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Interaction between β -hexachlorocyclohexane and ADIPOQ genotypes contributes to the risk of type 2 diabetes mellitus in East Chinese adults

View Article: PubMed Central - PubMed

ABSTRACT

Growing evidence links environmental exposure to hexachlorocyclohexanes (HCHs) to the risk of type 2 diabetes mellitus (T2DM), and ADIPOQ that encodes adiponectin is considered as an important gene for T2DM. However, the role of ADIPOQ-HCH interaction on T2DM risk remains unclear. Thus, a paired case-control study was conducted in an East Chinese community. A total of 1446 subjects, including 723 cases and 723 controls matched on age, gender and residence, were enrolled, and 4 types of HCH isomers were measured in serum samples using GC-MS/MS. Additionally, 4 candidate ADIPOQ SNPs (rs182052, rs266729, rs6810075, and rs16861194) were genotyped by TaqMan assay, and plasma adiponectin was measured using ELISA. No associations between 4 SNPs and T2DM risk were found, but T2DM risk significantly increased with serum levels of β-HCH (P < 0.001). Furthermore, the synergistic interaction between β-HCH and rs182052 significantly increased T2DM risk (OR I-additive model = 2.20, OR I-recessive model = 2.13). Additionally, individuals carrying only rs182052 (A allele) with high levels of β-HCH had significant reduction in adiponectin levels (P = 0.016). These results indicate that the interaction between rs182052 and β-HCH might increase the risk of T2DM by jointly decreasing the adiponectin level and potentially trigger T2DM development.

No MeSH data available.


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Plasma adiponectin levels among groups categorized by rs182052 genotype or serum β-HCH levels.(A) The adiponectin levels in cases and controls. (B) The distribution of the adiponectin levels among rs182052 genotype. (C) The distribution of the adiponectin levels among β-HCH groups. ND, not detectable; M1 and M2, median of detectable levels. Data were presented in Box (10–90 percentile) and whiskers, p values were calculated by nonparameteric test.
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f1: Plasma adiponectin levels among groups categorized by rs182052 genotype or serum β-HCH levels.(A) The adiponectin levels in cases and controls. (B) The distribution of the adiponectin levels among rs182052 genotype. (C) The distribution of the adiponectin levels among β-HCH groups. ND, not detectable; M1 and M2, median of detectable levels. Data were presented in Box (10–90 percentile) and whiskers, p values were calculated by nonparameteric test.

Mentions: To verify the impact of interaction between β-HCH and rs182052 on the risk of T2DM, the plasma levels of adiponectin was measured. As shown in Fig. 1, the median level of adiponectin was significantly lower in cases (13.34 μg/mL) than in controls (8.61 μg/mL; P < 0.01; Fig. 1A). After stratification, participants with rs182052 genotypes (AA) had a declined adiponectin levels in comparison with those who carried wild-type ADIPOQ; this difference was not significant (GG) (P > 0.05, Fig. 1B). However, participants with high levels of β-HCH had lower adiponectin levels than lower β-HCH level groups (reference or Median 1 groups) (P < 0.05, Fig. 1C). Furthermore, the levels of adiponectin in the rs182052 genotype (AG/AA) group and high β-HCH exposure group were lower than the levels in the wild type (GG) and low β-HCH exposure groups, but these differences were not significant (Table 4). However, individuals carrying rs182052 (mutant allele A, AG/AA) with high levels of β-HCH had a significant reduction in adiponectin levels (8.04 μg/mL) in comparison of those with low levels of β-HCH (P = 0.016, Table 4).


Interaction between β -hexachlorocyclohexane and ADIPOQ genotypes contributes to the risk of type 2 diabetes mellitus in East Chinese adults
Plasma adiponectin levels among groups categorized by rs182052 genotype or serum β-HCH levels.(A) The adiponectin levels in cases and controls. (B) The distribution of the adiponectin levels among rs182052 genotype. (C) The distribution of the adiponectin levels among β-HCH groups. ND, not detectable; M1 and M2, median of detectable levels. Data were presented in Box (10–90 percentile) and whiskers, p values were calculated by nonparameteric test.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5121886&req=5

f1: Plasma adiponectin levels among groups categorized by rs182052 genotype or serum β-HCH levels.(A) The adiponectin levels in cases and controls. (B) The distribution of the adiponectin levels among rs182052 genotype. (C) The distribution of the adiponectin levels among β-HCH groups. ND, not detectable; M1 and M2, median of detectable levels. Data were presented in Box (10–90 percentile) and whiskers, p values were calculated by nonparameteric test.
Mentions: To verify the impact of interaction between β-HCH and rs182052 on the risk of T2DM, the plasma levels of adiponectin was measured. As shown in Fig. 1, the median level of adiponectin was significantly lower in cases (13.34 μg/mL) than in controls (8.61 μg/mL; P < 0.01; Fig. 1A). After stratification, participants with rs182052 genotypes (AA) had a declined adiponectin levels in comparison with those who carried wild-type ADIPOQ; this difference was not significant (GG) (P > 0.05, Fig. 1B). However, participants with high levels of β-HCH had lower adiponectin levels than lower β-HCH level groups (reference or Median 1 groups) (P < 0.05, Fig. 1C). Furthermore, the levels of adiponectin in the rs182052 genotype (AG/AA) group and high β-HCH exposure group were lower than the levels in the wild type (GG) and low β-HCH exposure groups, but these differences were not significant (Table 4). However, individuals carrying rs182052 (mutant allele A, AG/AA) with high levels of β-HCH had a significant reduction in adiponectin levels (8.04 μg/mL) in comparison of those with low levels of β-HCH (P = 0.016, Table 4).

View Article: PubMed Central - PubMed

ABSTRACT

Growing evidence links environmental exposure to hexachlorocyclohexanes (HCHs) to the risk of type 2 diabetes mellitus (T2DM), and ADIPOQ that encodes adiponectin is considered as an important gene for T2DM. However, the role of ADIPOQ-HCH interaction on T2DM risk remains unclear. Thus, a paired case-control study was conducted in an East Chinese community. A total of 1446 subjects, including 723 cases and 723 controls matched on age, gender and residence, were enrolled, and 4 types of HCH isomers were measured in serum samples using GC-MS/MS. Additionally, 4 candidate ADIPOQ SNPs (rs182052, rs266729, rs6810075, and rs16861194) were genotyped by TaqMan assay, and plasma adiponectin was measured using ELISA. No associations between 4 SNPs and T2DM risk were found, but T2DM risk significantly increased with serum levels of &beta;-HCH (P&thinsp;&lt;&thinsp;0.001). Furthermore, the synergistic interaction between &beta;-HCH and rs182052 significantly increased T2DM risk (OR I-additive model&thinsp;=&thinsp;2.20, OR I-recessive model&thinsp;=&thinsp;2.13). Additionally, individuals carrying only rs182052 (A allele) with high levels of &beta;-HCH had significant reduction in adiponectin levels (P&thinsp;=&thinsp;0.016). These results indicate that the interaction between rs182052 and &beta;-HCH might increase the risk of T2DM by jointly decreasing the adiponectin level and potentially trigger T2DM development.

No MeSH data available.


Related in: MedlinePlus