL and α-HDL subpopulations and with a direct comparison in fasted and fed subjects have never been performed. Such studies have not been undertaken likely due to the complexity of preβ1-HDL metabolism, which is recycled in other HDL populations and originates from two different sources: (1) a direct synthesis from the liver and the intestine[5], and (2) an indirect synthesis from intestine-produced postprandial triglyceride-rich lipoproteins (TRL)[6], which have undergone hydrolysis by lipoprotein lipase[7,8].Of note, apolipoprotein C-III (apoC-III) inhibits TRL hydrolysis by acting on lipoprotein lipase[9] and food intake increases apoC-III plasma c oncentrations[10,11]. Our goals were to analyze the effects of food intake and plasma apoC-III on HDL metabolism, and to estimate the intestinal production rate of apoA-I
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