Journal of endocrinological investigation · 2018
Association of PON1 gene polymorphisms with polycystic ovarian syndrome risk: a meta-analysis of case-control studies.
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Liao D, Yu H, Han L, Zhong C, Ran X, Wang D, Mo L
Аннотация
PURPOSE: Evidences showed that paraoxonase 1 (PON1) gene polymorphism has an impact on women's susceptibility to polycystic ovarian syndrome (PCOS) by influencing the expression and activity of PON1. However, the effects of three PON1 polymorphisms (- 108 C>T, L55M and Q192R) on the incidence of PCOS have generated inconsistent results. Here, we conducted a meta-analysis to investigate the association between PON1 polymorphisms and PCOS risk.
METHODS: All eligible trials were identified via systematic searches of multiple literature databases. Outcome data were synthesized by using crude odds ratio with 95% confidence interval. Heterogeneity was assessed with the I2 test. Publication bias and subgroup analyses were also performed.
RESULTS: A total of 2449 cases and 1977 controls from nine studies were selected for analysis. The pooled results showed a significant association between PCOS risk and PON1 - 108 C/T polymorphism in the following genetic models [allelic, 0.72 (0.56-0.92); homozygote, 0.51 (0.32-0.82); heterozygote, 0.44 (0.25-0.78); and dominant 0.47 (0.29-0.77)]. For the PON1 192 Q/R polymorphism, a significant relationship was found in the allelic model [0.62 (0.41-0.93)] and recessive model [0.61 (0.37-0.98)]. PCOS risk was also linked to PON1 L55M polymorphism in the heterozygote model [0.62 (0.39-0.98)] and dominant model [0.63 (0.41-0.96)].
CONCLUSIONS: Our study has shown that PON1 - 108 C/T polymorphism might be associated with increased risk of PCOS under the allelic, homozygote, heterozygote, and dominant models. Additionally, PON1 192 Q/R and L55M polymorphisms were significantly related only in the allelic and recessive model, and in the heterozygote and dominant model, respectively.
METHODS: All eligible trials were identified via systematic searches of multiple literature databases. Outcome data were synthesized by using crude odds ratio with 95% confidence interval. Heterogeneity was assessed with the I2 test. Publication bias and subgroup analyses were also performed.
RESULTS: A total of 2449 cases and 1977 controls from nine studies were selected for analysis. The pooled results showed a significant association between PCOS risk and PON1 - 108 C/T polymorphism in the following genetic models [allelic, 0.72 (0.56-0.92); homozygote, 0.51 (0.32-0.82); heterozygote, 0.44 (0.25-0.78); and dominant 0.47 (0.29-0.77)]. For the PON1 192 Q/R polymorphism, a significant relationship was found in the allelic model [0.62 (0.41-0.93)] and recessive model [0.61 (0.37-0.98)]. PCOS risk was also linked to PON1 L55M polymorphism in the heterozygote model [0.62 (0.39-0.98)] and dominant model [0.63 (0.41-0.96)].
CONCLUSIONS: Our study has shown that PON1 - 108 C/T polymorphism might be associated with increased risk of PCOS under the allelic, homozygote, heterozygote, and dominant models. Additionally, PON1 192 Q/R and L55M polymorphisms were significantly related only in the allelic and recessive model, and in the heterozygote and dominant model, respectively.