AIMS/HYPOTHESIS: The associations between adiponectin polymorphisms and type 2 diabetes have been studied widely; however, results are inconsistent. METHODS: We searched electronic literature databases and reference lists of relevant articles. A fixed or random effects model was used on the basis of heterogeneity. Sub-group and meta-regression analyses were conducted to explore the sources of heterogeneity. RESULTS: There were no statistically significant associations between +45T>G (rs2241766), +276G>T (rs1501299), -11391G>A (rs17300539) and type 2 diabetes risk. However, for -11377C>G (rs266729), the pooled OR (95% CI) for G vs C allele was 1.07 (1.03-1.11, p = 0.001). Subgroup analysis by study design revealed that -11377C>G (rs266729) dominant model (CG+GG vs CC, p = 0.0008) and G vs C allele (p = 0.0004) might be associated with type 2 diabetes risk in population-based case-control studies. After stratification by ethnicity, we found that -11377C>G (rs266729) dominant model (CG+GG vs CC, p = 0.004) and G vs C allele (p = 0.001) might be associated with type 2 diabetes risk in white individuals. In individuals with a family history of diabetes, the presence of -11391G>A (rs17300539) dominant model (GA+AA vs GG) and A vs G allele might be associated with increased risk of type 2 diabetes. CONCLUSIONS/ INTERPRETATION: The presence of +45T>G (rs2241766), +276G>T (rs1501299) and -11391G>A (rs17300539) do not appear to influence the development of type 2 diabetes. However, G vs C allele of -11377C>G (rs266729) might be a risk factor for type 2 diabetes.
AIMS/HYPOTHESIS: The associations between adiponectin polymorphisms and type 2 diabetes have been studied widely; however, results are inconsistent. METHODS: We searched electronic literature databases and reference lists of relevant articles. A fixed or random effects model was used on the basis of heterogeneity. Sub-group and meta-regression analyses were conducted to explore the sources of heterogeneity. RESULTS: There were no statistically significant associations between +45T>G (rs2241766), +276G>T (rs1501299), -11391G>A (rs17300539) and type 2 diabetes risk. However, for -11377C>G (rs266729), the pooled OR (95% CI) for G vs C allele was 1.07 (1.03-1.11, p = 0.001). Subgroup analysis by study design revealed that -11377C>G (rs266729) dominant model (CG+GG vs CC, p = 0.0008) and G vs C allele (p = 0.0004) might be associated with type 2 diabetes risk in population-based case-control studies. After stratification by ethnicity, we found that -11377C>G (rs266729) dominant model (CG+GG vs CC, p = 0.004) and G vs C allele (p = 0.001) might be associated with type 2 diabetes risk in white individuals. In individuals with a family history of diabetes, the presence of -11391G>A (rs17300539) dominant model (GA+AA vs GG) and A vs G allele might be associated with increased risk of type 2 diabetes. CONCLUSIONS/ INTERPRETATION: The presence of +45T>G (rs2241766), +276G>T (rs1501299) and -11391G>A (rs17300539) do not appear to influence the development of type 2 diabetes. However, G vs C allele of -11377C>G (rs266729) might be a risk factor for type 2 diabetes.
Authors: A H Kissebah; G E Sonnenberg; J Myklebust; M Goldstein; K Broman; R G James; J A Marks; G R Krakower; H J Jacob; J Weber; L Martin; J Blangero; A G Comuzzie Journal: Proc Natl Acad Sci U S A Date: 2000-12-19 Impact factor: 11.205
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