Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

The metabolic cascade leading to eicosanoid precursors--desaturases, elongases, and phospholipases A2--is altered in Zucker fatty rats.

Authors: Fevre, C  Bellenger, S  Pierre, AS  Minville, M  Bellenger, J  Gresti, J  Rialland, M  Narce, M  Tessier, C 
Citation: Fevre C, etal., Biochim Biophys Acta. 2011 Jun;1811(6):409-17. Epub 2010 Dec 21.
Pubmed: (View Article at PubMed) PMID:21172452
DOI: Full-text: DOI:10.1016/j.bbalip.2010.12.004

Metabolic syndrome characterized by insulin resistance and obesity is accompanied by severe lipid metabolism perturbations and chronic low-grade inflammation. However, many unresolved questions remained regarding the regulation that underlie dyslipidemia, particularly the regulation of the metabolic cascade (synthesis and release) leading to eicosanoid precursors release. This study was undertaken to investigate the regulation of desaturases/elongases and phospholipases A(2) during the establishment of metabolic syndrome. Our results showed that delta-6 desaturase as well as elongase-6 expressions were upregulated in 3-month-old Zucker fatty rats as compared to lean littermates, independently of SREBP-1c activation. We also demonstrated for the first time an increase of liver group VII phospholipase A(2) gene expression in the obese animals together with a strong specific inhibition of type IVA and VIA phospholipases A(2). These results suggest that the regulation of unsaturated fatty acids biosynthesis and signalling cascade could contribute to the development of liver lipid dysregulation related to metabolic syndrome and may be considered as new potential targets in such pathological conditions.


Disease Annotations
Objects Annotated

Additional Information

RGD Object Information
RGD ID: 6482748
Created: 2012-05-01
Species: All species
Last Modified: 2012-05-01
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.