We have selectively reviewed recent findings regarding two candidate genes for DN. It is fair to state that the findings for many other candidate genes are far less consistent in most cases and are even conflicting in some. Although the cause of these discrepancies has not been precisely determined, certain explanations should be mentioned to help in the interpretation of these results as well to guide future studies. These explanations relate to the possibility that the "candidate genes" have only a minor impact on DN. Conceivably, the "detectability" of the contributions of these genes may depend on many additional factors such as study designs, the ethnicity of the study population, or the modulating effect of various environmental conditions (e.g., tobacco smoking, glycemic control, or hypertension control).
If an association is found in case-control studies, and is supported by family studies, it may be inferred that the DNA polymorphism is a marker of genetic susceptibility to DN. However, the biological interpretation of the association is not always clear. It may be owing to the polymorphism itself, including a disease-causing allele that directly affects the expression or function of a gene or gene product (e.g., by an amino acid change, frameshift mutation, or premature termination), or the association may result from linkage disequilibrium between the marker polymorphism and a causative polymorphism. This phenomenon is owing to the fact that particular alleles of polymorphisms lying in close genetic proximity to each other have a tendency to segregate together over successive generations (70). Therefore, whereas association between a polymorphism and DN may be demonstrated, confirmation that the polymorphism is actually the cause of genetic susceptibility can only be obtained from functional in vitro and in vivo studies that evaluate the impact of the polymorphism on the pathogenesis of DN.
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