Dataset Information

The Association and Interaction of Aldehyde Dehydrogenase 2 Polymorphisms with Food Group Intake and Probability of Having Non-Alcoholic Fatty Liver Disease.

ABSTRACT:

Purpose

This study investigated the association between the aldehyde dehydrogenase 2 (ALDH2) rs671 polymorphism, food group intake, and the probability of having non-alcoholic fatty liver disease (NAFLD) in a Chinese population.

Patients and methods

A total of 3506 adults were enrolled in this study, and all underwent physical examinations and genotyping of polymorphisms with polymerase chain reaction. Participants filled out a dietary questionnaire that was used to assess the frequency and quantity of food consumption.

Results

We found that milk groups were associated with a lower probability of developing NAFLD. On the contrary, meat and salted and smoked foods were associated with a higher probability of NAFLD. However, the influences of salted and smoked foods and fresh fruit and vegetables on NAFLD were obviously different in the two genotype groups. Salted and smoked foods intake was a factor associated with a higher probability of having NAFLD or nonalcoholic steatohepatitis (NASH) in the A genotype group, but there was no effect in the G genotype group. Moreover, eating salted and smoked foods several times per week was associated with a higher probability of having NAFLD than seldom consuming them. Consumption of fresh fruit and vegetables was not a factor influencing the probability of having NAFLD in the A genotype group, and there was no effect in the G genotype group. Further analysis of the interaction indicated that the GA?+AA genotype showed an interaction with fresh fruit and vegetables and salted and smoked foods. Moreover, it was not obvious that meat intake increased the probability of having NAFLD or NASH among different genotypes.

Conclusion

Our results indicate that ALDH2 rs671 GA and AA genotypes are factors associated with increased probability of NAFLD among Chinese subjects. This could stimulate the development of novel approaches for preventing NAFLD.

SUBMITTER: Hao X

PROVIDER: S-EPMC7765681 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Publications

The Association and Interaction of Aldehyde Dehydrogenase 2 Polymorphisms with Food Group Intake and Probability of Having Non-Alcoholic Fatty Liver Disease.

Hao Xiaoyan X Zeng Qiang Q

Diabetes, metabolic syndrome and obesity : targets and therapy 20201222

<h4>Purpose</h4>This study investigated the association between the <i>aldehyde dehydrogenase 2 (ALDH2) rs671</i> polymorphism, food group intake, and the probability of having non-alcoholic fatty liver disease (NAFLD) in a Chinese population.<h4>Patients and methods</h4>A total of 3506 adults were enrolled in this study, and all underwent physical examinations and genotyping of polymorphisms with polymerase chain reaction. Participants filled out a dietary questionnaire that was used to assess ...[more]

PMID: 33376374

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Project description:Aldehyde dehydrogenase 2 (ALDH2) is the major enzyme that metabolizes acetaldehyde produced from alcohol metabolism. Approximately 40-50% of East Asians carry an inactive ALDH2 gene and exhibit acetaldehyde accumulation after alcohol consumption. However, the role of ALDH2 deficiency in the pathogenesis of alcoholic liver injury remains obscure. In the present study, wild-type and ALDH2(-/-) mice were subjected to ethanol feeding and/or carbon tetrachloride (CCl4 ) treatment, and liver injury was assessed. Compared with wild-type mice, ethanol-fed ALDH2(-/-) mice had higher levels of malondialdehyde-acetaldehyde (MAA) adduct and greater hepatic inflammation, with higher hepatic interleukin (IL)-6 expression but surprisingly lower levels of steatosis and serum alanine aminotransferase (ALT). Higher IL-6 levels were also detected in ethanol-treated precision-cut liver slices from ALDH2(-/-) mice and in Kupffer cells isolated from ethanol-fed ALDH2(-/-) mice than those levels in wild-type mice. In vitro incubation with MAA enhanced the lipopolysaccharide (LPS)-mediated stimulation of IL-6 production in Kupffer cells. In agreement with these findings, hepatic activation of the major IL-6 downstream signaling molecule signal transducer and activator of transcription 3 (STAT3) was higher in ethanol-fed ALDH2(-/-) mice than in wild-type mice. An additional deletion of hepatic STAT3 increased steatosis and hepatocellular damage in ALDH2(-/-) mice. Finally, ethanol-fed ALDH2(-/-) mice were more prone to CCl4 -induced liver inflammation and fibrosis than ethanol-fed wild-type mice.ALDH2(-/-) mice are resistant to ethanol-induced steatosis but prone to inflammation and fibrosis by way of MAA-mediated paracrine activation of IL-6 in Kupffer cells. These findings suggest that alcohol, by way of acetaldehyde and its associated adducts, stimulates hepatic inflammation and fibrosis independent from causing hepatocyte death, and that ALDH2-deficient individuals may be resistant to steatosis and blood ALT elevation, but are prone to liver inflammation and fibrosis following alcohol consumption.

Project description:BackgroundCytosolic aldehyde dehydrogenase, or ALDH1A1, functions in ethanol detoxification, metabolism of neurotransmitters, and synthesis of retinoic acid. Because the promoter region of a gene can influence gene expression, the ALDH1A1 promoter regions were studied to identify polymorphism, to assess their functional significance, and to determine whether they were associated with a risk for developing alcoholism.MethodsSequence analysis was performed in the promoter region by using Asian, Caucasian, and African American subjects. The resulting polymorphisms were assessed for frequency in Asian, Caucasian, Jewish, and African American populations and tested for associations with alcohol dependence in Asian and African American populations of alcoholics and controls. The functional significance of each polymorphism was determined through in vitro expression analysis by using HeLa and HepG2 cells.ResultsTwo polymorphisms, a 17 base pair (bp) deletion (-416/-432) and a 3 bp insertion (-524), were discovered in the ALDH1A1 promoter region: ALDH1A1*2 and ALDH1A1*3, respectively. ALDH1A1*2 was observed at frequencies of 0.035, 0.023, 0.023, and 0.012 in the Asian, Caucasian, Jewish, and African American populations, respectively. ALDH1A1*3 was observed only in the African American population, at a frequency of 0.029. By using HeLa and HepG2 cells for in vitro expression, the activity of the luciferase reporter gene was significantly decreased after transient transfection of ALDH1A1*3-luciferase compared with the wild-type construct ALDH1A1*1-luciferase. In an African American population, a trend for higher frequencies of the ALDH1A1*2 and ALDH1A1*3 alleles was observed in a population of alcoholics (p = 0.03 and f = 0.12, respectively) compared with the control population.ConclusionsALDH1A1*2 and ALDH1A1*3 may influence ALDH1A1 gene expression. Both ALDH1A1*2 and ALDH1A1*3 produce a trend in an African American population that may be indicative of an association with alcoholism; however, more samples are required to validate this observation. The underlying mechanisms contributing to these trends are still unknown.

Dataset Information

The Association and Interaction of Aldehyde Dehydrogenase 2 Polymorphisms with Food Group Intake and Probability of Having Non-Alcoholic Fatty Liver Disease.

Purpose

Patients and methods

Results

Conclusion

Publications

The Association and Interaction of Aldehyde Dehydrogenase 2 Polymorphisms with Food Group Intake and Probability of Having Non-Alcoholic Fatty Liver Disease.

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