Background Type 2 diabetes mellitus (T2DM) is a global major health problem resulting from interaction of environmental and genetic factors, examples of the latter being KCNJ11 (coding for part of the ATP-sensitive potassium channel) and SDF-1β (coding for chemokine CXCL12). Our case-control study was conducted to assess whether recessive, dominant or additive genotype model associations of KCNJ11 (E23K, rs5219) and SDF-1β (G801A, rs1801157) were more strongly linked to type 2 diabetes. Subjects & Methods Genetic polymorphism analysis was performed by polymerase chain reaction-restriction fragment length polymorphism. Alleles and genotype frequencies between 200 cases and 200 controls were determined and compared. Results The dominant (EE v EK + KK, p = 0.022) and additive (EK v EE + KK, p = 0.021) models, but not the recessive model (KK v EE + EK, p = 0.727) of KCNJ11 were linked to diabetes. Similarly, the dominant (GG v GA + AA, p < 0.001) and additive (AG v GG + AA, p=<0.001) models, but not the recessive model (AA v AG + GG, p = 0.430) of SDF-1β were linked to diabetes. The A allele (p = 0.006) of SDF-1β was protective against the risk of T2DM. Conclusion Both dominant and additive models in both KCNJ11 (E23K, rs5219) and SDF-1β (G801A, rs1801157) genetic polymorphisms are significantly associated with type 2 diabetes.

TLR4 polymorphisms rs5030717 and rs5030718 may be useful in predicting those type 2 diabetics who are at risk of hypertension, nephropathy and/or dyslipidaemia.

Although no significant links were found between GST polymorphism and treatment response, null genotypes of GSTM1, GSTT1 and 'G' allele of GSTP1 bring a higher risk of severe gastrointestinal toxicity due to chemoradiation therapy in cervical cancer.

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