Dietary sucrose induces metabolic inflammation and atherosclerotic cardiovascular diseases more than dietary fat in LDLr−/− ApoB100/100 mice

Research output: Contribution to journal › Journal article › Research › peer-review

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Dietary sucrose induces metabolic inflammation and atherosclerotic cardiovascular diseases more than dietary fat in LDLr−/− ApoB100/100 mice. / Perazza, Laís R.; Mitchell, Patricia L.; Jensen, Benjamin A.H.; Daniel, Noëmie; Boyer, Marjorie; Varin, Thibault V.; Bouchareb, Rihab; Nachbar, Renato T.; Bouchard, Michaël; Blais, Mylène; Gagné, Andréanne; Joubert, Philippe; Sweeney, Gary; Roy, Denis; Arsenault, Benoit J.; Mathieu, Patrick; Marette, André.

In: Atherosclerosis, Vol. 304, 2020, p. 9-21.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Perazza, LR, Mitchell, PL, Jensen, BAH, Daniel, N, Boyer, M, Varin, TV, Bouchareb, R, Nachbar, RT, Bouchard, M, Blais, M, Gagné, A, Joubert, P, Sweeney, G, Roy, D, Arsenault, BJ, Mathieu, P & Marette, A 2020, 'Dietary sucrose induces metabolic inflammation and atherosclerotic cardiovascular diseases more than dietary fat in LDLr−/− ApoB100/100 mice', Atherosclerosis, vol. 304, pp. 9-21. https://doi.org/10.1016/j.atherosclerosis.2020.05.002

APA

Perazza, L. R., Mitchell, P. L., Jensen, B. A. H., Daniel, N., Boyer, M., Varin, T. V., Bouchareb, R., Nachbar, R. T., Bouchard, M., Blais, M., Gagné, A., Joubert, P., Sweeney, G., Roy, D., Arsenault, B. J., Mathieu, P., & Marette, A. (2020). Dietary sucrose induces metabolic inflammation and atherosclerotic cardiovascular diseases more than dietary fat in LDLr−/− ApoB100/100 mice. Atherosclerosis, 304, 9-21. https://doi.org/10.1016/j.atherosclerosis.2020.05.002

Vancouver

Perazza LR, Mitchell PL, Jensen BAH, Daniel N, Boyer M, Varin TV et al. Dietary sucrose induces metabolic inflammation and atherosclerotic cardiovascular diseases more than dietary fat in LDLr−/− ApoB100/100 mice. Atherosclerosis. 2020;304:9-21. https://doi.org/10.1016/j.atherosclerosis.2020.05.002

Author

Perazza, Laís R. ; Mitchell, Patricia L. ; Jensen, Benjamin A.H. ; Daniel, Noëmie ; Boyer, Marjorie ; Varin, Thibault V. ; Bouchareb, Rihab ; Nachbar, Renato T. ; Bouchard, Michaël ; Blais, Mylène ; Gagné, Andréanne ; Joubert, Philippe ; Sweeney, Gary ; Roy, Denis ; Arsenault, Benoit J. ; Mathieu, Patrick ; Marette, André. / Dietary sucrose induces metabolic inflammation and atherosclerotic cardiovascular diseases more than dietary fat in LDLr−/− ApoB100/100 mice. In: Atherosclerosis. 2020 ; Vol. 304. pp. 9-21.

Bibtex

@article{8ae8adb77bb945f894e791246dc1d906,
title = "Dietary sucrose induces metabolic inflammation and atherosclerotic cardiovascular diseases more than dietary fat in LDLr−/− ApoB100/100 mice",
abstract = "Background and aims: Poor dietary habits contribute to the obesity pandemic and related cardiovascular diseases but the respective impact of high saturated fat versus added sugar consumption remains debated. Herein, we aimed to disentangle the individual role of dietary fat versus sugar in cardiometabolic disease progression. Methods: We fed pro-atherogenic LDLr−/− ApoB100/100 mice either a low-fat/high-sucrose (LFHS) or a high-fat/low-sucrose (HFLS) diet for 24 weeks. Weekly body weight gain was registered. 16S rRNA gene-based gut microbial analysis was performed to investigate gut microbial modulations. Intraperitoneal insulin (ipITT) and oral glucose tolerance test (oGTT) were conducted to assess glucose homeostasis and insulin sensitivity. Cytokines were assessed in fasted plasma, epididymal white adipose tissue and liver lysates. Heart function was evaluated by echocardiography. Aortic atheroma lesions were quantified according to the en face technique. Results: HFLS feeding increased obesity, insulin resistance and dyslipidemia compared to LFHS feeding. Conversely, high sucrose consumption decreased gut microbial diversity while augmenting inflammation and the adaptative immune defense against metabolic endotoxemia and reduced macrophage cholesterol efflux capacity. This led to more severe cardiovascular complications as revealed by remarkably high level of atherosclerotic lesions and the early development of cardiac dysfunction in LFHS vs HFLS fed mice. Conclusions: We uncoupled obesity-associated insulin resistance from cardiovascular diseases and provided novel evidence that dietary sucrose, not fat, is the main driver of metabolic inflammation accelerating severe atherosclerosis in hyperlipidemic mice.",
keywords = "CVD, Fat, Inflammation, Insulin resistance, Obesity, Sugar",
author = "Perazza, {La{\'i}s R.} and Mitchell, {Patricia L.} and Jensen, {Benjamin A.H.} and No{\"e}mie Daniel and Marjorie Boyer and Varin, {Thibault V.} and Rihab Bouchareb and Nachbar, {Renato T.} and Micha{\"e}l Bouchard and Myl{\`e}ne Blais and Andr{\'e}anne Gagn{\'e} and Philippe Joubert and Gary Sweeney and Denis Roy and Arsenault, {Benoit J.} and Patrick Mathieu and Andr{\'e} Marette",
year = "2020",
doi = "10.1016/j.atherosclerosis.2020.05.002",
language = "English",
volume = "304",
pages = "9--21",
journal = "Journal of atherosclerosis research",
issn = "1567-5688",
publisher = "Elsevier Ireland Ltd",

}

RIS

TY - JOUR

T1 - Dietary sucrose induces metabolic inflammation and atherosclerotic cardiovascular diseases more than dietary fat in LDLr−/− ApoB100/100 mice

AU - Perazza, Laís R.

AU - Mitchell, Patricia L.

AU - Jensen, Benjamin A.H.

AU - Daniel, Noëmie

AU - Boyer, Marjorie

AU - Varin, Thibault V.

AU - Bouchareb, Rihab

AU - Nachbar, Renato T.

AU - Bouchard, Michaël

AU - Blais, Mylène

AU - Gagné, Andréanne

AU - Joubert, Philippe

AU - Sweeney, Gary

AU - Roy, Denis

AU - Arsenault, Benoit J.

AU - Mathieu, Patrick

AU - Marette, André

PY - 2020

Y1 - 2020

N2 - Background and aims: Poor dietary habits contribute to the obesity pandemic and related cardiovascular diseases but the respective impact of high saturated fat versus added sugar consumption remains debated. Herein, we aimed to disentangle the individual role of dietary fat versus sugar in cardiometabolic disease progression. Methods: We fed pro-atherogenic LDLr−/− ApoB100/100 mice either a low-fat/high-sucrose (LFHS) or a high-fat/low-sucrose (HFLS) diet for 24 weeks. Weekly body weight gain was registered. 16S rRNA gene-based gut microbial analysis was performed to investigate gut microbial modulations. Intraperitoneal insulin (ipITT) and oral glucose tolerance test (oGTT) were conducted to assess glucose homeostasis and insulin sensitivity. Cytokines were assessed in fasted plasma, epididymal white adipose tissue and liver lysates. Heart function was evaluated by echocardiography. Aortic atheroma lesions were quantified according to the en face technique. Results: HFLS feeding increased obesity, insulin resistance and dyslipidemia compared to LFHS feeding. Conversely, high sucrose consumption decreased gut microbial diversity while augmenting inflammation and the adaptative immune defense against metabolic endotoxemia and reduced macrophage cholesterol efflux capacity. This led to more severe cardiovascular complications as revealed by remarkably high level of atherosclerotic lesions and the early development of cardiac dysfunction in LFHS vs HFLS fed mice. Conclusions: We uncoupled obesity-associated insulin resistance from cardiovascular diseases and provided novel evidence that dietary sucrose, not fat, is the main driver of metabolic inflammation accelerating severe atherosclerosis in hyperlipidemic mice.

AB - Background and aims: Poor dietary habits contribute to the obesity pandemic and related cardiovascular diseases but the respective impact of high saturated fat versus added sugar consumption remains debated. Herein, we aimed to disentangle the individual role of dietary fat versus sugar in cardiometabolic disease progression. Methods: We fed pro-atherogenic LDLr−/− ApoB100/100 mice either a low-fat/high-sucrose (LFHS) or a high-fat/low-sucrose (HFLS) diet for 24 weeks. Weekly body weight gain was registered. 16S rRNA gene-based gut microbial analysis was performed to investigate gut microbial modulations. Intraperitoneal insulin (ipITT) and oral glucose tolerance test (oGTT) were conducted to assess glucose homeostasis and insulin sensitivity. Cytokines were assessed in fasted plasma, epididymal white adipose tissue and liver lysates. Heart function was evaluated by echocardiography. Aortic atheroma lesions were quantified according to the en face technique. Results: HFLS feeding increased obesity, insulin resistance and dyslipidemia compared to LFHS feeding. Conversely, high sucrose consumption decreased gut microbial diversity while augmenting inflammation and the adaptative immune defense against metabolic endotoxemia and reduced macrophage cholesterol efflux capacity. This led to more severe cardiovascular complications as revealed by remarkably high level of atherosclerotic lesions and the early development of cardiac dysfunction in LFHS vs HFLS fed mice. Conclusions: We uncoupled obesity-associated insulin resistance from cardiovascular diseases and provided novel evidence that dietary sucrose, not fat, is the main driver of metabolic inflammation accelerating severe atherosclerosis in hyperlipidemic mice.

KW - CVD

KW - Fat

KW - Inflammation

KW - Insulin resistance

KW - Obesity

KW - Sugar

U2 - 10.1016/j.atherosclerosis.2020.05.002

DO - 10.1016/j.atherosclerosis.2020.05.002

M3 - Journal article

C2 - 32563005

AN - SCOPUS:85086602065

VL - 304

SP - 9

EP - 21

JO - Journal of atherosclerosis research

JF - Journal of atherosclerosis research

SN - 1567-5688

ER -

ID: 245615902