Abstract
This study was conducted to determine the effects of dietary cholesterol (CHO) and cholesterol oxidation products (COPs) on the induction of pathological lesions in rabbit liver tissues. Liver lesions were induced only when the levels of CHO and COPs in the diet were very high. The amount of CHO measured in the liver increased when dietary CHO was increased; by comparison, dietary COPs affected liver CHO amounts to a lesser extent. The TBARS (thiobarbituric acid reactive substances) value measured for the liver samples also increased when dietary CHO and COP levels were elevated, and the TBARS value was more strongly affected by the amount of COPs in the diet than by the amount of CHO. At 6 and 12 weeks, COP levels were the highest in the group that received 1.2 g CHO + 0.8 g COPs, followed by the 0.5 g CHO + 0.5 g COPs and 1.6 g CHO + 0.4 g COPs groups; the control (0 g) group showed the lowest COP levels among all groups. In this study, we found that not only dietary CHO but also COPs were involved in hypercholesterolemia induced liver lesions when the amount of CHO and COPs was high.
Highlights
Cholesterol (CHO) is a crucial component of the human body, but a high level of CHO is considered a major risk factor for the development of atherosclerosis and coronary heart disease (CHD) [1]
The TBARS value measured for the liver samples increased when dietary CHO and cholesterol oxidation products (COPs) levels were elevated, and the TBARS value was more strongly affected by the amount of COPs in the diet than by the amount of CHO
The rabbits that were fed with the diets containing 1 g CHO, 0.9 g CHO + 0.1 g COPs, 0.8 g CHO + 0.2 g COPs, and 0.5 g CHO + 0.5 g COPs showed the least vacuolation of hepatocytes in the periacinar region of the hepatic lobule at 6 and 12 weeks
Summary
Cholesterol (CHO) is a crucial component of the human body, but a high level of CHO is considered a major risk factor for the development of atherosclerosis and coronary heart disease (CHD) [1]. The liver is the major site where CHO is removed by being directly secreted into the bile or by being broken down into bile acids; the liver plays a key role in maintaining whole body CHO homeostasis by controlling the uptake of extracellular CHO, CHO synthesis, and CHO storage [5]. An elevated level of plasma CHO is typically a risk factor for atherosclerosis, and several COPs are cytotoxic, atherogenic, mutagenic, or carcinogenic; COPs injure endothelial cells, leading to atherosclerosis [1]. Our objective was to determine the relationship between dietary CHO and COPs and the induction of lesions in liver tissues and the composition of CHO, COPs, TBARS, and fatty acids in the liver tissues of rabbits
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