Association between the catechol-O-methyltransferase (rs4680: Val158Met) polymorphism and serum alanine aminotransferase activity

Hiyoshi, Mineyoshi; Uemura, Hirokazu; Arisawa, Kokichi; Nakamoto, Mariko; Hishida, Asahi; Okada, Rieko; Matsuo, Keitaro; Kita, Yoshikuni; Niimura, Hideshi; Kuriyama, Nagato; Nanri, Hinako; Ohnaka, Keizo; Suzuki, Sadao; Mikami, Haruo; Kubo, Michiaki; Tanaka, Hideo; Hamajima, Nobuyuki

doi:10.1016/j.gene.2012.01.015

Cited by 3 publications

(2 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The effects of environmental factors such as air pollution on the incidence of NAFLD along with an increase in liver enzyme levels and consequent steatosis were previously reported (6,9,20). Exposure to diesel exhaust particles in diabetic obese mice is positively associated with NAFLD, and mortality due to diabetes mellitus is probably through increased oxidative stress (10).…”

Section: Discussionmentioning

confidence: 92%

Association of Delta-Aminolevulinic Acid Dehydratase Gene Variant with Serum Level of Alanine Aminotransferase

et al. 2019

View full text Add to dashboard Cite

Background:The enzyme ALAD (delta-aminolevulinic acid dehydratase), encoded by the ALAD gene, catalyzes the synthesis of porphobilinogen. The 177G>C (rs1800435) polymorphism participates in the hereditary deficiency of porphobilinogen synthase to cause acute lead poisoning. Objectives: The current study aimed at investigating the allelic frequency of the enzyme ALAD in patients with non-alcoholic fatty liver disease (NAFLD) compared to the control group. Methods: The fatty liver index (FLI) algorithm was used to diagnose NAFLD in participants of a prospective cohort of the Digestive Diseases Research Institute (DDRI). The ALAD genotypes, ALAD1 and ALAD2, were identified in 100 patients with NAFLD and 200 healthy controls using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP). Results: The C-allele of ALAD rs1800435 frequency was 5.5% in the group of patients with NAFLD compared to 3.3% in the control group, without significant differences (P = 0.37); however, alleles were in the Hardy-Weinberg equilibrium (P > 0.05). Serum ALT level was considerably higher in the ALAD2 carriers group than in the ones not carrying ALAD2 (29.4 ± 13.9 vs. 19.4 ± 10.1, P = 0.041).Nonetheless, each C-allele increased the serum ALT level by 1.24 IU/L (95% confidence interval: 0.22 -2.67; P = 0.04). Conclusions: The 177G>C (rs1800435) polymorphism in patients with NAFLD was similar to that of the normal population; however, it can be considered as a risk factor for serum ALT level increase.

show abstract

Section: Discussionmentioning

confidence: 92%

Association of Delta-Aminolevulinic Acid Dehydratase Gene Variant with Serum Level of Alanine Aminotransferase

et al. 2019

View full text Add to dashboard Cite

show abstract

“…In 2009, the research teams started a cross‐sectional study to examine correlations between lifestyle and medical factors, as assessed using questionnaires and medical examinations, and the distribution of possible related genotypes . Correlations were found between chronic kidney diseases and pro/anti‐inflammatory cytokine gene polymorphisms and metalloproteinase‐9 gene polymorphisms, between serum alanine aminotransferase activity and catechol‐ O ‐methyltransferase polymorphism, between clinical risk factors for diabetes mellitus and hemoglobin A1c and PPARG2 Pro12Ala polymorphism, between lifestyle risk factors on dyslipidemia and dysglycemia and apolipoprotein A5 polymorphisms, and between the timing of natural menopause and gene variants in PPARD and PPARGCIA . Although the Japanese genome‐cohort studies consist of different research teams with different financial sources, some of them are discussing collaboration to standardize the format of data collection for successful pooled analysis in the future.…”

Section: Molecular Epidemiologymentioning

confidence: 99%

Advances in cancer epidemiology in Japan

Tanaka

2013

Intl Journal of Cancer

Self Cite

View full text Add to dashboard Cite

Epidemiologists in Japan have been performing calculations to estimate nationwide cancer incidence rates as well as 5-year survival rates using population-based cancer registry data. There have been remarkable changes in cancer incidence and/or mortality in cancers of the lung, liver and stomach, which were thought to be attributed to the changing impact of exposure to cigarette smoking, chronic hepatitis C virus infection and Helicobacter pylori infection, respectively. In systematic reviews providing evidence in risk/protective factors for cancer sites using case-control and cohort studies of the Japanese population, there were associations between cancer sites (esophagus, stomach, colo-rectum, liver, pancreas, lung and breast) and various lifestyle factors. In the past 10 years, a hospital-based case-control study at Aichi Cancer Center provided valuable evidence of gene-environment interaction on the development of cancer [i.e., the effects of aldehyde dehydrogenase-2 (ALDH2) polymorphism and heavy alcohol drinking on esophageal cancer, ALDH2 polymorphism and smoking on lung cancer, methylenetetrahydrofolate reductase polymorphism and heavy alcohol drinking on pancreatic cancer]. The database with stored DNA was also used and identified seven loci containing significant but low-penetrance polymorphisms associated with the development of breast cancer. These findings together with established risk factors are likely to be useful to predict personalized breast cancer risk in East Asian women. In 2005, the Japan Multi-Institution Collaborative Cohort (J-MICC) study was launched to elucidate gene-environment interactions as well as to confirm preclinical diagnostic biomarkers of cancer. J-MICC, which has recruited 92,000 healthy individuals by the end of 2012, will follow the individuals until 2025.Over the past five decades, research on cancer epidemiology in Japan has been developing at a rapid pace. In descriptive epidemiology, Dr. Mitsuo Segi (well-known for "Segi's world population") started a population-based cancer registry in Miyagi prefecture in 1959. The population-based cancer registry expanded to cover the whole country of Japan in 2012, together with improving the quality of the data. These population-based data have been efficiently used in cancer control planning conducted by the Japanese Government since 2007. In analytical epidemiology, a "Large-Scale Census-Based Cohort Study" of cancer, and other major causes of death, was conducted by Dr. Takeshi Hirayama in 1965, recruiting 265,118 adults aged 40 years and over. From this cohort study, Dr. Hirayama first reported that passive smoking increased the risk of lung cancer in 1981.1 In 1991, the Japan Epidemiological Association (JEA) was established to promote epidemiological research. The recent trend in cancer epidemiology is focusing on molecular epidemiology, elucidating gene-environment interaction, as well as international collaboration of combining cohort data. This paper presents recent results in cancer epidemiology studies in Japan. Som...

show abstract