Role of cholesterol 7alpha-hydroxylase (CYP7A1) in nutrigenetics and pharmacogenetics of cholesterol lowering
Language English Country New Zealand Media print
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
16669607
DOI
10.1007/bf03256448
PII: 1023
Knihovny.cz E-resources
- MeSH
- Anticholesteremic Agents therapeutic use MeSH
- Cholesterol 7-alpha-Hydroxylase genetics MeSH
- Diet MeSH
- Pharmacogenetics MeSH
- Cardiovascular Diseases drug therapy genetics MeSH
- Cholesterol, LDL blood metabolism MeSH
- Humans MeSH
- Eating genetics MeSH
- Hydroxymethylglutaryl-CoA Reductase Inhibitors therapeutic use MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Anticholesteremic Agents MeSH
- Cholesterol 7-alpha-Hydroxylase MeSH
- Cholesterol, LDL MeSH
- Hydroxymethylglutaryl-CoA Reductase Inhibitors MeSH
The relationship between dietary composition/cholesterol-lowering therapy and final plasma lipid levels is to some extent genetically determined. It is clear that these responses are under polygenic control, with multiple variants in many genes participating in the total effect (and with each gene contributing a relatively small effect). Using different experimental approaches, several candidate genes have been analyzed to date.Interesting and consistent results have been published recently regarding the A-204C promoter variant in the cholesterol 7alpha-hydroxylase (CYP7A1) gene. CYP7A1 is a rate-limiting enzyme in bile acid synthesis and therefore plays an important role in maintaining cholesterol homeostasis. CYP7A1-204CC homozygotes have the greatest decrease in total cholesterol level in response to dietary changes in different types of dietary intervention studies. In contrast, one study has reported that the effect of statins in lowering low-density lipoprotein (LDL)-cholesterol levels was slightly greater in -204AA homozygotes. The CYP7A1 A-204C variant accounts for a significant proportion of the genetic predisposition of the response of plasma cholesterol levels.
See more in PubMed
N Engl J Med. 1994 Sep 15;331(11):706-10 PubMed
QJM. 1996 Sep;89(9):671-80 PubMed
Atherosclerosis. 2004 Aug;175(2):287-93 PubMed
Yi Chuan. 2004 May;26(3):283-6 PubMed
Am J Clin Nutr. 2003 May;77(5):1098-111 PubMed
Curr Opin Lipidol. 1998 Apr;9(2):113-8 PubMed
Physiol Res. 2004;53(5):565-8 PubMed
J Clin Invest. 1983 Dec;72(6):1930-6 PubMed
J Lipid Res. 1990 Dec;31(12):2219-26 PubMed
Biochem Soc Trans. 2004 Feb;32(Pt 1):92-6 PubMed
Am J Epidemiol. 1986 Feb;123(2):221-34 PubMed
Arterioscler Thromb. 1994 Jun;14(6):884-91 PubMed
Cas Lek Cesk. 2003;142(7):423-6 PubMed
J Lipid Res. 1980 May;21(4):455-66 PubMed
Clin Biochem. 2003 Jun;36(4):263-7 PubMed
J Lipid Res. 2000 Jan;41(1):1-11 PubMed
Atherosclerosis. 2001 Jul;157(1):1-11 PubMed
Eur J Hum Genet. 2004 Nov;12(11):935-41 PubMed
J Lipid Res. 1999 Oct;40(10):1883-9 PubMed
Genomics. 1992 Sep;14(1):153-61 PubMed
Genomics. 1994 Mar 15;20(2):320-3 PubMed
Atherosclerosis. 2005 Jun;180(2):407-15 PubMed
Nutrition. 2000 Sep;16(9):785-6 PubMed
J Nutr. 2004 Sep;134(9):2200-4 PubMed
Br J Nutr. 2000 Mar;83 Suppl 1:S127-36 PubMed
Eur J Clin Invest. 1999 Oct;29(10):827-34 PubMed
J Clin Invest. 1998 Mar 15;101(6):1283-91 PubMed
Proc Nutr Soc. 2002 Nov;61(4):427-34 PubMed
Arterioscler Thromb Vasc Biol. 1997 Nov;17(11):3064-70 PubMed
J Thromb Haemost. 2003 Jul;1(7):1398-402 PubMed
Gene. 2001 Jan 10;262(1-2):257-65 PubMed
Arteriosclerosis. 1988 Jan-Feb;8(1):1-21 PubMed
Circulation. 2003 May 20;107(19):2416-21 PubMed
Genes Dev. 1990 Dec;4(12B):2353-65 PubMed
Can J Cardiol. 1995 Oct;11 Suppl G:93G-96G PubMed
Global DNA methylation in rats´ liver is not affected by hypercholesterolemic diet
