Lack of stimulation of cholesteryl ester transfer protein by cholesterol in the presence of a high-fat diet

Cholesteryl ester transfer protein (CETP) is a key protein involved in the reverse cholesterol transport pathway. The regulation of CETP by dietary fats is not clearly understood. Transgenic mice expressing human CETP under the control of its natural flanking region were fed low- or high-fat diets enriched in monounsaturated fatty acids (MUFAs) or saturated fatty acids in the presence or absence of cholesterol. Addition of cholesterol to the low-fat MUFA diet increased CETP activity and mRNA expression, whereas addition of cholesterol to the high-fat MUFA diet led to a decrease in CETP activity and mRNA expression. In SW 872 cells, oleic acid and cholesterol stimulated CETP gene expression when given alone. However, addition of fatty acids along with cholesterol interfered with the stimulatory effect of cholesterol on CETP gene regulation. Cholesterol-mediated stimulation of CETP involves the transcription factor liver X receptor α (LXRα). High-fat MUFA diets inhibited the expression of LXRα, and addition of cholesterol to the high-fat MUFA diet did not rescue LXRα expression.Therefore, we present evidence for the first time that inhibition of LXRα expression by a high-fat MUFA diet leads to inhibition of CETP stimulation by cholesterol. Cholesteryl ester transfer protein (CETP) is a key protein involved in the reverse cholesterol transport pathway. The regulation of CETP by dietary fats is not clearly understood. Transgenic mice expressing human CETP under the control of its natural flanking region were fed low- or high-fat diets enriched in monounsaturated fatty acids (MUFAs) or saturated fatty acids in the presence or absence of cholesterol. Addition of cholesterol to the low-fat MUFA diet increased CETP activity and mRNA expression, whereas addition of cholesterol to the high-fat MUFA diet led to a decrease in CETP activity and mRNA expression. In SW 872 cells, oleic acid and cholesterol stimulated CETP gene expression when given alone. However, addition of fatty acids along with cholesterol interfered with the stimulatory effect of cholesterol on CETP gene regulation. Cholesterol-mediated stimulation of CETP involves the transcription factor liver X receptor α (LXRα). High-fat MUFA diets inhibited the expression of LXRα, and addition of cholesterol to the high-fat MUFA diet did not rescue LXRα expression. Therefore, we present evidence for the first time that inhibition of LXRα expression by a high-fat MUFA diet leads to inhibition of CETP stimulation by cholesterol. Cholesteryl ester transfer protein (CETP) is considered a key component in regulating cholesterol homeostasis as it transfers cholesteryl esters from HDL to apolipoprotein B-containing lipoproteins (1Bruce C. Chouinard Jr., R.A. Tall A.R. Plasma lipid transfer proteins, high density lipoproteins, and reverse cholesterol transport.Annu. Rev. Nutr. 1998; 18: 297-330Crossref PubMed Scopus (229) Google Scholar, 2Fielding C.J. Fielding P.E. Molecular physiology of reverse cholesterol transport.J. Lipid Res. 1995; 36: 211-228Abstract Full PubMed Google Scholar, of cholesteryl ester transfer protein to HDL cholesterol. in and PubMed Scopus Google Scholar, Tall A.R. Cholesteryl ester transfer protein and high density to cholesterol in to apolipoprotein Lipid Res. Full PubMed Google CETP in HDL and high or of CETP on the in of Res. PubMed Scopus Google Scholar, C. cholesteryl ester transfer protein and in Lipid Res. Full Full PubMed Scopus Google HDL a in reverse cholesterol a that involves the of cholesterol from to the liver for from the in and in with in CETP that absence of CETP is with the of cholesterol from of cholesterol and of cholesteryl ester transfer to apolipoprotein B-containing lipoproteins (1Bruce C. Chouinard Jr., R.A. Tall A.R. Plasma lipid transfer proteins, high density lipoproteins, and reverse cholesterol transport.Annu. Rev. Nutr. 1998; 18: 297-330Crossref PubMed Scopus (229) Google cholesterol to the a high CETP activity as it cholesterol from the the CETP that cholesteryl and the of HDL CETP is considered (1Bruce C. Chouinard Jr., R.A. Tall A.R. Plasma lipid transfer proteins, high density lipoproteins, and reverse cholesterol transport.Annu. Rev. Nutr. 1998; 18: 297-330Crossref PubMed Scopus (229) Google Scholar, 2Fielding C.J. Fielding P.E. Molecular physiology of reverse cholesterol transport.J. Lipid Res. 1995; 36: 211-228Abstract Full PubMed Google Scholar, of cholesteryl ester transfer protein to HDL cholesterol. in and PubMed Scopus Google Scholar, Tall A.R. Cholesteryl ester transfer protein and high density to cholesterol in to apolipoprotein Lipid Res. Full PubMed Google In CETP is with high HDL and a of C. of lipid transfer protein in a with increased PubMed Scopus Google Scholar, cholesteryl ester transfer protein by as a of increased of high density PubMed Scopus Google The absence of in of the first for the that CETP is C. of lipid transfer protein in a with increased PubMed Scopus Google Transgenic mice expressing human Tall A.R. high density cholesterol in human cholesteryl ester transfer protein Full PubMed Google or in mice expressing cholesteryl ester transfer PubMed Scopus Google CETP a in HDL that high of CETP protein increased of Plasma CETP activity in to diets in Tall A.R. and of lipid transfer protein Full PubMed Google lipid transfer in PubMed Google Scholar, Tall A.R. Plasma of cholesteryl ester transfer protein in the of dietary PubMed Scopus Google Tall Plasma lipid transfer protein as a of the of PubMed Scopus Google Scholar, dietary acid with acid HDL and CETP activity in Nutr. 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