Редактирование: ADH1B (раздел)

==Publications==

{{medline-entry
|title=Telomere shortening in alcohol dependence: Roles of alcohol and acetaldehyde.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30466069
|abstract=Heavy drinking leads to premature aging and precipitates the onset of age-related diseases. Acetaldehyde (AcH), a toxic metabolite of ethanol, has been implicated in various types of cancer. However, whether alcohol accelerates biological aging at a cellular level is controversial and the mechanism involved is unclear. We addressed these questions by measuring telomere length (TL) in peripheral blood leukocytes of Japanese patients with alcohol dependence (AD) and examined the association between TL, genetic variants of alcohol dehydrogenase (ADH)1B and aldehyde dehydrogenase (ALDH)2, and other clinical characteristics. A total of 134 male AD patients and 121 age- and sex-matched healthy controls were evaluated. All patients received endoscopic screening for cancer of the upper aerodigestive tract (UADT). TL was almost 50% shorter in AD patients relative to controls. There were no significant differences in TL between AD patients with and without UADT cancer, and no associations between [[ADH1B]] and [[ALDH2]] genotypes and TL. AD patients with thiamine (vitamin B1) deficiency at admission had significantly shorter TL than those with normal thiamine status. Although the exact mechanism underlying the shorter TL in AD patients remain unclear, our findings suggest that alcohol rather than AcH is associated with telomere shortening in AD, which may be accelerated by thiamine deficiency. Future studies should also focus on the association between telomere shortening and TD in the context of oxidative stress.
|mesh-terms=* Acetaldehyde
* Aged
* Aging, Premature
* Alcoholism
* Aldehyde Dehydrogenase, Mitochondrial
* Ethanol
* Humans
* Japan
* Male
* Middle Aged
* Telomere Shortening
* Thiamine Deficiency
|keywords=* ALDH2
* Age-related disease
* Alcohol dependence
* Premature aging
* Telomere length
* Thiamine/vitamin B1 deficiency
|full-text-url=https://sci-hub.do/10.1016/j.jpsychires.2018.11.007
}}
{{medline-entry
|title=Relationships of alcohol dehydrogenase 1B ([[ADH1B]]) and aldehyde dehydrogenase 2 ([[ALDH2]]) genotypes with alcohol sensitivity, drinking behavior and problem drinking in Japanese older men.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26825972
|abstract=Many East Asians have the genetic polymorphisms rs1229984 in alcohol dehydrogenase 1B ([[ADH1B]]) and rs671 in aldehyde dehydrogenase 2 ([[ALDH2]]). Here we analyzed the relationships of the two genotypes with alcohol sensitivity, drinking behavior and problem drinking among older and younger men living in rural areas of Japan. The subjects were 718 Japanese men aged 63.3 ± 10.8 (mean ± SD), categorized into the older (≥65 years, n = 357) and younger (<65 years, n = 361) groups. Facial flushing frequency, drinking behavior and positive CAGE results were compared among the genotypes using Bonferroni-corrected χ(2) test and a multivariate logistic regression analysis adjusting for age, BMI and lifestyle factors. The frequency of 'always' facial flushing among the [[ADH1B]]*1/*2 carriers was significantly lower than that among the [[ADH1B]]*2/*2 carriers in the older group (P < 0.01). The alcohol consumption (unit/day) in the [[ADH1B]]*1/*2 carriers tended to be higher compared with that in the [[ADH1B]]*2/*2 carriers among the older group (P = 0.050). In the younger group, no significant differences in alcohol sensitivity and drinking habits were generally found among the [[ADH1B]] genotypes. The [[ADH1B]]*1/*1 genotype tended to be positively associated with problem drinking in the older group (P = 0.080) but not in the younger group. The [[ALDH2]] genotypes consistently and strongly affected the alcohol sensitivity, drinking behavior and problem drinking in both the younger and older group. We for the first time observed a significant difference in alcohol sensitivity between [[ADH1B]]*1/*2 and [[ADH1B]]*2/*2 in older men aged 65 and above.
|mesh-terms=* Adult
* Aged
* Aged, 80 and over
* Alcohol Dehydrogenase
* Alcohol Drinking
* Alcoholism
* Aldehyde Dehydrogenase, Mitochondrial
* Face
* Genotype
* Humans
* Japan
* Male
* Middle Aged
* Polymorphism, Genetic
* Rural Population
|keywords=* Aging
* Alcohol dehydrogenase 1B
* Alcohol sensitivity
* Aldehyde dehydrogenase 2
* Problem drinking behavior
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4823221
}}
{{medline-entry
|title=Trends in gastrectomy and [[ADH1B]] and [[ALDH2]] genotypes in Japanese alcoholic men and their gene-gastrectomy, gene-gene and gene-age interactions for risk of alcoholism.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23296215
|abstract=The life-time drinking profiles of Japanese alcoholics have shown that gastrectomy increases susceptibility to alcoholism. We investigated the trends in gastrectomy and alcohol dehydrogenase-1B ([[ADH1B]]) and aldehyde dehydrogenase-2 ([[ALDH2]]) genotypes and their interactions in alcoholics. This survey was conducted on 4879 Japanese alcoholic men 40 years of age or older who underwent routine gastrointestinal endoscopic screening during the period 1996-2010. [[ADH1B]]/[[ALDH2]] genotyping was performed in 3702 patients. A history of gastrectomy was found in 508 (10.4%) patients. The reason for the gastrectomy was peptic ulcer in 317 patients and gastric cancer in 187 patients. The frequency of gastrectomy had gradually decreased from 13.3% in 1996-2000 to 10.5% in 2001-2005 and to 7.8% in 2006-2010 (P < 0.0001). [[ADH1B]]*1/*1 was less frequent in the gastrectomy group than in the non-gastrectomy group (age-adjusted prevalence: 20.4 vs. 27.6%, P = 0.006). [[ALDH2]] genotype distribution did not differ between the two groups. The frequency of inactive [[ALDH2]]*1/*2 heterozygotes increased slightly from 13.0% in 1996-2000 to 14.0% in 2001-2005 and to 15.4% in 2006-2010 (P < 0.08). Two alcoholism-susceptibility genotypes, [[ADH1B]]*1/*1 and [[ALDH2]]*1/*1, modestly but significantly tended not to occur in the same individual (P = 0.026). The frequency of [[ADH1B]]*1/*1 decreased with ascending age groups. The high frequency of history of gastrectomy suggested that gastrectomy is still a risk factor for alcoholism, although the percentage decreased during the period. The alcoholism-susceptibility genotype [[ADH1B]]*1/*1 was less frequent in the gastrectomy group, suggesting a competitive gene-gastrectomy interaction for alcoholism. A gene-gene interaction and gene-age interactions regarding the [[ADH1B]] genotype were observed.
|mesh-terms=* Adult
* Aged
* Aged, 80 and over
* Aging
* Alcohol Dehydrogenase
* Alcoholics
* Alcoholism
* Aldehyde Dehydrogenase
* Aldehyde Dehydrogenase, Mitochondrial
* Asian Continental Ancestry Group
* Cross-Sectional Studies
* Epistasis, Genetic
* Female
* Gastrectomy
* Gene Frequency
* Genetic Predisposition to Disease
* Genotype
* Humans
* Male
* Middle Aged
* Risk Factors

|full-text-url=https://sci-hub.do/10.1093/alcalc/ags135
}}
{{medline-entry
|title=Effect of [[ADH1B]] genotype on alcohol consumption in young Israeli Jews.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/17559546
|abstract=The alcohol dehydrogenase 1B ([[ADH1B]]) genotype affects the risk for alcoholism, with elevated prevalence of a protective allele in Jews. Alcohol consumption is increasing among younger Israeli Jews, reflecting environmental influences. We investigated whether the relationship of [[ADH1B]] genotype with alcohol consumption differed between younger and older adult Israelis. Israeli community residents aged 22 to 65 participated in a structured interview that included questions on the maximum number of drinks on an occasion (Maxdrinks). The [[ADH1B]] genotype was determined for 68 participants and dichotomized into nonprotective ([[ADH1B]](*)1/1) and protective ([[ADH1B]](*)1/2 or [[ADH1B]](*)2/2) genotypes. Using Maxdrinks as the dependent variable, Poisson's regression was used to test an age x genotype interaction. The [[ADH1B]] genotype interacted significantly with age (p=0.01) in a Poisson's model with Maxdrinks as the outcome. Among participants >or=33 years, Maxdrinks was low and unrelated to the [[ADH1B]] genotype. Among participants <33 years with [[ADH1B]](*)1/2 or [[ADH1B]](*)2/2, Maxdrinks was also low (mean, 2.6 drinks) but among those with [[ADH1B]](*)1/1, Maxdrinks was substantially higher (mean, 6.2 drinks). Maximum lifetime drinking among younger adult Israelis without genetic protection exceeded thresholds for risky and unsafe drinking (>or=5 drinks). Environmental influences promoting greater drinking among younger Israelis may particularly affect those with the nonprotective, more common [[ADH1B]] genotype.
|mesh-terms=* Adult
* Aged
* Aging
* Alcohol Dehydrogenase
* Alcohol Drinking
* Female
* Gene Frequency
* Genotype
* Humans
* Israel
* Jews
* Male
* Middle Aged
* Poisson Distribution
* Socioeconomic Factors

|full-text-url=https://sci-hub.do/10.1111/j.1530-0277.2007.00438.x
}}