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Insights into the Alteration of Lipid Metabolism in Cardiometabolic Diseases...
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Insights into the Alteration of Lipid Metabolism in Cardiometabolic Diseases Vol.2

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Lipid Metabolism".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 13325

Special Issue Editor

Dr. Wilfried Le Goff

E-Mail Website
Guest Editor
Sorbonne Université, Inserm, Institute of Cardiometabolism and Nutrition (ICAN), UMR_S1166, F-75013 Paris, France
Interests: lipids; lipidomic; lipoproteins; macrophages; cardiometabolic diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiometabolic diseases are characterized by major alterations in lipid metabolism affecting both systemic and cellular compartments. Consumption of lipid-enriched diets induces major modifications in the concentration and composition of circulating lipoproteins causing dyslipidemia. Importantly, dietary lipids profoundly impact the synthesis of lipoproteins in specialized tissues as well as the complex lipid composition of lipoproteins with consequences on their biological activities. At the cellular level, dietary lipids together with the disturbed lipoprotein phenotype induce a profound change of lipid metabolism in major tissues including but not limited to liver, adipose tissue, intestine, pancreas, muscle, and heart participating in their remodeling and in some cases in their metabolic activation as observed in macrophages. Such remodeling may occur through alterations in membrane lipid structure, signaling pathways, generation of bioactive or cytotoxic lipids, as well as in the capacity to handle this excess of lipids (storage vs. catabolism vs. recycling). All these modifications participate in the development of the spectrum of metabolic disorders including obesity, insulin resistance, diabetes, non-alcoholic fatty liver diseases, and atherosclerosis, contributing to cardiovascular diseases.

The second volume of this Special Issue of Metabolites, which follows the previous volume (https://www.mdpi.com/journal/metabolites/special_issues/lipid_metabolisms_cardiometabolic), is dedicated to publishing current advances on mechanisms underlying these alterations of the systemic and cellular lipid metabolism as well as their biological consequences in the context of cardiometabolic diseases. All the fields related to the study of lipids involving genetic/epigenetic, biochemical, molecular, cellular, and omics approaches will be covered in this issue.

Dr. Wilfried Le Goff
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • lipid
  • lipidomic
  • lipoprotein
  • membrane
  • obesity
  • diabetes
  • insulin resistance
  • NAFLD
  • atherosclerosis

Related Special Issue

Published Papers (5 papers)

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Research

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14 pages, 1343 KiB  
Article
Progressive, Qualitative, and Quantitative Alterations in HDL Lipidome from Healthy Subjects to Patients with Prediabetes and Type 2 Diabetes
by Christina E. Kostara, Kiriaki S. Karakitsou, Matilda Florentin, Eleni T. Bairaktari and Vasilis Tsimihodimos
Metabolites 2022, 12(8), 683; https://doi.org/10.3390/metabo12080683 - 25 Jul 2022
Cited by 9 | Viewed by 1860
Abstract
Prediabetes is a clinically silent, insulin-resistant state with increased risk for the development of type 2 diabetes (T2D) and cardiovascular disease (CVD). Since glucose homeostasis and lipid metabolism are highly intersected and interrelated, an in-depth characterization of qualitative and quantitative abnormalities in lipoproteins [...] Read more.
Prediabetes is a clinically silent, insulin-resistant state with increased risk for the development of type 2 diabetes (T2D) and cardiovascular disease (CVD). Since glucose homeostasis and lipid metabolism are highly intersected and interrelated, an in-depth characterization of qualitative and quantitative abnormalities in lipoproteins could unravel the metabolic pathways underlying the progression of prediabetes to T2D and also the proneness of these patients to developing premature atherosclerosis. We investigated the HDL lipidome in 40 patients with prediabetes and compared it to that of 40 normoglycemic individuals and 40 patients with established T2D using Nuclear Magnetic Resonance (NMR) spectroscopy. Patients with prediabetes presented significant qualitative and quantitative alterations, potentially atherogenic, in HDL lipidome compared to normoglycemic characterized by higher percentages of free cholesterol and triglycerides, whereas phospholipids were lower. Glycerophospholipids and ether glycerolipids were significantly lower in prediabetic compared to normoglycemic individuals, whereas sphingolipids were significantly higher. In prediabetes, lipids were esterified with saturated rather than unsaturated fatty acids. These changes are qualitatively similar, but quantitatively milder, than those found in patients with T2D. We conclude that the detailed characterization of the HDL lipid profile bears a potential to identify patients with subtle (but still proatherogenic) abnormalities who are at high risk for development of T2D and CVD. Full article
(This article belongs to the Special Issue Insights into the Alteration of Lipid Metabolism in Cardiometabolic Diseases Vol.2)
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16 pages, 1969 KiB  
Article
Post-Transcriptional Effects of miRNAs on PCSK7 Expression and Function: miR-125a-5p, miR-143-3p, and miR-409-3p as Negative Regulators
by Mahshid Malakootian, Parisa Naeli, Seyed Javad Mowla and Nabil G. Seidah
Metabolites 2022, 12(7), 588; https://doi.org/10.3390/metabo12070588 - 23 Jun 2022
Cited by 3 | Viewed by 1716
Abstract
The regulatory mechanism of PCSK7 gene is still unknown, although its encoded protein PC7 is the most ancient and highly conserved of all proprotein convertases and exhibits enzymatic and non-enzymatic functions in liver triglyceride regulation. Bioinformatics algorithms were used to predict regulatory microRNAs [...] Read more.
The regulatory mechanism of PCSK7 gene is still unknown, although its encoded protein PC7 is the most ancient and highly conserved of all proprotein convertases and exhibits enzymatic and non-enzymatic functions in liver triglyceride regulation. Bioinformatics algorithms were used to predict regulatory microRNAs (miRNAs) of PCSK7 expression. This led to the identification of four miRNAs, namely miR-125a-5p, miR-143-3p, miR-409-3p, and miR-320a-3p, with potential binding sites on the 3′-untranslated region (3′-UTR) of human PCSK7 mRNA. The expression patterns of these miRNAs and PCSK7 mRNA were assessed in three different cell lines with quantitative polymerase chain reaction (qPCR), which revealed reciprocal expression patterns between the expression levels of the four selected miRNAs and PCSK7. Next, the interactions and effects of these miRNAs on PCSK7 expression levels were investigated via cell-based expression analysis, dual-luciferase assay, and Western blot analysis. The data revealed that PCSK7 mRNA levels decreased in cells transfected with vectors overexpressing miR-125a-5p, miR-143-3p, and miR-409-3p, but not miR-320a-3p. The dual-luciferase assay demonstrated that the above three miRNAs could directly interact with putative target sites in PCSK7 3′-UTR and regulate its expression, whereas miR-320-3p exhibited no interaction. Western blot analysis further revealed that the overexpression of miR-125a-5p in Huh7 cells inhibits the expression and ability of PC7 to cleave human transferrin receptor 1. Our results support a regulatory role of these miRNAs on PCSK7 expression and function and open the way to assess their roles in the regulation of PC7 activity in vivo in the development of hepatic steatosis. Full article
(This article belongs to the Special Issue Insights into the Alteration of Lipid Metabolism in Cardiometabolic Diseases Vol.2)
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Review

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17 pages, 1174 KiB  
Review
Atherosclerosis Calcification: Focus on Lipoproteins
by Jaap G. Neels, Georges Leftheriotis and Giulia Chinetti
Metabolites 2023, 13(3), 457; https://doi.org/10.3390/metabo13030457 - 21 Mar 2023
Cited by 4 | Viewed by 4348
Abstract
Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipids in the vessel wall, leading to the formation of an atheroma and eventually to the development of vascular calcification (VC). Lipoproteins play a central role in the development of atherosclerosis and [...] Read more.
Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipids in the vessel wall, leading to the formation of an atheroma and eventually to the development of vascular calcification (VC). Lipoproteins play a central role in the development of atherosclerosis and VC. Both low- and very low-density lipoproteins (LDL and VLDL) and lipoprotein (a) (Lp(a)) stimulate, while high-density lipoproteins (HDL) reduce VC. Apolipoproteins, the protein component of lipoproteins, influence the development of VC in multiple ways. Apolipoprotein AI (apoAI), the main protein component of HDL, has anti-calcific properties, while apoB and apoCIII, the main protein components of LDL and VLDL, respectively, promote VC. The role of lipoproteins in VC is also related to their metabolism and modifications. Oxidized LDL (OxLDL) are more pro-calcific than native LDL. Oxidation also converts HDL from anti- to pro-calcific. Additionally, enzymes such as autotaxin (ATX) and proprotein convertase subtilisin/kexin type 9 (PCSK9), involved in lipoprotein metabolism, have a stimulatory role in VC. In summary, a better understanding of the mechanisms by which lipoproteins and apolipoproteins contribute to VC will be crucial in the development of effective preventive and therapeutic strategies for VC and its associated cardiovascular disease. Full article
(This article belongs to the Special Issue Insights into the Alteration of Lipid Metabolism in Cardiometabolic Diseases Vol.2)
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24 pages, 1604 KiB  
Review
Neurotransmitters in Type 2 Diabetes and the Control of Systemic and Central Energy Balance
by Amnah Al-Sayyar, Maha M. Hammad, Michayla R. Williams, Mohammed Al-Onaizi, Jehad Abubaker and Fawaz Alzaid
Metabolites 2023, 13(3), 384; https://doi.org/10.3390/metabo13030384 - 04 Mar 2023
Cited by 4 | Viewed by 2930
Abstract
Efficient signal transduction is important in maintaining the function of the nervous system across tissues. An intact neurotransmission process can regulate energy balance through proper communication between neurons and peripheral organs. This ensures that the right neural circuits are activated in the brain [...] Read more.
Efficient signal transduction is important in maintaining the function of the nervous system across tissues. An intact neurotransmission process can regulate energy balance through proper communication between neurons and peripheral organs. This ensures that the right neural circuits are activated in the brain to modulate cellular energy homeostasis and systemic metabolic function. Alterations in neurotransmitters secretion can lead to imbalances in appetite, glucose metabolism, sleep, and thermogenesis. Dysregulation in dietary intake is also associated with disruption in neurotransmission and can trigger the onset of type 2 diabetes (T2D) and obesity. In this review, we highlight the various roles of neurotransmitters in regulating energy balance at the systemic level and in the central nervous system. We also address the link between neurotransmission imbalance and the development of T2D as well as perspectives across the fields of neuroscience and metabolism research. Full article
(This article belongs to the Special Issue Insights into the Alteration of Lipid Metabolism in Cardiometabolic Diseases Vol.2)
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26 pages, 2748 KiB  
Review
High-Density Lipoprotein Alterations in Type 2 Diabetes and Obesity
by Damien Denimal, Serge Monier, Benjamin Bouillet, Bruno Vergès and Laurence Duvillard
Metabolites 2023, 13(2), 253; https://doi.org/10.3390/metabo13020253 - 09 Feb 2023
Cited by 7 | Viewed by 1773
Abstract
Alterations affecting high-density lipoproteins (HDLs) are one of the various abnormalities observed in dyslipidemia in type 2 diabetes mellitus (T2DM) and obesity. Kinetic studies have demonstrated that the catabolism of HDL particles is accelerated. Both the size and the lipidome and proteome of [...] Read more.
Alterations affecting high-density lipoproteins (HDLs) are one of the various abnormalities observed in dyslipidemia in type 2 diabetes mellitus (T2DM) and obesity. Kinetic studies have demonstrated that the catabolism of HDL particles is accelerated. Both the size and the lipidome and proteome of HDL particles are significantly modified, which likely contributes to some of the functional defects of HDLs. Studies on cholesterol efflux capacity have yielded heterogeneous results, ranging from a defect to an improvement. Several studies indicate that HDLs are less able to inhibit the nuclear factor kappa-B (NF-κB) proinflammatory pathway, and subsequently, the adhesion of monocytes on endothelium and their recruitment into the subendothelial space. In addition, the antioxidative function of HDL particles is diminished, thus facilitating the deleterious effects of oxidized low-density lipoproteins on vasculature. Lastly, the HDL-induced activation of endothelial nitric oxide synthase is less effective in T2DM and metabolic syndrome, contributing to several HDL functional defects, such as an impaired capacity to promote vasodilatation and endothelium repair, and difficulty counteracting the production of reactive oxygen species and inflammation. Full article
(This article belongs to the Special Issue Insights into the Alteration of Lipid Metabolism in Cardiometabolic Diseases Vol.2)
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