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.
Highlights
Palmitic acid (PA) is associated with higher blood concentrations of medium-chain acylcarnitines (MCACs), and we hypothesized that PA may inhibit progression of FA -oxidation
Expressed as a percent of resting energy expenditure, fat oxidation rate in the fed state was 147% higher during the high PA (HPA) diet (11.6 ± 3.0%) compared with the high oleic acid (HOA) diet (4.7 ± 2.4%) (P = 0.044)
There was evidence that the ratio of M + 1/M + 0 for the enrichment of plasma PA, just prior to the beginning of administering the PA tracer (110 min of formula feeding), was respectively 1.6–3% higher on day 2 compared with day 1 for the HPA and HOA diets (P < 0.001). In view of these data on spillover and the results presented below indicating that the rate of oxidation of PA was unaffected by the tracer employed, we examined whole body PA oxidation rate expressed either as micromoles per minute or as a fraction of PA intake, using only data from the day 1 study; on this basis, whole body PA oxidation rate during the HOA diet was respectively 198% increased or 35% increased, values which are very similar to those presented above where both tracers and both tracer days were considered
Summary
Palmitic acid (PA) is associated with higher blood concentrations of medium-chain acylcarnitines (MCACs), and we hypothesized that PA may inhibit progression of FA -oxidation. The [13-13C]PA/[1-13C]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. Increased palmitate intake: higher acylcarnitine concentrations without impaired progression of -oxidation. Impaired oxidation of FAs, including PA, may lead to the accumulation of lipids (diacylglycerol, ceramide), which activate serine kinases inhibiting activity of insulin-receptor substrate 1 [2,3,4]. In rodents fed a high saturated fat diet, insulin resistance was linked to “incomplete oxidation of FA,” with relative accumulation of chain-shortened acyl-CoAs esterified to carnitine. Relative to a high OA and low PA (HOA) diet, during a high PA (HPA) diet, insulin sensitivity in humans was inversely correlated with
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