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Contents

   



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1 Genetics  





2 Role in disease  





3 Pharmacology  





4 Interactive pathway map  





5 References  





6 Further reading  





7 External links  














Cholesteryl ester transfer protein






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From Wikipedia, the free encyclopedia
 


This is an old revision of this page, as edited by Donner60 (talk | contribs)at19:55, 19 April 2013 (Reverted 1 edit by 81.105.59.112 (talk) to last revision by Addbot. (TW)). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.
(diff)  Previous revision | Latest revision (diff) | Newer revision  (diff)

Template:PBB 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 homoexchange, trading a triglyceride for a cholesteryl ester or a cholesteryl ester for a triglyceride.

Genetics

The CETP gene is located on the sixteenth chromosome (16q21).

Role in disease

Rare mutations leading to increased function of CETP have been linked to accelerated atherosclerosis.[1] In contrast, a polymorphism (I405V) of the CETP gene leading to lower serum levels has also been linked to exceptional longevity [2] and to metabolic response to nutritional intervention.[3] However, this mutation also increases the prevalence of coronary heart disease in patients with hypertriglyceridemia.[4] The D442G mutation, which lowers CETP levels and increases HDL levels also increases coronary heart disease.[1]

Elaidic acid, a major component of trans fat, increases CETP activity.[5]

Pharmacology

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.[6] 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.[7] 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,[8][9] and, in a trial of a combination of torcetrapib and atorvastatin, an increase in cardiovascular events and mortality.[10]

A compound related to torcetrapib, Dalcetrapib (investigative name JTT-705/R1658), is also being studied.[11] It increases HDL levels by 30%, as compared to 60% by torcetrapib.[12] Another CETP inhibitor under development is Merck's MK-0859 anacetrapib, which in initial studies is not shown to increase blood pressure.[13]

Interactive pathway map

Click on genes, proteins and metabolites below to link to respective articles. [§ 1]

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Statin_Pathway_WP430go to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to article

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Statin_Pathway_WP430go to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to articlego to article

|alt=Statin pathway edit]] Statin pathway edit
  1. ^ The interactive pathway map can be edited at WikiPathways: "Statin_Pathway_WP430".

References

  1. ^ a b Zhong S, Sharp DS, Grove JS, Bruce C, Yano K, Curb JD, Tall AR (1996). "Increased coronary heart disease in Japanese-American men with mutation in the cholesteryl ester transfer protein gene despite increased HDL levels". J Clin Invest. 97 (12): 2917–23. doi:10.1172/JCI118751. ISSN 0021-9738. PMC 507389. PMID 8675707. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  • ^ Barzilai N, Atzmon G, Schechter C, Schaefer EJ, Cupples AL, Lipton R, Cheng S, Shuldiner AR (2003). "Unique lipoprotein phenotype and genotype associated with exceptional longevity". JAMA. 290 (15): 2030–40. doi:10.1001/jama.290.15.2030. ISSN 0098-7484. PMID 14559957. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  • ^ Darabi M; Abolfathi AA; Noori M; Kazemi A; Ostadrahimi A; Rahimipour A; et al. (2009). "Cholesteryl ester transfer protein I405V polymorphism influences apolipoprotein A-I response to a change in dietary fatty acid composition". Horm Metab Res. 41 (7): 554–8. doi:10.1055/s-0029-1192034. PMID 19242900. {{cite journal}}: Unknown parameter |author-separator= ignored (help)
  • ^ Bruce C, Sharp DS, Tall AR (1 May 1998). "Relationship of HDL and coronary heart disease to a common amino acid polymorphism in the cholesteryl ester transfer protein in men with and without hypertriglyceridemia". J Lipid Res. 39 (5): 1071–8. ISSN 0022-2275. PMID 9610775.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  • ^ Abbey M, Nestel PJ (1994). "Plasma cholesteryl ester transfer protein activity is increased when trans-elaidic acid is substituted for cis-oleic acid in the diet". Atherosclerosis. 106 (1): 99–107. doi:10.1016/0021-9150(94)90086-8. ISSN 0021-9150. PMID 8018112. {{cite journal}}: Unknown parameter |month= ignored (help)
  • ^ Barter PJ, Brewer HB Jr, Chapman MJ, Hennekens CH, Rader DJ, Tall AR (2003). "Cholesteryl ester transfer protein: a novel target for raising HDL and inhibiting atherosclerosis". Arterioscler Thromb Vasc Biol. 23 (2): 160–7. doi:10.1161/01.ATV.0000054658.91146.64. ISSN 1079-5642. PMID 12588754. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  • ^ Brousseau ME, Schaefer EJ, Wolfe ML, Bloedon LT, Digenio AG, Clark RW, Mancuso JP, Rader DJ (2004). "Effects of an inhibitor of cholesteryl ester transfer protein on HDL cholesterol". N Engl J Med. 350 (15): 1505–15. doi:10.1056/NEJMoa031766. ISSN 0028-4793. PMID 15071125. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  • ^ Nissen Se, Tardif JC; Investigators, Illustrate; Nicholls, Stephen J.; Revkin, James H.; Shear, Charles L.; Duggan, William T.; Ruzyllo, Witold; Bachinsky, William B.; Lasala, Gabriel P. (2007). "Effect of torcetrapib on the progression of coronary atherosclerosis". N Engl J Med. 356 (13): 1304–16. doi:10.1056/NEJMoa070635. ISSN 0028-4793. PMID 17387129. {{cite journal}}: Unknown parameter |month= ignored (help)
  • ^ Kastelein Jj, van Leuven SI, Investigators; Bots; Radiance 1, Leslie; Evans, Greg W.; Kuivenhoven, Jan A.; Barter, Philip J.; Revkin, James H.; Grobbee, Diederick E.; Riley, Ward A. (2007). "Effect of torcetrapib on carotid atherosclerosis in familial hypercholesterolemia" (abstract). N Engl J Med. 356 (16): 1620–30. doi:10.1056/NEJMoa071359. ISSN 0028-4793. PMID 17387131. {{cite journal}}: More than one of |author2= and |last2= specified (help); Unknown parameter |month= ignored (help)CS1 maint: numeric names: authors list (link)
  • ^ "Pfizer Stops All Torcetrapib Clinical Trials in Interest of Patient Safety" (Press release). U.S. Food and Drug Administration. 2006-12-03.
  • ^ El Harchaoui K, van der Steeg WA, Stroes ES, Kastelein JJ (2007). "The role of CETP inhibition in dyslipidemia". Curr Atheroscler Rep. 9 (2): 125–33. doi:10.1007/s11883-007-0008-5. ISSN 1523-3804. PMID 17877921. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  • ^ de Grooth GJ, Kuivenhoven JA, Stalenhoef AF, de Graaf J, Zwinderman AH, Posma JL, van Tol A, Kastelein JJ (2002). "Efficacy and safety of a novel cholesteryl ester transfer protein inhibitor, JTT-705, in humans: a randomized phase II dose-response study". Circulation. 105 (18): 2159–65. doi:10.1161/01.CIR.0000015857.31889.7B. ISSN 0009-7322. PMID 11994249. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  • ^ Reuters (2007-10-04). "Merck announces its investigational CETP-Inhibitor, MK-0859, produced positive effects on lipids with no observed blood pressure changes". Reuters, Inc. Retrieved 2007-11-04. {{cite news}}: |author= has generic name (help)
  • Further reading

    External links

    Template:PBB Controls


    Retrieved from "https://en.wikipedia.org/w/index.php?title=Cholesteryl_ester_transfer_protein&oldid=551180276"

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    This page was last edited on 19 April 2013, at 19:55 (UTC).

    This version of the page has been revised. Besides normal editing, the reason for revision may have been that this version contains factual inaccuracies, vandalism, or material not compatible with the Creative Commons Attribution-ShareAlike License.



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