Lipid Metabolism in Health and Disease 2023

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biomacromolecules: Lipids".

Deadline for manuscript submissions: closed (20 October 2023) | Viewed by 3111

Special Issue Editors


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Guest Editor
Department of Analytical Chemistry, Medical Univesrity of Białystok, Bialystok, Poland
Interests: oxidative stress and its consequences in various pathological conditions in humans (tick diseases, RA, skin diseases, cancer, hypertension); animal models and cell cultures; modification of the structure and function of phospholipids metabolites; proteins involved in metabolic processes
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Guest Editor
Institute Ruder Boskovic, Zagreb, Croatia
Interests: multidisciplinary areas of molecular medicine and life sciences; focused and stress and age-associated diseases; pathophysiology of lipid peroxidation as common fundamental processes of cancer; inflammation and degenerative processes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

While the pathophysiology of various diseases includes the onset of oxidative stress, the majority of chronic and aggressive stress-associated disorders also alter lipid metabolism. Therefore, increasing attention is given to the reactive oxygen species (ROS)- and enzyme-dependent metabolism of lipids.

The observed changes in lipid mediators involved in signal transduction at the (sub)cellular level and in particular organs or entire organisms help understand the metabolic functions of lipids in both physiology and pathology of various disease states. The development of analytical tools for metabolomic–lipidomic studies, such as platforms for separation techniques in combination with mass spectrometry and new chemometric methodologies, together with advanced immunochemical methods, supports a more accurate assessment of the lipidome, aiming to solve metabolic problems known for years.

The aim of this Special Issue is to publish papers focused on important pathophysiological changes in the lipidome of cells, tissues, or body fluids with respect to human diseases, including translational in vitro and in vivo models that might help the development of integrative biomedical diagnostics and treatments for stress-associated lipid disorders.

Prof. Dr. Elz̀bieta Skrzydlewska
Prof. Dr. Neven Zarkovic
Guest Editors

Manuscript Submission Information

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Keywords

  • redox homeostasis disorders
  • lipid metabolism
  • lipid peroxidation
  • lipid mediators
  • lipidomics
  • lipid biomarkers of diseases
  • pharmacotherapy

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Published Papers (2 papers)

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Research

35 pages, 10537 KiB  
Article
Metabolomics Analysis and Biochemical Profiling of Arsenic-Induced Metabolic Impairment and Disease Susceptibility
by Syed Muhammad Shoaib, Samina Afzal, Ali Feezan, Muhammad Sajid Hamid Akash, Ahmed Nadeem and Tahir Maqbool Mir
Biomolecules 2023, 13(9), 1424; https://0-doi-org.brum.beds.ac.uk/10.3390/biom13091424 - 20 Sep 2023
Viewed by 1391
Abstract
Our study aimed to conduct a comprehensive biochemical profiling and metabolomics analysis to investigate the effects of arsenic-induced metabolic disorders, with a specific focus on disruptions in lipid metabolism, amino acid metabolism, and carbohydrate metabolism. Additionally, we sought to assess the therapeutic potential [...] Read more.
Our study aimed to conduct a comprehensive biochemical profiling and metabolomics analysis to investigate the effects of arsenic-induced metabolic disorders, with a specific focus on disruptions in lipid metabolism, amino acid metabolism, and carbohydrate metabolism. Additionally, we sought to assess the therapeutic potential of resveratrol (RSV) as a remedy for arsenic-induced diabetes, using metformin (MF) as a standard drug for comparison. We measured the total arsenic content in mouse serum by employing inductively coupled plasma mass spectrometry (ICP-MS) after administering a 50-ppm solution of sodium arsenate (50 mg/L) in purified water. Our findings revealed a substantial increase in total arsenic content in the exposed group, with a mean value of 166.80 ± 8.52 ppb (p < 0.05). Furthermore, we investigated the impact of arsenic exposure on various biomarkers using enzyme-linked immunosorbent assay (ELISA) methods. Arsenic exposed mice exhibited significant hyperglycemia (p < 0.001) and elevated levels of homeostatic model assessment of insulin resistance (HOMA-IR), hemoglobin A1c (Hb1Ac), Inflammatory biomarkers as well as liver and kidney function biomarkers (p < 0.05). Additionally, the levels of crucial enzymes linked to carbohydrate metabolism, including α-glucosidase, hexokinase, and glucose-6-phosphatase (G6PS), and oxidative stress biomarkers, such as levels of glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD), were significantly reduced in the arsenic-exposed group compared to the control group (p < 0.05). However, the level of MDA was significantly increased. Molecular analysis of gene expression indicated significant upregulation of key enzymes involved in lipid metabolism, such as carnitine palmitoyl-transferase-I (CPT-I), carnitine palmitoyl-transferase-II (CPT-II), lecithin–cholesterol acyltransferase (LCAT), and others. Additionally, alterations in gene expression related to glucose transporter-2 (GLUT-2), glucose-6-phosphatase (G6PC), and glucokinase (GK), associated with carbohydrate metabolism, were observed. Amino acid analysis revealed significant decreases in nine amino acids in arsenic-exposed mice. Metabolomics analysis identified disruptions in lipid metabolomes, amino acids, and arsenic metabolites, highlighting their involvement in essential metabolic pathways. Histopathological observations revealed significant changes in liver architecture, hepatocyte degeneration, and increased Kupffer cells in the livers of arsenic-exposed mice. In conclusion, these findings enhance our comprehension of the impact of environmental toxins on metabolic health and offer potential avenues for remedies against such disruptions. Full article
(This article belongs to the Special Issue Lipid Metabolism in Health and Disease 2023)
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16 pages, 2055 KiB  
Article
Eicosapentaenoic Acid Influences the Lipid Profile of an In Vitro Psoriatic Skin Model Produced with T Cells
by Sophie Morin, Andréa Tremblay, Elizabeth Dumais, Pierre Julien, Nicolas Flamand and Roxane Pouliot
Biomolecules 2023, 13(9), 1413; https://0-doi-org.brum.beds.ac.uk/10.3390/biom13091413 - 19 Sep 2023
Cited by 1 | Viewed by 1350
Abstract
Psoriasis is a skin disease characterized by epidermal hyperplasia and an inappropriate activation of the adaptive immunity. A dysregulation of the skin’s lipid mediators is reported in the disease with a predominance of the inflammatory cascade derived from n-6 polyunsaturated fatty acids (n-6 [...] Read more.
Psoriasis is a skin disease characterized by epidermal hyperplasia and an inappropriate activation of the adaptive immunity. A dysregulation of the skin’s lipid mediators is reported in the disease with a predominance of the inflammatory cascade derived from n-6 polyunsaturated fatty acids (n-6 PUFAs). Bioactive lipid mediators derived from arachidonic acid (AA) are involved in the inflammatory functions of T cells in psoriasis, whereas n-3 PUFAs’ derivatives are anti-inflammatory metabolites. Here, we sought to evaluate the influence of a supplementation of the culture media with eicosapentaenoic acid (EPA) on the lipid profile of a psoriatic skin model produced with polarized T cells. Healthy and psoriatic skin substitutes were produced following the auto-assembly technique. Psoriatic skin substitutes produced with or without T cells presented increased epidermal and dermal linolenic acid (LA) and AA levels. N-6 PUFA lipid mediators were strongly measured in psoriatic substitutes, namely, 13-hydroxyoctadecadienoic acid (13-HODE), prostaglandin E2 (PGE2) and 12-hydroxyeicosatetraenoic acid (12-HETE). The added EPA elevated the amounts of EPA, n-3 docosapentaenoic acid (DPA) and docosahexaenoic acid (DHA) in the epidermal and dermal phospholipids. The EPA supplementation balanced the production of epidermal lipid mediators, with an increase in prostaglandin E3 (PGE3), 12-hydroxyeicosapentaenoic acid (12-HEPE) and N-eicosapentaenoyl-ethanolamine (EPEA) levels. These findings show that EPA modulates the lipid composition of psoriatic skin substitutes by encouraging the return to a cutaneous homeostatic state. Full article
(This article belongs to the Special Issue Lipid Metabolism in Health and Disease 2023)
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