title: Effect of conjugated linoleic acid isomers on lipoproteins and atherosclerosis in the Syrian Golden hamster.
abstract: Conjugated linoleic acid (CLA) is a group of positional and geometric isomers of linoleic acid (LA, C18:2 cis-9, cis-12) that are reported to have important biological activities, including protection against atherosclerosis. In this study, the potential role of the individual cis-9, trans-11 and trans-10, cis-12 isomers of CLA in atherogenesis were compared with LA in the Syrian Golden hamster. Supplementation of a high-fat, high-cholesterol diet (HFHC) with 1% (w/w) cis-9, trans-11 CLA or trans-10, cis-12 CLA did not significantly affect plasma cholesterol levels compared to supplementation with 1% (w/w) LA. Very low density lipoprotein cholesterol (VLDL-C) was lower and plasma triglycerides (TG) were higher in diets where C18:2 fatty acid was added to the HFHC diet, but neither the cis-9, trans-11 CLA group nor trans-10, cis-12 CLA group was significantly different from the LA control group. CLA supplementation did not significantly affect low density lipoprotein cholesterol (LDL-C). Trans-10, cis-12 CLA increased high density lipoprotein cholesterol (HDL-C) levels compared to LA or cis-9, trans-11 CLA (P<0.02), and although the ratio of non-HDL-C:HDL-C in the cis-9, trans-11 CLA group (1.11+/-0.54) and the trans-10, cis-12 CLA group (1.11+/-0.21) was lower than the LA group (1.29+/-0.45), the reduction did not reach statistical significance. Atherosclerosis was assessed in the ascending aorta by measuring the number of aortic cross-sections containing Oil Red O-stained intimal lesions. Compared to the LA group (60+/-11%), both the cis-9, trans-11 CLA group (38+/-8%) and the trans-10, cis-12 CLA group (28+/-7%) had fewer sections displaying a fatty streak lesion, although the differences did not reach statistical significance. These results suggest that individual CLA isomers may reduce atherosclerotic lesion development in the hamster, but when compared to LA, the apparent atheroprotective effects do not correlate with beneficial changes in lipoprotein profile.
authors.affiliation: Department of Biochemistry and Molecular Biology, Dalhousie University, 5850 College Street, Halifax, Nova Scotia, Canada B3H 1X5.
authors.forename: Patricia L
authors.initials: PL
authors.lastname: Mitchell
authors.forename: Morgan A
authors.initials: MA
authors.lastname: Langille
authors.forename: Deborah L
authors.initials: DL
authors.lastname: Currie
authors.forename: Roger S
authors.initials: RS
authors.lastname: McLeod
mesh_terms: D000818:Animals; D001011:Aorta / Q000473:pathology; D001161:Arteriosclerosis / Q000097:blood / Q000378:metabolism* / Q000473:pathology; D002791:Cholesterol, Dietary / Q000494:pharmacology; D006224:Cricetinae; D004032:Diet; D004041:Dietary Fats / Q000494:pharmacology; D008041:Linoleic Acids / Q000008:administration & dosage / Q000494:pharmacology*; D044243:Linoleic Acids, Conjugated / Q000494:pharmacology; D008074:Lipoproteins / Q000097:blood / Q000378:metabolism*; D008647:Mesocricetus; D013997:Time Factors; D044242:Trans Fatty Acids / Q000494:pharmacology
chemical_list: D002791:Cholesterol, Dietary; D004041:Dietary Fats; D008041:Linoleic Acids; D044243:Linoleic Acids, Conjugated; D008074:Lipoproteins; D044242:Trans Fatty Acids