[Study on the association between polymorphism of TAP1 637 A/G alleles polymorphism and metabolic syndrome].
OBJECTIVE
To explore the effect of the transporter 1 associated with antigen processing (TAP1) gene 637 A/G polymorphism on the risk of metabolic syndrome(MS).


METHODS
A case-control study was conducted on 138 based-community patients (68 males and 70 females, 61.31 +/- 11.00 years old) diagnosed as MS with 162 healthy subjects (74 males and 88 females, 48.73 +/- 11.66 years old) came from the same origin as cases. The allele polymorphisms TAP1 637 A/G was examined by the specificity restriction fragment length polymorphism-polymerase chain reaction(RFLP-PCR) method with genomic DNA. The effect of TAP1 637 A/G polymorphisms on MS were analyzed by multivariable unconditional logistic regression models.


RESULTS
The TAPI 637 A/G allele genotypes frequencies (83.3%, 16.7%) contribution in control group were consistent with the distribution predicted by Hardy-Weinberg equilibrium (chi2 = 1.46, P > 0.05). TAP1 637 G allele genotypes frequencies (26.1%) of cases were significantly higher than controls (16.7%) with P = 0.005. There were significant differences of AA (58.0%), AG (31.9%) and GG (10.1%) genotypes in cases than controls, AA (68.5%). AG (29.6%) and GG (1.9%) for recessive model and addictive model after age was adjusted with P value as 0.006 and 0.044, but no significant differences for dominant model (P = 0. 298). Results from recessive model with OR = 6.62, 95% CI :1.73-25.31, Addictive model with OR = 1.56, 95% CI:1.01-2.41 and one-way ANOVA analysis showed that systolic blood pressure(SBP) and diastolic blood pressure (DBP) levels of GG genotype were significantly higher than AA or AG genotype (P < 0.05) whereas no significantly statistical differences for other clinical characteristics.


CONCLUSIONS
The TAP1 637 allele A to G alteration or genotype AA to GG and AG to GG alterations could increase the risk of MS significantly, especially for SBP and DBP levels, and this positive association results might be helpful to support the biological role of TAP1 in MS but in need of larger sample size to provide more powerful evidences.
Hu
Xiao-shu
XS
Department of Chronic Noninfectious Disease Prevention and Control, Jiangsu Centers for Disease Prevention and Control, Nanjing 210009, China.
Guo
Zhi-rong
ZR
Shen
Chong
C
Wu
Ming
M
Yu
Rong-bin
RB
Yao
Cai-liang
CL
D000071181:ATP Binding Cassette Transporter, Subfamily B, Member 2; D018528:ATP-Binding Cassette Transporters / Q000235:genetics*; D000328:Adult; D016022:Case-Control Studies; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D024821:Metabolic Syndrome / Q000235:genetics*; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length
D000071181:ATP Binding Cassette Transporter, Subfamily B, Member 2; D018528:ATP-Binding Cassette Transporters; C073119:TAP1 protein, human