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Comment
. 2010 Oct;59(10):2351-3.
doi: 10.2337/db10-0912.

Targeting ceramide synthesis to reverse insulin resistance

Carsten Schmitz-Peiffer  1
Affiliations
Comment

Targeting ceramide synthesis to reverse insulin resistance

Carsten Schmitz-Peiffer. Diabetes. 2010 Oct.
No abstract available

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Figures

FIG. 1.
FIG. 1.
Roles of SPT, CerS, and sphingomyelinase (SMase) in the metabolism of ceramides. De novo synthesis of ceramide is initiated by the condensation of serine with palmitoyl-CoA by SPT to generate the sphingoid backbone. A range of saturated and unsaturated fatty acids (acyl-CoA) can be subsequently incorporated by CerS (LASS) isoforms to form the ceramide sidechain. The salvage pathway, responsible for the cycling between ceramide and complex sphingolipids, also involves CerS activity and can also promote ceramide accumulation upon fatty acid oversupply. See references (9) and (24) for further details of sphingolipid metabolism. Inflammation can promote ceramide release from sphingomyelin through the activation of SMase by cytokines. Studies in intact cells and in vivo suggest that ceramide (and possibly also complex sphingolipids) can affect insulin action at least in part by inducing further stress signaling and mitochondrial dysfunction as well as by directly inhibiting insulin signal transduction.
See this image and copyright information in PMC

Comment on

References

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