Major changes in the sphingophospholipidome of HDL in non-diabetic patients with metabolic syndrome

Denimal, Damien; Nguyen, Amandine; Barros, Jean‐Paul Pais de; Bouillet, Benjamin; Petit, Jean‐Michel; Vergès, Bruno; Duvillard, Laurence

doi:10.1016/j.atherosclerosis.2015.12.042

Cited by 31 publications

(35 citation statements)

References 47 publications

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“…These data confirm previous observations that found no link between either TG or LPC circulating levels and insulin resistance in the context of obesity ( Coen and Goodpaster, 2012 ; del Bas et al, 2016 ; Eisinger et al, 2014 ; Tulipani et al, 2016 ). However, the reduced cardiac SM levels observed in HFD rats might participate in the cardiac insulin resistance observed in these animals since a direct correlation between levels of SM and 18 F-FDG uptake was observed, confirming previous data ( Denimal et al, 2016 ; Tonks et al, 2016 ). In agreement with this observation, we have found that cardiac SM levels are independent predictors of GLUT4 cardiac levels in HFD ( Marin-Royo et al, 2017 ).…”

Section: Discussionsupporting

confidence: 90%

Inhibition of galectin-3 ameliorates the consequences of cardiac lipotoxicity in a rat model of diet-induced obesity

Marín-Royo

Gallardo

Martínez‐Martínez

et al. 2018

Disease Models &Amp; Mechanisms

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Obesity is accompanied by metabolic alterations characterized by insulin resistance and cardiac lipotoxicity. Galectin-3 (Gal-3) induces cardiac inflammation and fibrosis in the context of obesity; however, its role in the metabolic consequences of obesity is not totally established. We have investigated the potential role of Gal-3 in the cardiac metabolic disturbances associated with obesity. In addition, we have explored whether this participation is, at least partially, acting on mitochondrial damage. Gal-3 inhibition in rats that were fed a high-fat diet (HFD) for 6 weeks with modified citrus pectin (MCP; 100 mg/kg/day) attenuated the increase in cardiac levels of total triglyceride (TG). MCP treatment also prevented the increase in cardiac protein levels of carnitine palmitoyl transferase IA, mitofusin 1, and mitochondrial complexes I and II, reactive oxygen species accumulation and decrease in those of complex V but did not affect the reduction in 18F-fluorodeoxyglucose uptake observed in HFD rats. The exposure of cardiac myoblasts (H9c2) to palmitic acid increased the rate of respiration, mainly due to an increase in the proton leak, glycolysis, oxidative stress, β-oxidation and reduced mitochondrial membrane potential. Inhibition of Gal-3 activity was unable to affect these changes. Our findings indicate that Gal-3 inhibition attenuates some of the consequences of cardiac lipotoxicity induced by a HFD since it reduced TG and lysophosphatidyl choline (LPC) levels. These reductions were accompanied by amelioration of the mitochondrial damage observed in HFD rats, although no improvement was observed regarding insulin resistance. These findings increase the interest for Gal-3 as a potential new target for therapeutic intervention to prevent obesity-associated cardiac lipotoxicity and subsequent mitochondrial dysfunction.

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Section: Discussionsupporting

confidence: 90%

Inhibition of galectin-3 ameliorates the consequences of cardiac lipotoxicity in a rat model of diet-induced obesity

Marín-Royo

Gallardo

Martínez‐Martínez

et al. 2018

Disease Models &Amp; Mechanisms

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“…Ether-PCs were previously reported to be decreased in HDL CHD (20) and in HDL of patients with metabolic syndrome (21), whereas others found them increased in HDL T2DM (18). Sphingomyelins were reported to be decreased in HDL of patients with metabolic syndrome in 1 study but not in another (18,22). An increased content of HDL in (polyunsaturated) PEs was previously reported for acute coronary syndrome patients and associated with increased thrombogenicity (23)(24)(25).…”

Section: Discussionmentioning

confidence: 82%

Structure-function relationships of HDL in diabetes and coronary heart disease

Cardner¹,

Yalçinkaya²,

Goetze³

et al. 2020

JCI Insight

103

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“…Lyso derivatives of alkylphosphatidylcholines, ether lipids without the sn-2 esterified fatty acid, were also negatively associated with T2D [34]. A recent study identified changes to the lipidome of HDL subpopulations, with decreases in choline plasmalogens associated with metabolic syndrome [46]. Due to the vinylether bond, plasmalogens are more prone to oxidation and act as a sacrificial antioxidant in lipid membranes and lipoproteins [47,48].…”

Section: Lipidomic Profiling In Diabetesmentioning

confidence: 99%

Lipidomic Profiles in Diabetes and Dementia

Huynh

Martins

Meikle

2017

JAD

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Lipids are a diverse class of hydrophobic and amphiphilic molecules which make up the bulk of most biological systems and are essential for human life. The role of lipids in health and disease has been recognized for many decades, as evidenced by the early identification of cholesterol as an important risk factor of heart disease and the development and introduction of statins as a one of the most successful therapeutic interventions to date. While several studies have demonstrated an increased risk of dementia, including Alzheimer's disease (AD), in those with diabetes mellitus, the nature of this risk is not well understood. Recent developments in the field of lipidomics, driven primarily by technological advances in high pressure liquid chromatography and particularly mass spectrometry, have enabled the detailed characterization of the many hundreds of individual lipid species in mammalian systems and their association with disease states. Diabetes mellitus and AD have received particular attention due to their prominence in Western societies as a result of the ongoing obesity epidemic and the aging populations. In this review, we examine how these lipidomic studies are informing on the relationship between lipid metabolism with diabetes and AD and how this may inform on the common pathological pathways that link diabetes risk with dementia.

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Major changes in the sphingophospholipidome of HDL in non-diabetic patients with metabolic syndrome

Cited by 31 publications

References 47 publications

Inhibition of galectin-3 ameliorates the consequences of cardiac lipotoxicity in a rat model of diet-induced obesity

Inhibition of galectin-3 ameliorates the consequences of cardiac lipotoxicity in a rat model of diet-induced obesity

Structure-function relationships of HDL in diabetes and coronary heart disease

Lipidomic Profiles in Diabetes and Dementia

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