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Diabetologia

, Volume 53, Issue 5, pp 1007–1008 | Cite as

Sulphated galactosylceramide

  • K. Buschard
Letter

Keywords

Ceramides IL-6 Inflammation Sulphated galactosylceramide Sulfatide 

To the Editor: In the December 2009 issue of Diabetologia, an article by de Mello et al. [1] and a commentary by Gill and Sattar [2] draw attention to ceramides as being associated with inflammation, which plays a role in the development of type 2 diabetes and the metabolic syndrome. In this context, some variants of ceramides are interesting too. In beta cells, ceramide is taken up and ligated with galactose by ceramide galactosyltransferase to β-galactosylceramide (GalCer) [3] and, furthermore in the Golgi apparatus, a sulphate group is linked by galactosylceramide sulfotransferase to form sulphated galactosylceramide, also called sulfatide [4]. The same process takes place in the brain and is likely to occur in the liver. Like ceramides, sulfatide is present in the blood, where its concentration is inversely correlated with insulin resistance [5]. The sulfatide level is lower in type 2 diabetic patients than in matched healthy controls [5]. Sulfatide inhibits the production of IL-6, as well as other cyto- and chemokines, both in fat cells and in peripheral leucocytes, and thus acts as an anti-inflammatory agent [6, 7]. Sulfatide has several other beneficial properties, including a possible role in insulin secretion from pancreatic beta cells (see [8]).

Ceramide is a precursor of sulfatide; thus, high concentrations of the former might facilitate production of the latter. However, in insulin-resistant individuals, high concentrations of ceramide but low levels of sulfatide are observed. This raises the question of whether the pathway involved in sulfatide synthesis is involved in the pathogenesis of the disease.

Thus, a derivative of ceramide known as sulphated galactosylceramide or sulfatide is positively correlated with insulin sensitivity and acts as an anti-inflammatory agent by, among other things, inhibiting the production of IL-6. Lower blood concentrations of sulfatide are observed in type 2 diabetic patients.

Notes

Duality of interest

The author declares that there is no duality of interest associated with this manuscript.

References

  1. 1.
    de Mello V, Lankinen M, Schwab U et al (2009) Link between plasma ceramides, inflammation and insulin resistance: association with serum IL-6 concentration in patients with coronary heart disease. Diabetologia 52:2612–2615CrossRefPubMedGoogle Scholar
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    Gill JM, Sattar N (2009) Ceramides: a new player in the inflammation-insulin resistance paradigm? Diabetologia 52:2475–2477CrossRefPubMedGoogle Scholar
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    Coetzee T, Li X, Fujita N et al (1996) Molecular cloning, chromosomal mapping, and characterization of the mouse UDP-galactose:ceramide galactosyltransferase gene. Genomics 35:215–222CrossRefPubMedGoogle Scholar
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    Honke K, Tsuda M, Koyota S et al (2001) Molecular cloning and characterization of a human beta-Gal-3′-sulfotransferase that acts on both type 1 and type 2 (Gal beta 1-3/1-4GlcNAc-R) oligosaccharides. J Biol Chem 276:267–274CrossRefPubMedGoogle Scholar
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    Buschard K, Fredman P, Bog-Hansen E et al (2005) Low serum concentration of sulfatide and presence of sulfated lactosylceramid are associated with type 2 diabetes. The Skaraborg Project. Diabet Med 22:1190–1198CrossRefPubMedGoogle Scholar
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    Bruun JM, Roeske-Nielsen A, Richelsen B, Fredman P, Buschard K (2007) Sulfatide increases adiponectin and decreases TNF-alpha, IL-6, and IL-8 in human adipose tissue in vitro. Mol Cell Endocrinol 263:142–148CrossRefPubMedGoogle Scholar
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    Roeske-Nielsen A, Fredman P, Mansson JE, Bendtzen K, Buschard K (2004) Beta-galactosylceramide increases and sulfatide decreases cytokine and chemokine production in whole blood cells. Immunol Lett 91:205–211CrossRefPubMedGoogle Scholar
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    Buschard K, Blomqvist M, Osterbye T, Fredman P (2005) Involvement of sulfatide in beta cells and type 1 and type 2 diabetes. Diabetologia 48:1957–1962CrossRefPubMedGoogle Scholar

Copyright information

© Springer-Verlag 2010

Authors and Affiliations

  1. 1.Bartholin InstituttetCopenhagenDenmark

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