Divergent mechanisms of c is 9, trans 11-and trans 10, cis 12-conjugated linoleic acid affecting insulin resistance and inflammation in apolipoprotein E knockout mice: a proteomics approach B. de Roos * ,1 , G. Rucklidge * , M. Reid * , K. Ross * , G. Duncan * , M. A. Navarro † , J. M. Arbones-Mainar † , M. A. Guzman-Garcia † , J. Osada † , J. Browne ‡ , C. E. Loscher ‡ and H. M. Roche ‡ * Rowett Research Institute, Aberdeen, UK; † Department of Biochemistry, Veterinary School, University of Zaragoza, Zaragoza, Spain; and ‡ Nutrigenomics Research Group, Department of Clinical Medicine, Institute of Molecular Medicine, St. James’s Hospital, Dublin, Ireland 1 Correspondence: Rowett Research Institute, Greenburn Rd., Bucksburn, Aberdeen AB21 9SB, Scotland, UK. E-mail: b.deroos@rowett.ac.uk <h3>SPECIFIC AIMS</h3> Conjugated linoleic acids (CLA) are present as minor constituents of meat, milk, and dairy products or other foods derived from ruminant animals. These fatty acids affect atherosclerosis, but mechanisms are not well understood. The present study compares both the physiological and biochemical properties of cis 9, trans 11-CLA and trans 10, cis 12-CLA in a single well-validated animal model for atherosclerosis, the apolipoprotein E (apoE)
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Divergent mechanisms of cis9, trans11-and trans10, cis12-conjugated linoleic acid affecting insulin resistance and inflammation in apolipoprotein E knockout mice: a proteomics approach
de Roos, B.; Rucklidge, G.; Reid, M.; Ross, K.; Duncan, G.; Navarro, M. A.; Arbones-Mainar, J. M.; Guzman-Garcia, M. A.; Osada, J.; Browne, J.; Loscher, C. E.; Roche, H. M.
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, Volume 19 (12): 1746
Fed of American Socs for Experimental Biology – Oct 1, 2005
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