Increased palmitate intake: higher acylcarnitine concentrations without impaired progression of β-oxidation

Abstract

Palmitic acid (PA) is associated with higher blood concentrations of medium-chain acylcarnitines (MCACs), and we hypothesized that PA may inhibit progression of FA β-oxidation. Using a cross-over design, 17 adults were fed high PA (HPA) and low PA/high oleic acid (HOA) diets, each for 3 weeks. The [1-(13)C]PA and [13-(13)C]PA tracers were administered with food in random order with each diet, and we assessed PA oxidation (PA OX) and serum AC concentration to determine whether a higher PA intake promoted incomplete PA OX. Dietary PA was completely oxidized during the HOA diet, but only about 40% was oxidized during the HPA diet. The [13-(13)C]PA/[1-(13)C]PA ratio of PA OX had an approximate value of 1.0 for either diet, but the ratio of the serum concentrations of MCACs to long-chain ACs (LCACs) was significantly higher during the HPA diet. Thus, direct measurement of PA OX did not confirm that the HPA diet caused incomplete PA OX, despite the modest, but statistically significant, increase in the ratio of MCACs to LCACs in blood.

Keywords: cytokines; dehydrogenases; diet and dietary lipids; fatty acid; fatty acid/oxidation; incomplete β-oxidation of fatty acids; inflammation; innate immunity; lipids/oxidation; macrophages/monocytes; mass spectrometry; nutrition; oleic acid; palmitic acid; stable isotopes.

Copyright © 2015 by the American Society for Biochemistry and Molecular Biology, Inc.

Figures

Fig. 1.

Consort diagram for the trial.

Fig. 2.

PA oxidation and retention is increased on the HPA diet. As described in detail in the Materials and Methods, studies of the oxidation of [1-13C]PA and [13-13C]PA tracers were carried out in random order, in the fed state, using an oral tracer administration protocol for the HPA, low PA, and HOA diets. Both whole body and muscle parameters are calculated based on data obtained from blood samples (see the Materials and Methods, as well as detailed equations in the online data supplement). Black bars indicate the HPA diet and white bars indicate the HOA diet. **P ≤ 0.01 or ***P ≤ 0.0001 for diet differences. A: The whole body rate of oxidation of PA (PA OX) based either on the [1-13C]PA tracer or the [13-13C]PA tracer (micromoles per minute) (n = 17). B: The whole body rate of oxidation of PA, using either tracer, expressed as a fraction of PA intake (n = 17). C: Whole body PA retention (PA intake − PA oxidation) (micromoles per minute). Data are presented for the [1-13C]PA tracer only as described in the text (n = 17). D: Skeletal muscle oxidation of PA (micromoles per minute, across the forearm muscle) based either on the [1-13C]PA tracer (n = 15) or the [13-13C]PA tracer (n = 12). E: Skeletal muscle PA uptake (micromoles per minute, across the forearm muscle). Average uptake on both tracer days for each diet is presented because position of label has no effect (n = 16 for the [1-13C]PA tracer and n = 13 for the [13-13C]PA tracer). The values for both tracer days were averaged when both values were available. F: Skeletal muscle PA retention based on the [1-13C]PA tracer (micromoles per minute, across the forearm muscle) (n = 15).

Fig. 3.

Discordant interpretation of completeness of FA OX based on tracer data and AC profiling. The oxidation of PA was assessed during a 7 h protocol in which tracers for PA and diet formula were administered by mouth every 20 min. The [1-13C]PA and [13-13C]PA tracers were administered in random order for each of the experimental diets (HPA, HOA). As described in Materials and Methods, oxidation of each tracer was based on plateau samples obtained during the last hour of tracer administration. AC profiling was conducted on blood obtained at the end of the tracer administration protocol (n = 17 for all diet comparisons). Black bars indicate the HPA diet and white bars indicate HOA diet. *P ≤ 0.05, **P < 0.01, and ***P < 0.001, for differences between tracers (repeated measures ANOVA, except for AC statistics, which were based on a paired t-test). A: Ratio of the whole body rates of PA oxidation measured with tracers for PA labeled on positions C1 and C13 (C13/C1 data presented). B: Serum AC profile averaged for the two tracer days on each diet (see text for calculation). C: Effects of diets on the serum concentrations of specific saturated ACs. D: Effects of diets on the serum concentrations of specific monounsaturated ACs.