The genetics of alcohol metabolism: role of alcohol dehydrogenase and aldehyde dehydrogenase variants.
paper
Cited
Public
- Authors
- Edenberg, Howard J
- Year
- 2007
- Journal
- Alcohol research & health : the journal of the National Institute on Alcohol Abuse and Alcoholism
- PMID
- 17718394
- PMCID
- PMC3860432
The primary enzymes involved in alcohol metabolism are alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH). Both enzymes occur in several forms that are encoded by different genes; moreover, there are variants (i.e., alleles) of some of these genes that encode enzymes with different characteristics and which have different ethnic distributions. Which ADH or ALDH alleles a person carries influence his or her level of alcohol consumption and risk of alcoholism. Researchers to date primarily have studied coding variants in the ADH1 B, ADH1C, and ALDH2 genes that are associated with altered kinetic properties of the resulting enzymes. For example, certain ADH1B and ADH1C alleles encode particularly active ADH enzymes, resulting in more rapid conversion of alcohol (i.e., ethanol) to acetaldehyde; these alleles have a protective effect on the risk of alcoholism. A variant of the ALDH2 gene encodes an essentially inactive ALDH enzyme, resulting in acetaldehyde accumulation and a protective effect. It is becoming clear that noncoding variants in both ADH and ALDH genes also may influence alcohol metabolism and, consequently, alcoholism risk; the specific nature and effects of these variants still need further study.
Relative sizes and positions of the seven human alcohol dehydrogenase (ADH) genes on the long arm of chromosome 4 (i.e., chromosome 4q). They are shown in the direction in which the genes are transcribed (arrows), but this is opposite to their orientation on chromosome 4q (i.e., ADH5 is closest to the region where the chromosome arms are joined [i.e., the centromere]). The distances between the genes are indicated in kilobasepairs (kb).
Linkage disequilibrium (LD) among single-nucleotide polymorphisms (SNPs) in the alcohol dehydrogenase (ADH) genes. The positions of the genes are indicated at the top. SNPs in which particular combinations of alleles are commonly inherited together have a high LD, depicted in the figure as darker-shaded boxes at the intersections of the SNPs that are being compared. SNPs in which combinations of alleles essentially are random have a lower LD (indicated by lighter shades). SNPs within genes generally are in high LD with each other, whereas SNPs in different genes typically have a lower LD between them. One region of moderately high LD spans most of the genes except ADH7. At one site of the ADH7 gene, frequent rearrangement of the genetic information (i.e., recombination) has occurred so that SNPs upstream of that site are randomly associated with SNPs downstream of that site (as indicated by the area of mostly white boxes).SOURCE: Modified from Edenberg et al. 2006.
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| Name | Type |
|---|---|
| 66-bp insertion/deletion local | variant |
| acetaldehyde | drug |
| acetic acid | drug |
| ADH | gene |
| ADH1A | gene |
| ADH1B | gene |
| ADH1B*1 local | variant |
| ADH1C | gene |
| ADH1C expression local | phenotype |
| ADH1C promoter haplotype local | variant |
| ADH1C*Thr352 local | variant |
| ADH4 | gene |
| ADH4 -136bp SNP local | variant |
| ADH5 | gene |
| ADH6 | gene |
| ADH7 | gene |
| ADH genes | gene |
| African | cohort |
| African-American families local | cohort |
| African descent | cohort |
| alcohol | phenotype |
| alcohol dependence | phenotype |
| alcohol flush reaction | phenotype |
| alcoholism | phenotype |
| alcoholism risk | phenotype |
| alcohol metabolism | phenotype |
| ALDH1 local | drug |
| ALDH1A1 | gene |
| ALDH1 enzyme local | drug |
| ALDH2 | gene |
| ALDH2*1 local | variant |
| ALDH2*1 allele local | variant |
| ALDH2_enzyme local | drug |
| ALDH2 promoter variant local | variant |
| ALDH2 SNPs local | variant |
| ALDH gene local | gene |
| Asian | cohort |
| Australian community-based sample local | cohort |
| binge drinking | phenotype |
| Chinese descent local | cohort |
| Chinese men | cohort |
| Chinese (Taiwan) local | cohort |
| class I enzymes local | gene |
| coding variant | cohort |
| complex diseases | phenotype |
| disulfiram | drug |
| East Asian | cohort |
| Elevated BACs local | phenotype |
| ethanol consumption | phenotype |
| ethanol elimination rate local | phenotype |
| ethanol oxidation local | phenotype |
| ethanol-oxidizing capacity local | phenotype |
| European-American families local | cohort |
| European population | cohort |
| fetal alcohol syndrome | phenotype |
| formaldehyde dehydrogenase local | drug |
| Haplotype of five minor alleles in ALDH2 local | variant |
| healthy young European Americans local | cohort |
| human alcoholics | phenotype |
| Japanese alcoholics local | cohort |
| Japanese descent local | cohort |
| Jewish descent local | cohort |
| Korean descent local | cohort |
| NAD+ | drug |
| Native Americans | cohort |
| noncoding variant | variant |
| oxidative capacity local | phenotype |
| oxidizing capacity local | phenotype |
| protective allele local | variant |
| retinol oxidation local | phenotype |
| Self-reported intoxication local | phenotype |
| SNP | cohort |
| Southwest California Indians | cohort |
| three SNPs in ADH1C regulatory region local | variant |
| Two individual SNPs in ALDH2 local | variant |
| Ξ± subunit | drug |
| Ξ² subunit | drug |
| Ξ³1Ξ³1 homodimeric enzyme local | drug |
| Ξ³2Ξ³2 enzyme local | drug |
| Ξ³ subunit | drug |
| Ο-ADH local | drug |
| Ο-ADH local | gene |
| Ο-ADH local | drug |
| Ο-ADH local | drug |
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