In males, rs9860747 and rs17366568 predicted CHD (0.22 [0.05-0.92] and 1.50 [1.01-2.20]; P ≤ 0.042), while rs1648707 and rs1063537 predicted IS (2.36 [1.32-4.23] and 2.09 [1.17-3.72]; P ≤ 0.012).
Moreover, the stratified analysis found that the genotype of rs3774262 (GA/AA), rs4686803 (CT/TT), and rs1063537 (CT/TT) variants were associated with increased risk of OSA by 2.935-, 2.935- and 2.786-fold in overweight participants.
On the other hand, while initial univariate logistic regression analysis pointed to rs1063537 C > T (p = 0.010), rs2082940 C > T (p = 0.035) and rs1063539 G > C (p = 0.035) as being associated with myocardial infarction, significance levels of these relationships were diminished following adjustment for the influence of confounding covariates.
ADIPOQ genetic polymorphisms rs2241766 (+45T>G), rs1063537, rs2241767 and rs2082940 were correlated with the progression of DN in Taiwanese male patients with T2D.
One intron SNP (rs13306519) in LEPR and one 3'UTR SNP (rs1063537) in ADIPOQ demonstrated a significant association with T2DM (P = 0.024 and 0.014 respectively).
In males, rs9860747 and rs17366568 predicted CHD (0.22 [0.05-0.92] and 1.50 [1.01-2.20]; P ≤ 0.042), while rs1648707 and rs1063537 predicted IS (2.36 [1.32-4.23] and 2.09 [1.17-3.72]; P ≤ 0.012).
In two-factor gene-environment interaction analyses, rs1063538 presented significant interactions with smoking status, family history of cancer and alcohol use, with ORs of 4.52 (95%CI: 2.78-7.34), 3.18 (95%CI: 1.73-5.82) and 1.97 (95%CI: 1.27-3.04) for smokers, individuals with family history of cancer or drinkers with CC genotype compared with non-smokers, individuals without family history of cancer or non-drinkers with TT genotype, respectively.
Further stratified analysis of the patients indicated that there were significant correlations for rs1342387A/G (P = 0.027) and rs16861205A/G (P = 0.000) with tumor location; rs16850799A/G (P = 0.004) and rs2058033C/A (P = 0.003) with invasion depth; rs16850799A/G (P = 0.019) with the tumor-node-metastasis stage; rs16850799A/G (P = 0.016), rs1501299A/C (P = 0.005) and rs1063538C/T (P = 0.017) with alcohol consumption; rs11612414A/G (P = 0.040) and rs12733285T/C (P = 0.005) with salted food; rs1063538C/T (P = 0.043) with family history of gastric cancer; and rs11612414A/G (P = 0.029) with gender.
In two-factor gene-environment interaction analyses, rs1063538 presented significant interactions with smoking status, family history of cancer and alcohol use, with ORs of 4.52 (95%CI: 2.78-7.34), 3.18 (95%CI: 1.73-5.82) and 1.97 (95%CI: 1.27-3.04) for smokers, individuals with family history of cancer or drinkers with CC genotype compared with non-smokers, individuals without family history of cancer or non-drinkers with TT genotype, respectively.
Varied association of ADIPOQ genotypes with T2DM was seen according to the genetic model used: rs17300539 and rs266729 were significantly associated with T2DM under the three models, while rs16861194 was association with T2DM under additive and dominant models, and rs822396, rs2241766, and rs1063538 were associated with T2DM under the dominant models only.
In the case-control analysis, PPARG rs1801282 (Pro12Ala) (OR=1.48 (1.02-2.16)), ADIPOQ rs1063539 (OR=1.17 (1.01-1.35)), and HNF4A rs1884614 (OR=1.16 (1.00-1.32) were associated with T2D (P(allelic)<0.05).
Among these mutations, the 4545G/C mutation (rs1063539) contributed to the genetic risk of T2D in the non-obese group (OR=2.34, 95%CI: 1.31-4.21, P=0.004), and 57% of the risk is related to this polymorphism.
rs266729, rs2241766, rs2082940 and rs1063539 in the <i>AD</i> gene and rs7539542 and rs12342 in the <i>ADR</i> gene are possibly not associated with genetic susceptibility to RA, but the <i>A</i><i>D</i> gene rs1063539 locus was possibly associated with anti-CCP in RA female patients.
On the other hand, while initial univariate logistic regression analysis pointed to rs1063537 C > T (p = 0.010), rs2082940 C > T (p = 0.035) and rs1063539 G > C (p = 0.035) as being associated with myocardial infarction, significance levels of these relationships were diminished following adjustment for the influence of confounding covariates.
We observed an epistatic interaction between survivin rs9904341 CC+CG genotype and ADIPOQ rs1063539 GG genotype increasing the risk of EC compared to those with other genotypes [OR: 4.86(1.88-12.54), P=0.001].
We observed an epistatic interaction between survivin rs9904341 CC+CG genotype and ADIPOQ rs1063539 GG genotype increasing the risk of EC compared to those with other genotypes [OR: 4.86(1.88-12.54), P=0.001].
The silence SNP G15G (+45TN G) in exon 1 and SNP+349ANG in intron 2 also showed a weak association with type 2 diabetes (P=0.06 and P=0.07, respectively),while SNPs−3971ANG in intron 1 and Y111H, R112C and H241P in exon 3 showed no association (P N 0.05).
Six polymorphisms (rs182052G > A, rs16861205G > A, rs822391T > C, rs822396A > G, rs12495941G > T and rs3774261A > G) that had a minor allele frequency of over 1% were strongly associated with stroke (p < 0.05).
The association between the rs12495941 variant and obesity is modulated by the PEA, so that the relationship between the G allele and a higher incidence of obesity was present in those individuals within the lower PEA group.
CONCLUSIONS TDT confirms that rs17300539 of ADIPOQ is strongly associated with the risk of PCOS in a Chinese Han population, but rs12495941 of ADIPOQ is not associated with the occurrence of PCOS.
In Cox regression after adjustment for the most parsimonious models, log<sub>e</sub>(serum adiponectin) and the ADIPOQ variant rs12495941 were inversely associated with incident CHD (hazard ratio [95% confidence interval] 0.79 [0.65-0.98] and 0.64 [0.44-0.94], respectively), while rs1648707 was positively associated with incident IS (2.05 [1.37-3.06]; all P ≤ 0.028).