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==Role in disease== |
==Role in disease== |
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Rare mutations leading to increased function of CETP have been linked to accelerated [[atherosclerosis]].<ref name=Zhong1996>{{cite journal |author= Zhong S, Sharp DS, Grove JS, Bruce C, Yano K, Curb JD, Tall AR |date=June 1996 |title= Increased coronary heart disease in Japanese-American men with mutation in the cholesteryl ester transfer protein gene despite increased HDL levels |journal=J Clin Invest |volume=97 |issue=12 |pages=2917–23 |pmid=8675707 |url=http://www.jci.org/cgi/content/full/97/12/2917 |doi= 10.1172/JCI118751 |issn=0021-9738 |pmc=507389}}</ref> In contrast, a polymorphism (I405V) of the ''CETP'' gene leading to lower serum levels has also been linked to exceptional longevity <ref>{{cite journal |author=Barzilai N, Atzmon G, Schechter C, Schaefer EJ, Cupples AL, Lipton R, Cheng S, Shuldiner AR |date=October 2003 |title=Unique lipoprotein phenotype and genotype associated with exceptional longevity |journal=JAMA |volume=290 |issue=15 |pages=2030–40 |pmid=14559957 |url=http://jama.ama-assn.org/cgi/content/full/290/15/2030 |doi=10.1001/jama.290.15.2030 |issn=0098-7484}}</ref> and to metabolic response to nutritional intervention.<ref name="pmid19242900">{{cite journal| author=Darabi M| title=Cholesteryl ester transfer protein I405V polymorphism influences apolipoprotein A-I response to a change in dietary fatty acid composition | journal=Horm Metab Res |year= 2009 | volume= 41 | issue= 7 | pages= 554–8 | pmid=19242900 | doi=10.1055/s-0029-1192034| author-separator=,| author2=Abolfathi AA| author3=Noori M| author4=Kazemi A| author5=Ostadrahimi A| author6=Rahimipour A| display-authors=6| last7=Darabi| first7=M.| last8=Ghatrehsamani| first8=K.}} </ref> However, this mutation also increases the prevalence of coronary heart disease in patients with hypertriglyceridemia.<ref>{{cite journal |author=Bruce C, Sharp DS, Tall AR |date=1 May 1998|title= 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|journal=J Lipid Res |volume=39 |issue=5 |pages=1071–8 |pmid=9610775 |url=http://www.jlr.org/cgi/content/full/39/5/1071 |issn=0022-2275}}</ref> The D442G mutation, which lowers CETP levels and increases HDL levels also increases coronary heart disease.<ref name=Zhong1996/> |
Rare mutations leading to increased function of CETP have been linked to accelerated [[atherosclerosis]].<ref name=Zhong1996>{{cite journal |author= Zhong S, Sharp DS, Grove JS, Bruce C, Yano K, Curb JD, Tall AR |date=June 1996 |title= Increased coronary heart disease in Japanese-American men with mutation in the cholesteryl ester transfer protein gene despite increased HDL levels |journal=J Clin Invest |volume=97 |issue=12 |pages=2917–23 |pmid=8675707 |url=http://www.jci.org/cgi/content/full/97/12/2917 |doi= 10.1172/JCI118751 |issn=0021-9738 |pmc=507389|last2=Sharp |last3=Grove |last4=Bruce |last5=Yano |last6=Curb |last7=Tall }}</ref> In contrast, a polymorphism (I405V) of the ''CETP'' gene leading to lower serum levels has also been linked to exceptional longevity <ref>{{cite journal |author=Barzilai N, Atzmon G, Schechter C, Schaefer EJ, Cupples AL, Lipton R, Cheng S, Shuldiner AR |date=October 2003 |title=Unique lipoprotein phenotype and genotype associated with exceptional longevity |journal=JAMA |volume=290 |issue=15 |pages=2030–40 |pmid=14559957 |url=http://jama.ama-assn.org/cgi/content/full/290/15/2030 |doi=10.1001/jama.290.15.2030 |issn=0098-7484|last2=Atzmon |last3=Schechter |last4=Schaefer |last5=Cupples |last6=Lipton |last7=Cheng |last8=Shuldiner }}</ref> and to metabolic response to nutritional intervention.<ref name="pmid19242900">{{cite journal| author=Darabi M| title=Cholesteryl ester transfer protein I405V polymorphism influences apolipoprotein A-I response to a change in dietary fatty acid composition | journal=Horm Metab Res |year= 2009 | volume= 41 | issue= 7 | pages= 554–8 | pmid=19242900 | doi=10.1055/s-0029-1192034| author-separator=,| author2=Abolfathi AA| author3=Noori M| author4=Kazemi A| author5=Ostadrahimi A| author6=Rahimipour A| display-authors=6| last7=Darabi| first7=M.| last8=Ghatrehsamani| first8=K.}} </ref> However, this mutation also increases the prevalence of coronary heart disease in patients with hypertriglyceridemia.<ref>{{cite journal |author=Bruce C, Sharp DS, Tall AR |date=1 May 1998|title= 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|journal=J Lipid Res |volume=39 |issue=5 |pages=1071–8 |pmid=9610775 |url=http://www.jlr.org/cgi/content/full/39/5/1071 |issn=0022-2275|last2=Sharp|last3=Tall}}</ref> The D442G mutation, which lowers CETP levels and increases HDL levels also increases coronary heart disease.<ref name=Zhong1996/> |
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[[Elaidic acid]], a major component of [[trans fat]], increases CETP activity.<ref name="pmid8018112">{{cite journal |author=Abbey M, Nestel PJ |title=Plasma cholesteryl ester transfer protein activity is increased when trans-elaidic acid is substituted for cis-oleic acid in the diet |journal=Atherosclerosis |volume=106 |issue=1 |pages=99–107 |pmid=8018112 |doi=10.1016/0021-9150(94)90086-8 |date=March 1994 |issn=0021-9150}}</ref> |
[[Elaidic acid]], a major component of [[trans fat]], increases CETP activity.<ref name="pmid8018112">{{cite journal |author=Abbey M, Nestel PJ |title=Plasma cholesteryl ester transfer protein activity is increased when trans-elaidic acid is substituted for cis-oleic acid in the diet |journal=Atherosclerosis |volume=106 |issue=1 |pages=99–107 |pmid=8018112 |doi=10.1016/0021-9150(94)90086-8 |date=March 1994 |issn=0021-9150|last2=Nestel }}</ref> |
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==Pharmacology== |
==Pharmacology== |
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{{see also|CETP inhibitor}} |
{{see also|CETP inhibitor}} |
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As [[High-density lipoprotein|HDL]] can alleviate atherosclerosis and other [[cardiovascular disease]]s, 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.<ref>{{cite journal |author=Barter PJ, Brewer HB Jr, Chapman MJ, Hennekens CH, Rader DJ, Tall AR |date=February 2003 |title=Cholesteryl ester transfer protein: a novel target for raising HDL and inhibiting atherosclerosis |journal=Arterioscler Thromb Vasc Biol |volume=23 |issue=2 |pages=160–7 |pmid=12588754 |url=http://atvb.ahajournals.org/cgi/content/full/23/2/160 |doi=10.1161/01.ATV.0000054658.91146.64 |issn=1079-5642}}</ref> 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.<ref>{{cite journal |author=Brousseau ME, Schaefer EJ, Wolfe ML, Bloedon LT, Digenio AG, Clark RW, Mancuso JP, Rader DJ |date=April 2004 |title=Effects of an inhibitor of cholesteryl ester transfer protein on HDL cholesterol |journal=N Engl J Med |volume=350 |issue=15 |pages=1505–15 |pmid=15071125 |url=http://content.nejm.org/cgi/content/full/350/15/1505 |doi=10.1056/NEJMoa031766 |issn=0028-4793}}</ref> 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,<ref>{{cite journal |date=March 2007 |title=Effect of torcetrapib on the progression of coronary atherosclerosis |journal=N Engl J Med |volume=356 |issue=13 |pages=1304–16 |pmid=17387129 |doi=10.1056/NEJMoa070635 |issn=0028-4793 |author1=Steven E. Nissen, M.D. |author2=Jean-Claude Tardif, M.D. |author3=Stephen J. Nicholls, M.B., B.S., Ph.D. |author4=James H. Revkin, M.D. |author5=Charles L. Shear, Dr.P.H. |author6=William T. Duggan, Ph.D. |author7=Witold Ruzyllo, M.D. |author8=William B. Bachinsky, M.D. |author9=Gabriel P. Lasala, M.D. |author10=E. Murat Tuzcu, M.D. for the ILLUSTRATE Investigators |displayauthors=11 |deadurl=no }}</ref><ref>{{cite journal |date=April 2007 |title=Effect of torcetrapib on carotid atherosclerosis in familial hypercholesterolemia |journal=N Engl J Med |volume=356 |issue=16 |pages=1620–30 |pmid=17387131 |url=http://content.nejm.org/cgi/content/abstract/356/16/1620 |doi=10.1056/NEJMoa071359 |format=abstract |issn=0028-4793 |author1=Kastelein JJ, van Leuven SI |last2=Van Leuven |first2=Michiel L. |last3=Burgess |first3=Leslie |last4=Evans |first4=Greg W. |last5=Kuivenhoven |first5=Jan A. |last6=Barter |first6=Philip J. |last7=Revkin |first7=James H. |last8=Grobbee |first8=Diederick E. |last9=Riley |first9=Ward A. |last10=Shear |first10=Charles L. |last11=Duggan |last12=Bots |first12=Michiel L. |last13=Radiance 1 |first13=Investigators}}</ref> and, in a trial of a combination of torcetrapib and [[atorvastatin]], an increase in cardiovascular events and mortality.<ref name=FDA2006>{{cite press release |title=Pfizer Stops All Torcetrapib Clinical Trials in Interest of Patient Safety |publisher=U.S. Food and Drug Administration |date=2006-12-03 |url=http://www.fda.gov/bbs/topics/news/2006/new01514.html}}</ref> |
As [[High-density lipoprotein|HDL]] can alleviate atherosclerosis and other [[cardiovascular disease]]s, 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.<ref>{{cite journal |author=Barter PJ, Brewer HB Jr, Chapman MJ, Hennekens CH, Rader DJ, Tall AR |date=February 2003 |title=Cholesteryl ester transfer protein: a novel target for raising HDL and inhibiting atherosclerosis |journal=Arterioscler Thromb Vasc Biol |volume=23 |issue=2 |pages=160–7 |pmid=12588754 |url=http://atvb.ahajournals.org/cgi/content/full/23/2/160 |doi=10.1161/01.ATV.0000054658.91146.64 |issn=1079-5642|last2=Brewer Jr |last3=Chapman |last4=Hennekens |last5=Rader |last6=Tall }}</ref> 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.<ref>{{cite journal |author=Brousseau ME, Schaefer EJ, Wolfe ML, Bloedon LT, Digenio AG, Clark RW, Mancuso JP, Rader DJ |date=April 2004 |title=Effects of an inhibitor of cholesteryl ester transfer protein on HDL cholesterol |journal=N Engl J Med |volume=350 |issue=15 |pages=1505–15 |pmid=15071125 |url=http://content.nejm.org/cgi/content/full/350/15/1505 |doi=10.1056/NEJMoa031766 |issn=0028-4793|last2=Schaefer |last3=Wolfe |last4=Bloedon |last5=Digenio |last6=Clark |last7=Mancuso |last8=Rader }}</ref> 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,<ref>{{cite journal |date=March 2007 |title=Effect of torcetrapib on the progression of coronary atherosclerosis |journal=N Engl J Med |volume=356 |issue=13 |pages=1304–16 |pmid=17387129 |doi=10.1056/NEJMoa070635 |issn=0028-4793 |author1=Steven E. Nissen, M.D. |author2=Jean-Claude Tardif, M.D. |author3=Stephen J. Nicholls, M.B., B.S., Ph.D. |author4=James H. Revkin, M.D. |author5=Charles L. Shear, Dr.P.H. |author6=William T. Duggan, Ph.D. |author7=Witold Ruzyllo, M.D. |author8=William B. Bachinsky, M.D. |author9=Gabriel P. Lasala, M.D. |author10=E. Murat Tuzcu, M.D. for the ILLUSTRATE Investigators |displayauthors=11 |deadurl=no |last11=Illustrate |first11=Investigators }}</ref><ref>{{cite journal |date=April 2007 |title=Effect of torcetrapib on carotid atherosclerosis in familial hypercholesterolemia |journal=N Engl J Med |volume=356 |issue=16 |pages=1620–30 |pmid=17387131 |url=http://content.nejm.org/cgi/content/abstract/356/16/1620 |doi=10.1056/NEJMoa071359 |format=abstract |issn=0028-4793 |author1=Kastelein JJ, van Leuven SI |last2=Van Leuven |first2=Michiel L. |last3=Burgess |first3=Leslie |last4=Evans |first4=Greg W. |last5=Kuivenhoven |first5=Jan A. |last6=Barter |first6=Philip J. |last7=Revkin |first7=James H. |last8=Grobbee |first8=Diederick E. |last9=Riley |first9=Ward A. |last10=Shear |first10=Charles L. |last11=Duggan |last12=Bots |first12=Michiel L. |last13=Radiance 1 |first13=Investigators}}</ref> and, in a trial of a combination of torcetrapib and [[atorvastatin]], an increase in cardiovascular events and mortality.<ref name=FDA2006>{{cite press release |title=Pfizer Stops All Torcetrapib Clinical Trials in Interest of Patient Safety |publisher=U.S. Food and Drug Administration |date=2006-12-03 |url=http://www.fda.gov/bbs/topics/news/2006/new01514.html}}</ref> |
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A compound related to torcetrapib, [[Dalcetrapib]] (investigative name JTT-705/R1658), was also being studied, but trials have since been ceased.<ref>{{cite journal |author=El Harchaoui K, van der Steeg WA, Stroes ES, Kastelein JJ |date=August 2007 |title=The role of CETP inhibition in dyslipidemia |journal=Curr Atheroscler Rep |volume=9 |issue=2 |pages=125–33 |pmid=17877921 |doi=10.1007/s11883-007-0008-5 |issn=1523-3804}}</ref> It increases HDL levels by 30%, as compared to 60% by torcetrapib.<ref>{{cite journal |author=de Grooth GJ, Kuivenhoven JA, Stalenhoef AF, de Graaf J, Zwinderman AH, Posma JL, van Tol A, Kastelein JJ |date=May 2002 |title=Efficacy and safety of a novel cholesteryl ester transfer protein inhibitor, JTT-705, in humans: a randomized phase II dose-response study |journal=Circulation |volume=105 |issue=18 |pages=2159–65 |pmid=11994249 |url=http://circ.ahajournals.org/cgi/content/full/circulationaha;105/18/2159 |doi=10.1161/01.CIR.0000015857.31889.7B |issn=0009-7322}}</ref> Another CETP inhibitor under development is Merck's MK-0859 [[anacetrapib]], which in initial studies is not shown to increase blood pressure.<ref>{{cite news |author=Reuters|title=Merck announces its investigational CETP-Inhibitor, MK-0859, produced positive effects on lipids with no observed blood pressure changes | url=http://www.reuters.com/article/inPlayBriefing/idUSIN20071004163052MRK20071004 |publisher=Reuters, Inc. |date=2007-10-04 |deadurl=no |accessdate=26 November 2013}}</ref> |
A compound related to torcetrapib, [[Dalcetrapib]] (investigative name JTT-705/R1658), was also being studied, but trials have since been ceased.<ref>{{cite journal |author=El Harchaoui K, van der Steeg WA, Stroes ES, Kastelein JJ |date=August 2007 |title=The role of CETP inhibition in dyslipidemia |journal=Curr Atheroscler Rep |volume=9 |issue=2 |pages=125–33 |pmid=17877921 |doi=10.1007/s11883-007-0008-5 |issn=1523-3804|last2=Van Der Steeg |last3=Stroes |last4=Kastelein }}</ref> It increases HDL levels by 30%, as compared to 60% by torcetrapib.<ref>{{cite journal |author=de Grooth GJ, Kuivenhoven JA, Stalenhoef AF, de Graaf J, Zwinderman AH, Posma JL, van Tol A, Kastelein JJ |date=May 2002 |title=Efficacy and safety of a novel cholesteryl ester transfer protein inhibitor, JTT-705, in humans: a randomized phase II dose-response study |journal=Circulation |volume=105 |issue=18 |pages=2159–65 |pmid=11994249 |url=http://circ.ahajournals.org/cgi/content/full/circulationaha;105/18/2159 |doi=10.1161/01.CIR.0000015857.31889.7B |issn=0009-7322|last2=Kuivenhoven |last3=Stalenhoef |last4=De Graaf |last5=Zwinderman |last6=Posma |last7=Van Tol |last8=Kastelein }}</ref> Another CETP inhibitor under development is Merck's MK-0859 [[anacetrapib]], which in initial studies is not shown to increase blood pressure.<ref>{{cite news |author=Reuters|title=Merck announces its investigational CETP-Inhibitor, MK-0859, produced positive effects on lipids with no observed blood pressure changes | url=http://www.reuters.com/article/inPlayBriefing/idUSIN20071004163052MRK20071004 |publisher=Reuters, Inc. |date=2007-10-04 |deadurl=no |accessdate=26 November 2013}}</ref> |
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==Interactive pathway map== |
==Interactive pathway map== |
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*{{cite journal |author=Okajima F |title=[Distribution of sphingosine 1-phosphate in plasma lipoproteins and its role in the regulation of the vascular cell functions] |journal=Tanpakushitsu Kakusan Koso |volume=47 |issue= 4 Suppl |pages=480–7 |pmid= 11915346 |date=March 2002 |issn=0039-9450}} |
*{{cite journal |author=Okajima F |title=[Distribution of sphingosine 1-phosphate in plasma lipoproteins and its role in the regulation of the vascular cell functions] |journal=Tanpakushitsu Kakusan Koso |volume=47 |issue= 4 Suppl |pages=480–7 |pmid= 11915346 |date=March 2002 |issn=0039-9450}} |
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*{{cite journal |author=Barter PJ |title=Cholesteryl ester transfer protein: a novel target for raising HDL and inhibiting atherosclerosis |journal=Arterioscler. Thromb. Vasc. Biol. |volume=23 |issue= 2 |pages= 160–7 |pmid= 12588754 |doi=10.1161/01.ATV.0000054658.91146.64 |date=February 2003 |issn=1079-5642 |url=http://atvb.ahajournals.org/cgi/pmidlookup?view=long&pmid=12588754 |format=Free full text |author-separator=, |author2=Brewer HB |author3=Chapman MJ |display-authors=3 |last4=Hennekens |first4=CH |last5=Rader |first5=DJ |last6=Tall |first6=AR}} |
*{{cite journal |author=Barter PJ |title=Cholesteryl ester transfer protein: a novel target for raising HDL and inhibiting atherosclerosis |journal=Arterioscler. Thromb. Vasc. Biol. |volume=23 |issue= 2 |pages= 160–7 |pmid= 12588754 |doi=10.1161/01.ATV.0000054658.91146.64 |date=February 2003 |issn=1079-5642 |url=http://atvb.ahajournals.org/cgi/pmidlookup?view=long&pmid=12588754 |format=Free full text |author-separator=, |author2=Brewer HB |author3=Chapman MJ |display-authors=3 |last4=Hennekens |first4=CH |last5=Rader |first5=DJ |last6=Tall |first6=AR}} |
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*{{cite journal |author=Dallinga-Thie GM, Dullaart RP, van Tol A |title=Concerted actions of cholesteryl ester transfer protein and phospholipid transfer protein in type 2 diabetes: effects of apolipoproteins |journal=Curr. Opin. Lipidol. |volume=18 |issue= 3 |pages= 251–7 |pmid=17495597 |doi=10.1097/MOL.0b013e3280e12685 |date=June 2007 | issn=0957-9672}} |
*{{cite journal |author=Dallinga-Thie GM, Dullaart RP, van Tol A |title=Concerted actions of cholesteryl ester transfer protein and phospholipid transfer protein in type 2 diabetes: effects of apolipoproteins |journal=Curr. Opin. Lipidol. |volume=18 |issue= 3 |pages= 251–7 |pmid=17495597 |doi=10.1097/MOL.0b013e3280e12685 |date=June 2007 | issn=0957-9672|last2=Dullaart |last3=Van Tol }} |
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}} |
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{{Refend}} |
{{Refend}} |
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 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 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]
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), was also being studied, but trials have since been ceased.[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]
Click on genes, proteins and metabolites below to link to respective articles. [§ 1]
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Fatty acid |
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Hormone |
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Metal/element |
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Vitamin |
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Pigment |
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Other |
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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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