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Special Issue Editor

Special Issue Information

Dear Colleagues,

A strong case is emerging that bioactive sphingolipids, although only a minor constituent of the global lipid milieu in cells and tissues, play a central role in regulating metabolic functions. Specific bioactive sphingolipids have been identified as pathogenic mediators in metabolic disorders such as non-alcoholic fatty liver disease (NAFLD), diabetes, or cardiovascular dysfunction. Circulating mediators that are released from adipose tissue (e.g., adipokines, inflammatory cytokines) specifically modulate enzymes that are involved in sphingolipid synthesis and degradation. The accumulation of specific sphingolipid species in tissues such as the liver, muscle, heart, pancreas, and vasculature may contribute to the onset and development of metabolic diseases including insulin resistance, pancreatic β-cell failure, liver dysfunction, neuro-muscolar degeneration, cardiomyopathy, and vascular and microenviromental dysfunctions. Striking progress has been made in the last few years in elucidating the complex crosstalk between sphingolipids and the development of metabolic diseases, as scientists have figured out that pharmacological intervention or genetic ablation of enzymes controlling sphingolipid synthesis or degradation have beneficial effects in these disorders.

The Guest Editor also encourages the submission of manuscripts (reviews or research articles) regarding the involvement of sphingolipids in pathongen infections, including coronavirus.

Prof. Dr. Elisabetta Meacci
Guest Editor

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Keywords

sphingolipids
ceramide
sphingosine
sphingosine 1-phosphate
ceramide 1-phosphate
glycosphingolipids
diabetes
insulin resistance
beta-cell failure
NAFLD
cardiovascular disease
metabolic dysfunction

Published Papers (2 papers)

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Research

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24 pages, 5985 KiB

Open AccessArticle

Different Metabolism and Toxicity of TRANS Fatty Acids, Elaidate and Vaccenate Compared to Cis-Oleate in HepG2 Cells

by Farkas Sarnyai, Éva Kereszturi, Kitti Szirmai, Judit Mátyási, Johanna Iman Al-Hag, Tamás Csizmadia, Péter Lőw, Péter Szelényi, Viola Tamási, Kinga Tibori, Veronika Zámbó, Blanka Tóth and Miklós Csala

Int. J. Mol. Sci. 2022, 23(13), 7298; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23137298 - 30 Jun 2022

Cited by 4 | Viewed by 1996

Abstract

Trans fatty acids (TFAs) are not synthesized in the human body but are generally ingested in substantial amounts. The widespread view that TFAs, particularly those of industrial origin, are unhealthy and contribute to obesity, cardiovascular diseases and diabetes is based mostly on in vivo studies, and the underlying molecular mechanisms remain to be elucidated. Here, we used a hepatoma model of palmitate-induced lipotoxicity to compare the metabolism and effects of the representative industrial and ruminant TFAs, elaidate and vaccenate, respectively, with those of cis-oleate. Cellular FAs, triacylglycerols, diacylglycerols and ceramides were quantitated using chromatography, markers of stress and apoptosis were assessed at mRNA and protein levels, ultrastructural changes were examined by electron microscopy and viability was evaluated by MTT assay. While TFAs were just slightly more damaging than oleate when applied alone, they were remarkably less protective against palmitate toxicity in cotreatments. These differences correlated with their diverse incorporation into the accumulating diacylglycerols and ceramides. Our results provide in vitro evidence for the unfavorable metabolic features and potent stress-inducing character of TFAs in comparison with oleate. These findings strengthen the reasoning against dietary trans fat intake, and they can also help us better understand the molecular mechanisms of lipotoxicity. Full article

(This article belongs to the Special Issue Sphingolipids: Metabolic Functions and Disorders 2.0)

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Other

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18 pages, 5698 KiB

Open AccessHypothesis

SARS-CoV-2 Infection: A Role for S1P/S1P Receptor Signaling in the Nervous System?

by Elisabetta Meacci, Mercedes Garcia-Gil and Federica Pierucci

Int. J. Mol. Sci. 2020, 21(18), 6773; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186773 - 15 Sep 2020

Cited by 22 | Viewed by 4003

Abstract

The recent coronavirus disease (COVID-19) is still spreading worldwide. The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the virus responsible for COVID-19, binds to its receptor angiotensin-converting enzyme 2 (ACE2), and replicates within the cells of the nasal cavity, then spreads along the airway tracts, causing mild clinical manifestations, and, in a majority of patients, a persisting loss of smell. In some individuals, SARS-CoV-2 reaches and infects several organs, including the lung, leading to severe pulmonary disease. SARS-CoV-2 induces neurological symptoms, likely contributing to morbidity and mortality through unknown mechanisms. Sphingosine 1-phosphate (S1P) is a bioactive sphingolipid with pleiotropic properties and functions in many tissues, including the nervous system. S1P regulates neurogenesis and inflammation and it is implicated in multiple sclerosis (MS). Notably, Fingolimod (FTY720), a modulator of S1P receptors, has been approved for the treatment of MS and is being tested for COVID-19. Here, we discuss the putative role of S1P on viral infection and in the modulation of inflammation and survival in the stem cell niche of the olfactory epithelium. This could help to design therapeutic strategies based on S1P-mediated signaling to limit or overcome the host–virus interaction, virus propagation and the pathogenesis and complications involving the nervous system. Full article

(This article belongs to the Special Issue Sphingolipids: Metabolic Functions and Disorders 2.0)

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