ArticleMolecular genetics & genomic medicine2020
DDAH1 promoter -396 4N insertion variant is associated with increased risk of type 2 diabetes in a gender-dependent manner.
Article in Molecular genetics & genomic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 3 citations in OpenAlex.
- Effects of AGXT2 variants on blood pressure and blood sugar among 750 older Japanese subjects recruited by the complete enumeration survey method.BMC genomics · 2021Article
- DDAH1 promoter -396 4N insertion variant is associated with increased risk of type 2 diabetes in a gender-dependent manner.Molecular genetics & genomic medicine · 2020Article
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4 authors at 2 institutions in 1 country.
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Abstract
backgroundAsymmetrical dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthases, making it a contributing factor for diabetes. Endogenous ADMA is hydrolyzed by dimethylarginine dimethylaminohydrolase 1 (DDAH1), and a DDAH1 promoter -396 4N deletion/insertion polymorphism (DDAH1: -396_-395insGCGT) regulates its transcriptional activity. This study aimed to explore the association between this polymorphism and type 2 diabetes (T2DM).
methodsIn a case-control study, all participants were genotyped for this polymorphism within two sets of populations (discovery: 1,227 T2DM patients and 1,339 controls; replication: 1,190 patients and 1,651 controls). The disease association was assessed by a unconditional logistic regression model. Homeostasis model assessment calculations were conducted among different genotypes.
resultsWe identified that DDAH1: -396_-395insGCGT insertion allele was significantly associated with increased risk of T2DM (discovery: adjusted odds ratio [OR] = 1.380, 95% CI = 1.128-1.687, p = .002; replication: OR = 1.231, 95% CI = 1.007-1.504, p = .043). The homeostasis model assessment of insulin resistance was increased in participants carrying Ins/Ins alleles (p = .0452). Interestingly, the insertion allele increased the risk of T2DM in males but not in females (male discovery: OR = 1.528, 95% CI = 1.141-2.047, p = .004; replication: OR = 1.439, 95% CI = 1.083-1.911, p = .012; female discovery: OR = 1.218, 95% CI = 0.913-1.626, p = .18; replication: OR = 1.161, 95% CI = 0.871-1.548, p = .308).
conclusionThe DDAH1: -396_-395insGCGT insertion allele is associated with increased risk of T2DM in a gender-dependent manner, affects males but not females.
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