Cinnamate supplementation enhances hepatic lipid metabolism and antioxidant defense systems in high cholesterol-fed rats.
This study investigated the effect of cinnamate, a phenolic compound found in cinnamon bark and other plant materials, on lipid metabolism and antioxidant enzyme activities in rats fed a high cholesterol diet. Three groups of rats were given a diet containing 1 g of cholesterol/kg for 6 weeks. The control group only received the high cholesterol diet, whereas the other two groups received a diet supplemented with lovastatin or cinnamate (0.1 g/100 g of diet). The plasma high-density lipoprotein-cholesterol levels were significantly higher in the cinnamate group than in either the control or lovastatin groups, and the atherogenic index was significantly lower in rats with cinnamate supplementation. Supplementation with cinnamate resulted in significantly lower hepatic cholesterol and triglyceride levels. Accumulation of hepatic lipid droplets was higher in the control group than in the rats supplemented with either cinnamate or lovastatin. Hepatic 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase activity was significantly lower in the cinnamate group compared with the other groups, whereas only acyl-CoA:cholesterol acyltransferase activity was significantly lower in the lovastatin group compared with the control group. Cinnamate supplementation resulted in higher catalase and glutathione peroxidase activities, while hepatic thiobarbituric acid-reactive substances were significantly lower in both the cinnamate and lovastatin groups. The fecal acidic sterol was higher in the lovastatin group than in the control or cinnamate groups. These results suggest that dietary cinnamate inhibits hepatic HMG-CoA reductase activity, resulting in lower hepatic cholesterol content, and suppresses lipid peroxidation via enhancement of hepatic antioxidant enzyme activities.
Lee
Jeong-Sun
JS
Department of Food Science and Nutrition, Kyungpook National University, Daegu, Korea.
Jeon
Seon-Min
SM
Park
Eun-Mi
EM
Huh
Tae-Lin
TL
Kwon
Oh-Shin
OS
Lee
Mi-Kyung
MK
Choi
Myung-Sook
MS
D000818:Animals; D000924:Anticholesteremic Agents / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D002791:Cholesterol, Dietary / Q000008:administration & dosage* / Q000378:metabolism; D008076:Cholesterol, HDL / Q000097:blood / Q000378:metabolism; D002934:Cinnamates / Q000494:pharmacology*; D019587:Dietary Supplements; D005243:Feces / Q000737:chemistry; D005979:Glutathione Peroxidase / Q000378:metabolism; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology*; D008099:Liver / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D008148:Lovastatin / Q000494:pharmacology; D008297:Male; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013261:Sterols / Q000737:chemistry; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014280:Triglycerides / Q000097:blood / Q000378:metabolism
D000924:Anticholesteremic Agents; D002791:Cholesterol, Dietary; D008076:Cholesterol, HDL; D002934:Cinnamates; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D013261:Sterols; D017392:Thiobarbituric Acid Reactive Substances; D014280:Triglycerides; D008148:Lovastatin; D002374:Catalase; D005979:Glutathione Peroxidase