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'''Cholesteryl ester transfer protein''' (CETP), also called '''plasma lipid transfer protein''', is a [[blood plasma|plasma]] [[protein]] that facilitates the transport of [[cholesteryl ester]]s and [[triglyceride]]s between the [[lipoprotein]]s. It collects triglycerides from [[Very-low-density lipoprotein|very-low-density]] (VLDL) or [[low-density lipoprotein]]s (LDL) and exchanges them for cholesteryl esters from [[high-density lipoprotein]]s (HDL), and vice versa. Most of the time, however, CETP does a heteroexchange, trading a triglyceride for a cholesteryl ester or a cholesteryl ester for a triglyceride. |
'''Cholesteryl ester transfer protein''' (CETP), also called '''plasma lipid transfer protein''', is a [[blood plasma|plasma]] [[protein]] that facilitates the transport of [[cholesteryl ester]]s and [[triglyceride]]s between the [[lipoprotein]]s. It collects triglycerides from [[Very-low-density lipoprotein|very-low-density]] (VLDL) or [[low-density lipoprotein]]s (LDL) and exchanges them for cholesteryl esters from [[high-density lipoprotein]]s (HDL), and vice versa. Most of the time, however, CETP does a heteroexchange, trading a triglyceride for a cholesteryl ester or a cholesteryl ester for a triglyceride. |
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Cholesteryl ester transfer protein (CETP), also called plasma lipid transfer protein, is a plasma protein that facilitates the transport of cholesteryl esters and triglycerides between the lipoproteins. It collects triglycerides from very-low-density (VLDL) or low-density lipoproteins (LDL) and exchanges them for cholesteryl esters from high-density lipoproteins (HDL), and vice versa. Most of the time, however, CETP does a heteroexchange, trading a triglyceride for a cholesteryl ester or a cholesteryl ester for a triglyceride.
The CETP gene is located on the sixteenth chromosome (16q21).
Rare mutations leading to reduced function of CETP have been linked to accelerated atherosclerosis.[3] In contrast, a polymorphism (I405V) of the CETP gene leading to lower serum levels has also been linked to exceptional longevity [4] and to metabolic response to nutritional intervention.[5] However, this mutation also increases the prevalence of coronary heart disease in patients with hypertriglyceridemia.[6] The D442G mutation, which lowers CETP levels and increases HDL levels also increases coronary heart disease.[3]
Elaidic acid, a major component of trans fat, increases CETP activity.[7]
AsHDL can alleviate atherosclerosis and other cardiovascular diseases, and certain disease states such as the metabolic syndrome feature low HDL, pharmacological inhibition of CETP is being studied as a method of improving HDL levels.[8] To be specific, in a 2004 study, the small molecular agent torcetrapib was shown to increase HDL levels, alone and with a statin, and lower LDL when co-administered with a statin.[9] Studies into cardiovascular endpoints, however, were largely disappointing. While they confirmed the change in lipid levels, most reported an increase in blood pressure, no change in atherosclerosis,[10][11] and, in a trial of a combination of torcetrapib and atorvastatin, an increase in cardiovascular events and mortality.[12]
A compound related to torcetrapib, Dalcetrapib (investigative name JTT-705/R1658), was also studied, but trials have ceased.[13] It increases HDL levels by 30%, as compared to 60% by torcetrapib.[14] Two CETP inhibitors are currently under development. One is Merck's MK-0859 anacetrapib, which in initial studies did not increase blood pressure.[15] The other is Eli Lilly's evacetrapib, which failed in Phase 3 trials.
Click on genes, proteins and metabolites below to link to respective articles. [§ 1]
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| Fatty acid |
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Lipids: lipoprotein particle metabolism
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| Lipoprotein particle classes and subclasses |
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| Apolipoproteins |
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| Extracellular enzymes |
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| Lipid transfer proteins |
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| Cell surface receptors |
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| ATP-binding cassette transporter |
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