The role of angiotensin I-converting enzyme gene polymorphism and global DNA methylation in the negative associations between urine di-(2-ethylhexyl) phthalate metabolites and serum adiponectin in a young Taiwanese population.

Chien-Yu Lin, Hui-Ling Lee, Ching-Way Chen, Chikang Wang, Fung-Chang Sung, Ta-Chen Su

Journal: Clinical epigenetics 2023;15(1):87

PMID: 37198693

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Abstract

BACKGROUND

Adiponectin is a key protein produced in adipose tissue, with crucial involvement in multiple metabolic processes. Di-(2-ethylhexyl) phthalate (DEHP), one of the phthalate compounds used as a plasticizer, has been shown to decrease adiponectin levels in vitro and in vivo studies. However, the role of angiotensin I-converting enzyme (ACE) gene polymorphism and epigenetic changes in the relationship between DEHP exposure and adiponectin levels is not well understood.

METHODS

This study examined the correlation between urine levels of DEHP metabolite, epigenetic marker 5mdC/dG, ACE gene phenotypes, and adiponectin levels in a sample of 699 individuals aged 12-30 from Taiwan.

RESULTS

Results showed a positive relationship between mono-2-ethylhexyl phthalate (MEHP) and 5mdC/dG, and a negative association between both MEHP and 5mdC/dG with adiponectin. The study found that the inverse relationship between MEHP and adiponectin was stronger when levels of 5mdC/dG were above the median. This was supported by differential unstandardized regression coefficients (- 0.095 vs. - 0.049, P value for interaction = 0.038)). Subgroup analysis also showed a negative correlation between MEHP and adiponectin in individuals with the I/I ACE genotype, but not in those with other genotypes, although the P value for interaction was borderline significant (0.06). The structural equation model analysis indicated that MEHP has a direct inverse effect on adiponectin and an indirect effect via 5mdC/dG.

CONCLUSIONS

In this young Taiwanese population, our findings suggest that urine MEHP levels are negatively correlated with serum adiponectin levels, and epigenetic modifications may play a role in this association. Further study is needed to validate these results and determine causality.

Address: Department of Internal Medicine, En Chu Kong Hospital, New Taipei City, 237, Taiwan.; School of Medicine, Fu Jen Catholic University, New Taipei City, 242, Taiwan.; Department of Environmental Engineering and Health, Yuanpei University of Medical Technology, Hsinchu, 300, Taiwan.; Department of Chemistry, Fu Jen Catholic University, New Taipei City, 242, Taiwan.; Department of Cardiology, National Taiwan University Hospital Yunlin Branch, Yunlin, 640, Taiwan.; Department of Health Services Administration, College of Public Health, China Medical University, Taichung, 404, Taiwan.; Department of Environmental and Occupational Medicine, National Taiwan University Hospital, Taipei, 10002, Taiwan. [email protected].; Department of Internal Medicine and Cardiovascular Center, National Taiwan University Hospital, Taipei, 100, Taiwan. [email protected].; Institute of Environmental and Occupational Health Sciences, College of Public Health, National Taiwan University, Taipei, 100, Taiwan. [email protected].; The Experimental Forest, National Taiwan University, Nantou, 558, Taiwan. [email protected].

DOI: 10.1186/s13148-023-01502-z

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MeSH Terms: Adiponectin, Diethylhexyl Phthalate, DNA Methylation, Peptidyl-Dipeptidase A, Humans, Taiwan