Substitution of dietary monounsaturated fatty acids from olive oil for saturated fatty acids from lard increases LDL apolipoprotein B-100 fractional catabolic rate in subjects with dyslipidemia associated with insulin resistance: a randomized controlled trial.

insulin resistance lipidomics lipoprotein metabolism monounsaturated fatty acids saturated fatty acids

Journal

The American journal of clinical nutrition
ISSN: 1938-3207
Titre abrégé: Am J Clin Nutr
Pays: United States
ID NLM: 0376027

Informations de publication

Date de publication:
20 Mar 2024
Historique:
received: 17 10 2023
revised: 21 02 2024
accepted: 18 03 2024
medline: 23 3 2024
pubmed: 23 3 2024
entrez: 22 3 2024
Statut: aheadofprint

Résumé

The substitution of monounsaturated acids (MUFAs) for saturated fatty acids (SFAs) is recommended for cardiovascular disease prevention but its impact on lipoprotein metabolism in subjects with dyslipidemia associated with insulin resistance (IR) remains largely unknown. This study aimed to evaluate the impact of substituting MUFAs for SFAs on the in vivo kinetics of apolipoprotein (apo)B-containing lipoproteins and on the plasma lipidomic profile in adults with IR-induced dyslipidemia. Males and females with dyslipidemia associated with IR (n = 18) were recruited for this crossover double-blind randomized controlled trial. Subjects consumed, in random order, a diet rich in SFAs (SFAs: 13.4%E; MUFAs: 14.4%E) and a diet rich in MUFAs (SFAs: 7.1%E; MUFAs: 20.7%E) in fully controlled feeding conditions for periods of 4 wk each, separated by a 4-wk washout. At the end of each diet, fasting plasma samples were taken together with measurements of the in vivo kinetics of apoB-containing lipoproteins. Substituting MUFAs for SFAs had no impact on TRL apoB-48 fractional catabolic rate (FCR) (Δ = -8.9%, P = 0.4) and production rate (PR) (Δ = 0.0%, P = 0.9), although it decreased VLDL apoB-100 pool size (PS) (Δ = -22.5%; P = 0.01). This substitution also reduced LDL-C (Δ = -7.0%; P = 0.01), non-HDL cholesterol (Δ = -2.5%; P = 0.04) and LDL apoB-100 PS (Δ = -6.0%; P = 0.05). These differences were partially attributed to an increase in LDL apoB-100 FCR (Δ = +1.6%; P = 0.05). The MUFA diet showed reduced sphingolipid concentrations and elevated glycerophospholipid levels compared with the SFA diet. This study demonstrated that substituting dietary MUFAs for SFAs decreases LDL-C levels and LDL PS by increasing LDL apoB-100 FCR and results in an overall improved plasma lipidomic profile in individuals with IR-induced lipidemia. clinicaltrials.gov NCT03872349.

Sections du résumé

BACKGROUND BACKGROUND
The substitution of monounsaturated acids (MUFAs) for saturated fatty acids (SFAs) is recommended for cardiovascular disease prevention but its impact on lipoprotein metabolism in subjects with dyslipidemia associated with insulin resistance (IR) remains largely unknown.
OBJECTIVE OBJECTIVE
This study aimed to evaluate the impact of substituting MUFAs for SFAs on the in vivo kinetics of apolipoprotein (apo)B-containing lipoproteins and on the plasma lipidomic profile in adults with IR-induced dyslipidemia.
DESIGN METHODS
Males and females with dyslipidemia associated with IR (n = 18) were recruited for this crossover double-blind randomized controlled trial. Subjects consumed, in random order, a diet rich in SFAs (SFAs: 13.4%E; MUFAs: 14.4%E) and a diet rich in MUFAs (SFAs: 7.1%E; MUFAs: 20.7%E) in fully controlled feeding conditions for periods of 4 wk each, separated by a 4-wk washout. At the end of each diet, fasting plasma samples were taken together with measurements of the in vivo kinetics of apoB-containing lipoproteins.
RESULTS RESULTS
Substituting MUFAs for SFAs had no impact on TRL apoB-48 fractional catabolic rate (FCR) (Δ = -8.9%, P = 0.4) and production rate (PR) (Δ = 0.0%, P = 0.9), although it decreased VLDL apoB-100 pool size (PS) (Δ = -22.5%; P = 0.01). This substitution also reduced LDL-C (Δ = -7.0%; P = 0.01), non-HDL cholesterol (Δ = -2.5%; P = 0.04) and LDL apoB-100 PS (Δ = -6.0%; P = 0.05). These differences were partially attributed to an increase in LDL apoB-100 FCR (Δ = +1.6%; P = 0.05). The MUFA diet showed reduced sphingolipid concentrations and elevated glycerophospholipid levels compared with the SFA diet.
CONCLUSIONS CONCLUSIONS
This study demonstrated that substituting dietary MUFAs for SFAs decreases LDL-C levels and LDL PS by increasing LDL apoB-100 FCR and results in an overall improved plasma lipidomic profile in individuals with IR-induced lipidemia.
TRIAL REGISTRATION BACKGROUND
clinicaltrials.gov NCT03872349.

Identifiants

pubmed: 38518848
pii: S0002-9165(24)00382-4
doi: 10.1016/j.ajcnut.2024.03.015
pii:
doi:

Banques de données

ClinicalTrials.gov
['NCT03872349']

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024 American Society for Nutrition. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests ☒ The authors declare the following financial interests/personal relationships which may be considered as potential competing interestsPatrick Couture reports financial support was provided by Canadian Institutes of Health Research. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Louis-Charles Desjardins (LC)

Centre Nutrition, santé et société (NUTRISS), Institute of Nutrition and Functional Foods (INAF), Université Laval, Quebec, G1V 0A6, Canada; School of nutrition, Université Laval, Quebec, G1V 0A6, Canada.

Francis Brière (F)

Centre Nutrition, santé et société (NUTRISS), Institute of Nutrition and Functional Foods (INAF), Université Laval, Quebec, G1V 0A6, Canada; Faculty of medicine, Université Laval, Quebec, G1V 0A6, Canada.

André J Tremblay (AJ)

Centre Nutrition, santé et société (NUTRISS), Institute of Nutrition and Functional Foods (INAF), Université Laval, Quebec, G1V 0A6, Canada.

Maryka Rancourt-Bouchard (M)

Centre Nutrition, santé et société (NUTRISS), Institute of Nutrition and Functional Foods (INAF), Université Laval, Quebec, G1V 0A6, Canada; School of nutrition, Université Laval, Quebec, G1V 0A6, Canada; Faculty of pharmacy, Université Laval, Quebec, G1V 0A6, Canada.

Jean-Philippe Drouin-Chartier (JP)

Centre Nutrition, santé et société (NUTRISS), Institute of Nutrition and Functional Foods (INAF), Université Laval, Quebec, G1V 0A6, Canada; Faculty of pharmacy, Université Laval, Quebec, G1V 0A6, Canada.

Jacques Corbeil (J)

Centre Nutrition, santé et société (NUTRISS), Institute of Nutrition and Functional Foods (INAF), Université Laval, Quebec, G1V 0A6, Canada; Faculty of medicine, Université Laval, Quebec, G1V 0A6, Canada; Big Data Research Centre, Université Laval, Quebec, G1V 0A6, Canada.

Valéry Lemelin (V)

CHU de Québec-Université Laval Research Center, Quebec, QC, G1V 4G2, Canada.

Amélie Charest (A)

Centre Nutrition, santé et société (NUTRISS), Institute of Nutrition and Functional Foods (INAF), Université Laval, Quebec, G1V 0A6, Canada; School of nutrition, Université Laval, Quebec, G1V 0A6, Canada.

Ernst J Schaefer (EJ)

Boston Heart Diagnostics, Framingham, MA, 01702, USA.

Benoît Lamarche (B)

Centre Nutrition, santé et société (NUTRISS), Institute of Nutrition and Functional Foods (INAF), Université Laval, Quebec, G1V 0A6, Canada; School of nutrition, Université Laval, Quebec, G1V 0A6, Canada.

Patrick Couture (P)

Centre Nutrition, santé et société (NUTRISS), Institute of Nutrition and Functional Foods (INAF), Université Laval, Quebec, G1V 0A6, Canada; Faculty of medicine, Université Laval, Quebec, G1V 0A6, Canada; CHU de Québec-Université Laval Research Center, Quebec, QC, G1V 4G2, Canada. Electronic address: patrick.couture@fmed.ulaval.ca.

Classifications MeSH