Year-end Sale % OFF 
Abstract
BackgroundLipoproteins are major players in the development and progression of atherosclerotic plaques leading to coronary stenosis and myocardial infarction. Epidemiological, genetic and experimental observations have implicated the association of sphingolipids and intermediates of sphingolipid synthesis in atherosclerosis. We aimed to investigate relationships between quantitative changes in serum sphingolipids, the regulation of the metabolism of lipoproteins (LDL, HDL), and endophenotypes of coronary artery disease (CAD).MethodsWe carried out untargeted liquid chromatography – mass spectrometry (UPLC-MS) lipidomics of serum samples of subjects belonging to a cross-sectional study and recruited on the basis of absence or presence of angiographically-defined CAD, and extensively characterized for clinical and biochemical phenotypes.ResultsAmong the 2998 spectral features detected in the serum samples, 1328 metabolic features were significantly correlated with at least one of the clinical or biochemical phenotypes measured in the cohort. We found evidence of significant associations between 34 metabolite signals, corresponding to a set of sphingomyelins, and serum HDL cholesterol. Many of these metabolite associations were also observed with serum LDL and total cholesterol levels but not as much with serum triglycerides.ConclusionAmong patients with CAD, sphingolipids in the form of sphingomyelins are directly correlated with serum levels of lipoproteins and total cholesterol. Results from this study support the fundamental role of sphingolipids in modulating lipid serum levels, highlighting the importance to identify novel targets in the sphingolipid metabolic pathway for anti-atherogenic therapies.
Highlights
Coronary artery disease (CAD) is the leading cause of mortality caused by a complex interplay of genetic and environmental factors [1]
Accumulation of fatty deposits in the intima layer of arteries leads to arterial stiffness and formation of plaques that result in narrowing of arteries and eventually coronary artery stenosis [2]
Clinical and biochemical data analysis The study population consisted of 109 individuals with a mean age of 53.38 ± 1.07 years, a mean body weight of 77.59 ± 1.56 kg, a mean body mass index (BMI) of 27.77 ± 0.47 kg/m2, a mean total cholesterol of 189.91 ± 3.74 mg/dL, a mean LDL of 116.52 ± 3.13 mg/dL, a mean high-density lipoprotein cholesterol (HDL-C) level of 39.94 ± 0.98 mg/dL and a mean fasting plasma glucose of 107.81 ± 3.96 mg/ dL (Table 1)
Summary
Coronary artery disease (CAD) is the leading cause of mortality caused by a complex interplay of genetic and environmental factors [1]. Metabolomics and lipidomics are powerful strategies to qualitatively and quantitatively analyze a wide range of small molecules in a biological sample, Zalloua et al Lipids in Health and Disease (2019) 18:38 which represent endpoints of genome expression [6]. They provide a source of molecular endophenotypes (i.e. intermediate phenotypes) that can massively refine phenotypic information in patients and healthy individuals [7]. We aimed to investigate relationships between quantitative changes in serum sphingolipids, the regulation of the metabolism of lipoproteins (LDL, HDL), and endophenotypes of coronary artery disease (CAD)
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
