Effects of Therapeutic Lifestyle Change diets high and low in dietary fish-derived FAs on lipoprotein metabolism in middle-aged and elderly subjects

Abstract

The effects of Therapeutic Lifestyle Change (TLC) diets, low and high in dietary fish, on apolipoprotein metabolism were examined. Subjects were provided with a Western diet for 6 weeks, followed by 24 weeks of either of two TLC diets (10/group). Apolipoprotein kinetics were determined in the fed state using stable isotope methods and compartmental modeling at the end of each phase. Only the high-fish diet decreased median triglyceride-rich lipoprotein (TRL) apoB-100 concentration (-23%), production rate (PR, -9%), and direct catabolism (-53%), and increased TRL-to-LDL apoB-100 conversion (+39%) as compared with the baseline diet (all P < 0.05). This diet also decreased TRL apoB-48 concentration (-24%), fractional catabolic rate (FCR, -20%), and PR (-50%) as compared with the baseline diet (all P < 0.05). The high-fish and low-fish diets decreased LDL apoB-100 concentration (-9%, -23%), increased LDL apoB-100 FCR (+44%, +48%), and decreased HDL apoA-I concentration (-15%, -14%) and PR (-11%, -12%) as compared with the baseline diet (all P < 0.05). On the high-fish diet, changes in TRL apoB-100 PR were negatively correlated with changes in plasma eicosapentaenoic and docosahexaenoic acids. In conclusion, the high-fish diet decreased TRL apoB-100 and TRL apoB-48 concentrations chiefly by decreasing their PR. Both diets decreased LDL apoB-100 concentration by increasing LDL apoB-100 FCR and decreased HDL apoA-I concentration by decreasing HDL apoA-I PR.

Fig. 1.

A: Compartment model describing TRL, IDL and LDL apoB-100 kinetics The apoB-100 model consisted of seven compartments. Compartment 1 represents the precursor compartment, the plasma leucine pool. Compartment 2 is an intracellular delay compartment that accounts for the synthesis and secretion of apoB-100 into the TRL pool (compartment 3). Compartments 3 and 4 account for the kinetics of apoB-100 in the TRL fraction. Compartment 5 accounts for the kinetics of IDL apoB-100. The kinetics of LDL apoB-100 are described by a plasma compartment (compartment 7). In order to fit the LDL apoB-100 tracer data, a delay compartment (compartment 6) between the TRL and LDL compartments was required. B: Compartment model describing TRL apoB-48 and HDL apoA-I kinetics The kinetics of TRL apoB-48 and HDL apoA-I were described by a three-compartment model. Compartment 1 represents the precursor compartment, which is the plasma leucine pool. Compartment 2 is an intracellular delay compartment that accounts for the synthesis and secretion of apoB-48 or apoA-I into the TRL or the HDL pool, respectively (compartment 3). Compartment 3 accounts for the kinetics of apoB-48 or apoA-I in the TRL or HDL fraction, respectively. Of note, the TRL apoB-100 plateau was used as the tracer plateau for HDL apoA-I kinetic analysis.

Fig. 2.

Correlations between the changes in TRL apoB-100 concentration with changes in plasma oleic acid (A), the changes in TRL apoB-100 production rate with changes in plasma oleic acid (B), EPA (C), and DHA (D), and the changes in TRL-to-LDL apoB-100 conversion rate with changes in plasma EPA (E) in the NCEP high-fish diet group (n = 9; the plasma FA profile of one subject was not measured during the study). Spearman correlation analyses were performed to examine the statistical associations between changes from baseline in variables.