Effect of dietary cholesterol on the activities of key enzymes of cholesterol metabolism in hyperlipidemia- and atherosclerosis-prone Japanese quail.
The hyperlipidemia- and atherosclerosis-prone (HAP) Japanese quail is a strain developed for the study of atherosclerosis by genetic selection from the commercially available (CA) Japanese quail. To delineate the characteristics of cholesterol metabolism in this strain, concentrations of serum lipids as well as hepatic enzyme activities were compared between HAP and CA quail. The hepatic enzymes studied are involved in the key step reaction in cholesterol metabolism: HMG-CoA reductase, ACAT, and cholesterol 7 alpha-hydroxylase. The animals were fed ad libitum with either 1% cholesterol or cholesterol-free semipurified diet for 28 days. Although a significant increase (p < 0.01) in serum cholesterol was observed in both strains on elapse of cholesterol feeding, formation of atheroma was seen exclusively in HAP quail of the cholesterol-fed group. The serum and liver cholesterol levels of HAP quail fed the cholesterol diet were significantly higher (p < 0.01) than those of CA quail. No significant differences were seen in the rate of cholesterol biosynthesis (HMG-CoA reductase activity), cholesterol ester formation (ACAT activity) and cholesterol catabolism (7 alpha-hydroxylase activity) between CA and HAP quail. Furthermore, the fecal excretions of acidic and neutral sterol showed no significant difference between strains. Although the formation of atheroma in HAP quail may be presumably due to the contribution of the marked increase in serum cholesterol level, the rate of cholesterol catabolism and synthesis in HAP quail compared well with those of CA quail. These observations suggest that the retarded rate of cholesterol biosynthesis or catabolism is not responsible for hypercholesterolemia in HAP quail.
Laboratory of Applied Biochemistry, Faculty of Agriculture, School of Medicine, University of the Ryukyus, Okinawa, Japan.
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Nagata
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Oku
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Toda
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Chinen
D000818:Animals; D001161:Arteriosclerosis / Q000201:enzymology*; D002784:Cholesterol / Q000097:blood / Q000378:metabolism*; D002791:Cholesterol, Dietary / Q000494:pharmacology*; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D015243:Cholesterol, VLDL / Q000097:blood; D003370:Coturnix / Q000378:metabolism*; D005243:Feces; D006903:Hydroxymethylglutaryl CoA Reductases / Q000378:metabolism; D006949:Hyperlipidemias / Q000201:enzymology*; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood; D008099:Liver / Q000378:metabolism; D008297:Male; D008862:Microsomes, Liver / Q000378:metabolism; D013261:Sterols / Q000378:metabolism
D002791:Cholesterol, Dietary; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D015243:Cholesterol, VLDL; D008055:Lipids; D013261:Sterols; D002784:Cholesterol; D006903:Hydroxymethylglutaryl CoA Reductases