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Background  Single nucleotide polymorphisms (SNPs) from  GCK ,  GCKR ,  G6PC2  and  MTNR1B  were found to modulate the fasting glucose levels. The current study aimed to replicate this association in the Chinese population and further analyze their effects on biphasic insulin secretion.    Methods/Principal Findings  SNPs from  GCK ,  GCKR ,  G6PC2  and  MTNR1B  were genotyped in the Shanghai Chinese, including 3,410 type 2 diabetes patients and 3,412 controls. The controls were extensively phenotyped for the traits related to glucose metabolism and insulin secretion. We replicated the association between  GCK  rs1799884,  G6PC2  rs16856187 and  MTNR1B  rs10830963 and fasting glucose in our samples ( p  = 0.0003∼2.0×10 −8 ).  GCK  rs1799884 and  G6PC2  rs16856187 showed association to HOMA-β, insulinogenic index and both first- and second-phases insulin secretion ( p  = 0.0030∼0.0396).  MTNR1B  rs10830963 was associated to HOMA-β, insulinogenic index and first-phase insulin secretion ( p  = 0.0102∼0.0426), but not second-phase insulin secretion ( p  = 0.9933). Combined effect analyses showed individuals carrying more risk allele for high fasting glucose tended to have a higher glucose levels at both fasting and 2 h during OGTTs ( p  = 1.7×10 −13  and 0.0009, respectively), as well as lower HOMA-β, insulinogenic index and both first- and second-phases insulin secretion ( p  = 0.0321∼1.1×10 −7 ).    Conclusions/Significance  We showed that SNPs from  GCK ,  G6PC2  and  MTNR1B  modulated the fasting glucose levels in the normoglycaemic population while SNPs from  G6PC2  and  GCKR  was associated with type 2 diabetes. Moreover, we found  GCK  and  G6PC2  genetic variants were associated to both first- and second-phases insulin secretion while  MTNR1B  genetic variant was associated with first-phase insulin secretion, but not second-phase insulin secretion.

Effects of GCK, GCKR, G6PC2 and MTNR1B Variants on Glucose Metabolism and Insulin Secretion