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  1. AU="Ali-Berrada, Sarah"
  2. AU=Wang Xiangjun
  3. AU="Abbracchio, Maria P"
  4. AU="Pesios, D"
  5. AU="Chidumayo, Emmanuel N."
  6. AU="Abdalla, Marwah"
  7. AU=Newton Mark A
  8. AU="Stajich, Jeffrey M"
  9. AU="Thunberg, Sarah"
  10. AU="Kolla, Jayaprakash Narayana"
  11. AU="Yeo, Chang Dong"
  12. AU="Söderberg, Simon"
  13. AU="Wei, Fuwen"
  14. AU="Christie, Corey"
  15. AU="Cole, Naida M"
  16. AU="Vasudevan, Anju"
  17. AU="Garg, Muskan"
  18. AU="Scott, Michelle"
  19. AU="Hartmann, Annette M" AU="Hartmann, Annette M"
  20. AU="Stewart, Darren E"
  21. AU="Khosravi, Amir"
  22. AU="Kang, Christopher Y"
  23. AU="Martins, Stella Maris Seixas"
  24. AU=Rybniker Jan AU=Rybniker Jan
  25. AU="Kroes, Rob"
  26. AU="Gancitano, Giuseppe"
  27. AU="Beaty, B J"
  28. AU="Kiès, Philippine"
  29. AU="Zlatko Trajanoski"
  30. AU="Hopke, Philip K"
  31. AU="Kothandaraman, Venkatraman"
  32. AU="Wiencek, Joesph R"
  33. AU="Gachon, Philippe"
  34. AU="Tsuboi, Yoshio"
  35. AU=Woolard Stacie N AU=Woolard Stacie N
  36. AU="Rowland, Jonathan"
  37. AU="Chloe C. Y. Wong"

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  1. Artikel ; Online: Circulating Sphingolipids and Glucose Homeostasis: An Update.

    Ali-Berrada, Sarah / Guitton, Jeanne / Tan-Chen, Sophie / Gyulkhandanyan, Anna / Hajduch, Eric / Le Stunff, Hervé

    International journal of molecular sciences

    2023  Band 24, Heft 16

    Abstract: Sphingolipids are a family of lipid molecules produced through different pathways in mammals. Sphingolipids are structural components of membranes, but in response to obesity, they are implicated in the regulation of various cellular processes, including ...

    Abstract Sphingolipids are a family of lipid molecules produced through different pathways in mammals. Sphingolipids are structural components of membranes, but in response to obesity, they are implicated in the regulation of various cellular processes, including inflammation, apoptosis, cell proliferation, autophagy, and insulin resistance which favors dysregulation of glucose metabolism. Of all sphingolipids, two species, ceramides and sphingosine-1-phosphate (S1P), are also found abundantly secreted into the bloodstream and associated with lipoproteins or extracellular vesicles. Plasma concentrations of these sphingolipids can be altered upon metabolic disorders and could serve as predictive biomarkers of these diseases. Recent important advances suggest that circulating sphingolipids not only serve as biomarkers but could also serve as mediators in the dysregulation of glucose homeostasis. In this review, advances of molecular mechanisms involved in the regulation of ceramides and S1P association to lipoproteins or extracellular vesicles and how they could alter glucose metabolism are discussed.
    Mesh-Begriff(e) Animals ; Sphingolipids ; Ceramides ; Homeostasis ; Glucose ; Mammals
    Chemische Substanzen Sphingolipids ; Ceramides ; sphingosine 1-phosphate (26993-30-6) ; Glucose (IY9XDZ35W2)
    Sprache Englisch
    Erscheinungsdatum 2023-08-12
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms241612720
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Ceramide analog C2-cer induces a loss in insulin sensitivity in muscle cells through the salvage/recycling pathway.

    Bandet, Cécile L / Tan-Chen, Sophie / Ali-Berrada, Sarah / Campana, Mélanie / Poirier, Maxime / Blachnio-Zabielska, Agnieszka / Pais-de-Barros, Jean-Paul / Rouch, Claude / Ferré, Pascal / Foufelle, Fabienne / Le Stunff, Hervé / Hajduch, Eric

    The Journal of biological chemistry

    2023  Band 299, Heft 6, Seite(n) 104815

    Abstract: Ceramides have been shown to play a major role in the onset of skeletal muscle insulin resistance and therefore in the prevalence of type 2 diabetes. However, many of the studies involved in the discovery of deleterious ceramide actions used a ... ...

    Abstract Ceramides have been shown to play a major role in the onset of skeletal muscle insulin resistance and therefore in the prevalence of type 2 diabetes. However, many of the studies involved in the discovery of deleterious ceramide actions used a nonphysiological, cell-permeable, short-chain ceramide analog, the C2-ceramide (C2-cer). In the present study, we determined how C2-cer promotes insulin resistance in muscle cells. We demonstrate that C2-cer enters the salvage/recycling pathway and becomes deacylated, yielding sphingosine, re-acylation of which depends on the availability of long chain fatty acids provided by the lipogenesis pathway in muscle cells. Importantly, we show these salvaged ceramides are actually responsible for the inhibition of insulin signaling induced by C2-cer. Interestingly, we also show that the exogenous and endogenous monounsaturated fatty acid oleate prevents C2-cer to be recycled into endogenous ceramide species in a diacylglycerol O-acyltransferase 1-dependent mechanism, which forces free fatty acid metabolism towards triacylglyceride production. Altogether, the study highlights for the first time that C2-cer induces a loss in insulin sensitivity through the salvage/recycling pathway in muscle cells. This study also validates C2-cer as a convenient tool to decipher mechanisms by which long-chain ceramides mediate insulin resistance in muscle cells and suggests that in addition to the de novo ceramide synthesis, recycling of ceramide could contribute to muscle insulin resistance observed in obesity and type 2 diabetes.
    Mesh-Begriff(e) Humans ; Ceramides/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Insulin/metabolism ; Insulin Resistance/physiology ; Muscle Cells/metabolism ; Muscle, Skeletal/metabolism
    Chemische Substanzen Ceramides ; Insulin ; N-acetylsphingosine
    Sprache Englisch
    Erscheinungsdatum 2023-05-11
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1016/j.jbc.2023.104815
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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