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Lovastatin inhibits diet induced atherosclerosis in F1B golden Syrian hamsters
1Lipid Metabolism Laboratory, USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA.
Insights
Lovastatin, a cholesterol-lowering drug, was found to prevent diet-induced atherosclerosis in hamsters. This study shows lovastatin reduces non-high density lipoprotein (HDL) cholesterol and aortic lipid deposition.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Atherosclerosis Studies
Background:
- 3-Hydroxy-3-methylglutaryl-CoA (HMG CoA) reductase inhibitors, commonly prescribed for high cholesterol, effectively reduce low-density lipoprotein (LDL) cholesterol.
- The role of these inhibitors in preventing diet-induced atherosclerosis remains less understood.
- This study investigates lovastatin's impact on atherosclerosis development in a hamster model.
Purpose of the Study:
- To evaluate the efficacy of lovastatin in preventing diet-induced atherosclerosis.
- To analyze changes in lipoprotein profiles and atherogenesis extent.
- To determine lovastatin's effect on aortic lipid deposition.
Main Methods:
- Two studies were conducted using F1B strain hamsters fed an atherogenic diet (high fat, cholesterol) with or without lovastatin.
- Animals were randomized into groups receiving basal chow, atherogenic diet, or atherogenic diet plus lovastatin at different dosages and durations.
- Lipoprotein cholesterol, liver enzymes, and aortic foam cell development were assessed post-treatment.
Main Results:
- Lovastatin significantly reduced non-high density lipoprotein (HDL) cholesterol in hamsters on a high-fat diet compared to those without lovastatin.
- No significant difference in non-HDL cholesterol was observed between the low-fat diet group and the lovastatin-treated group.
- Aortic lipid staining was significantly reduced in both the lovastatin-treated and low-fat diet groups compared to the unsupplemented high-fat diet group.
Conclusions:
- Lovastatin demonstrates preventative effects against diet-induced atherosclerosis in this animal model.
- The drug effectively reduces atherogenic lipid deposition in the aorta.
- These findings suggest potential therapeutic benefits of lovastatin in managing diet-related cardiovascular risks.
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.