Postprandial Responses to Meals Enriched With Canola or Coconut Oil in Men and Women With a Risk Phenotype for Cardiometabolic Diseases: A Randomized Crossover Trial

Abstract

We investigated the metabolic response to meals with canola or coconut oil (rich in unsaturated vs. rich in saturated fatty acids [FAs]). Although the longer-term metabolic effects of these fats are well evidenced, their postprandial effects remain inconclusive. In this randomized crossover trial, 29 participants with increased cardiometabolic risk consumed four isoenergetic meals containing 25 or 50 g (low-fat meals [LFMs], high-fat meals [HFMs]) of canola or coconut oil. Blood samples for analysis of triglycerides (TGs), glucose, insulin, nonesterified FAs (NEFAs), IL-6, and individual FAs were collected in the fasting state and 6 h postprandially (every 0.5-1 h). The incremental areas under the curves (iAUCs) of TGs and IL-6 were higher after canola than after coconut oil. Concentrations of lauric and myristic acid were higher after coconut oil, while concentrations of oleic, linoleic, and α-linolenic acid were higher after canola oil. The TG iAUC was higher after HFMs than after corresponding LFMs. NEFAs decreased more after LFMs than after HFMs. The glucose and insulin iAUCs were higher after LFMs than after HFMs. Canola and coconut oil induced different metabolic responses. The manner and strength of the postprandial effects differed depending on the parameter.

Keywords: arterial stiffness; canola oil; cardiometabolic risk; coconut oil; triglyceride response.

FIGURE 1

Flowchart of inclusion and exclusion of participants.

FIGURE 2

Fasting and postprandial concentrations of serum triglycerides in response to test meals in adults with increased cardiometabolic risk. Canola oil consumption resulted in a higher triglyceride concentration than coconut oil consumption. Data are shown as mean ± SEM (n = 29). A linear mixed model with repeated measures was used to test for effects of interventions, time points, and their interactions. ***p < 0.001 for fixed factor time, €p < 0.05 for fixed factor fat type, ##p < 0.01 for fixed factor fat amount, §p < 0.05 for fat type × time interaction. Abbreviations: HFM, high‐fat meal; LFM, low‐fat meal.

FIGURE 3

Fasting and postprandial concentrations of serum nonesterified fatty acids in response to test meals in adults with increased cardiometabolic risk. Low‐fat meal consumption resulted in a lower NEFA concentration than high‐fat meal consumption. Data are shown as mean ± SEM (n = 29). A linear mixed model with repeated measures was used to test for effects of interventions, time points, and their interactions. ***p < 0.001 for fixed factor time, ###p < 0.001 for fixed factor fat amount, $$p < 0.01 for fat amount × time interaction. Abbreviations: HFM, high‐fat meal; LFM, low‐fat meal; NEFA, nonesterified fatty acid.

FIGURE 4

Fasting and postprandial concentrations of plasma glucose (A) and serum insulin (B) in response to test meals in adults with increased cardiometabolic risk. Low‐fat meal consumption resulted in higher glucose and insulin concentrations than high‐fat meal consumption. Data are shown as mean ± SEM (n = 29). A linear mixed model with repeated measures was used to test for effects of interventions, time points, and their interactions. ***p < 0.001 for fixed factor time, #p < 0.05 for fixed factor fat amount, ###p < 0.001 for fixed factor fat amount, $$$p < 0.001 for fat amount × time interaction. Abbreviations: HFM, high‐fat meal; LFM, low‐fat meal.

FIGURE 5

Fasting and postprandial concentrations of plasma IL‐6 in response to test meals in adults with increased cardiometabolic risk. Canola oil consumption resulted in a higher IL‐6 concentration than coconut oil consumption. Data are shown as mean ± SEM (n = 29). A linear mixed model with repeated measures was used to test for effects of interventions, time points, and their interactions. ***p < 0.001 for fixed factor time, €p < 0.05 for fixed factor fat type. Abbreviations: HFM, high‐fat meal; LFM, low‐fat meal.

FIGURE 6

Fasting and postprandial concentrations of plasma α‐tocopherol (A) and plasma γ‐tocopherol (B) in response to test meals in adults with increased cardiometabolic risk. Canola oil consumption resulted in a higher γ‐tocopherol concentration than coconut oil consumption. Data are shown as mean ± SEM (n = 29). A linear mixed model with repeated measures was used to test for effects of interventions, time points, and their interactions. ***p < 0.001 for fixed factor time, €€€p < 0.001 for fixed factor fat type, §§§p < 0.001 for fat type × time interaction, $p < 0.05 for fat amount × time interaction. Abbreviations: HFM, high‐fat meal; LFM, low‐fat meal.