title: Lovastatin inhibits diet induced atherosclerosis in F1B golden Syrian hamsters.
abstract: 3-Hydroxy-3-methylglutaryl-CoA (HMG CoA) reductase inhibitors are the drugs most commonly prescribed in the US to lower blood cholesterol. Previous studies have shown their efficacy in reducing plasma low density lipoprotein (LDL) cholesterol. However, little is known about their effects on preventing diet induced atherosclerosis. We have investigated the changes in lipoprotein profiles and extent of atherogenesis in hamsters (F1B strain) consuming an atherogenic diet with and without lovastatin. Thirty-six animals were randomized into 3 groups of 12 animals each, with similar plasma cholesterol levels. One group of animals received a basal chow diet, and the other two groups a basal diet plus 10% (w/w) coconut oil and 0.05% cholesterol. After 2.5 weeks, one of the groups received the latter diet supplemented with lovastatin (25 mg/kg/day). A second study was carried out in which animals received the same diets, but lovastatin was given during the 10 week period at a dose of 12.5 mg/kg/day. At the end of the experimental period, animals were sacrificed and lipoprotein cholesterol, liver enzymes, and aortic foam cell development were determined. Animals fed the high fat diet plus lovastatin had significantly lower levels of non-high density lipoprotein (HDL) cholesterol than those fed the unsupplemented high fat diet. No differences were observed in mean levels of this parameter between animals fed the low fat diet and those receiving lovastatin. The amount of aortic lipid staining was significantly less in the lovastatin and low fat groups when compared to the unsupplemented high fat groups. These results indicate that lovastatin can prevent diet induced aortic lipid deposition in this animal model.
authors.affiliation: Lipid Metabolism Laboratory, USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA.
authors.forename: J
authors.initials: J
authors.lastname: Otto
authors.forename: J M
authors.initials: JM
authors.lastname: Ordovas
authors.forename: D
authors.initials: D
authors.lastname: Smith
authors.forename: D
authors.initials: D
authors.lastname: van Dongen
authors.forename: R J
authors.initials: RJ
authors.lastname: Nicolosi
authors.forename: E J
authors.initials: EJ
authors.lastname: Schaefer
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001161:Arteriosclerosis / Q000378:metabolism / Q000517:prevention & control*; D001835:Body Weight; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D006224:Cricetinae; D004036:Diet, Atherogenic; D004195:Disease Models, Animal; D005487:Foam Cells / Q000378:metabolism; D008055:Lipids / Q000097:blood; D008099:Liver / Q000201:enzymology; D008148:Lovastatin / Q000008:administration & dosage / Q000494:pharmacology*; D008297:Male; D008647:Mesocricetus; D014280:Triglycerides / Q000097:blood
chemical_list: D008076:Cholesterol, HDL; D008055:Lipids; D014280:Triglycerides; D002784:Cholesterol; D008148:Lovastatin