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Combined effects of single-nucleotide polymorphisms in GCK, GCKR, G6PC2 and MTNR1B on fasting plasma glucose and type 2 diabetes risk.


ABSTRACT: AIMS/HYPOTHESIS: Variation in fasting plasma glucose (FPG) within the normal range is a known risk factor for the development of type 2 diabetes. Several reports have shown that genetic variation in the genes for glucokinase (GCK), glucokinase regulatory protein (GCKR), islet-specific glucose 6 phosphatase catalytic subunit-related protein (G6PC2) and melatonin receptor type 1B (MTNR1B) is associated with FPG. In this study we examined whether these loci also contribute to type 2 diabetes susceptibility. METHODS: A random selection from the Dutch New Hoorn Study was used for replication of the association with FGP (2,361 non-diabetic participants). For the genetic association study we extended the study sample with 2,628 participants with type 2 diabetes. Risk allele counting was used to calculate a four-gene risk allele score for each individual. RESULTS: Variants of the GCK, G6PC2 and MTNR1B genes but not GCKR were associated with FPG (all, p

SUBMITTER: Reiling E 

PROVIDER: S-EPMC2723681 | biostudies-literature | 2009 Sep

REPOSITORIES: biostudies-literature

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Combined effects of single-nucleotide polymorphisms in GCK, GCKR, G6PC2 and MTNR1B on fasting plasma glucose and type 2 diabetes risk.

Reiling E E   van 't Riet E E   Groenewoud M J MJ   Welschen L M C LM   van Hove E C EC   Nijpels G G   Maassen J A JA   Dekker J M JM   't Hart L M LM  

Diabetologia 20090617 9


<h4>Aims/hypothesis</h4>Variation in fasting plasma glucose (FPG) within the normal range is a known risk factor for the development of type 2 diabetes. Several reports have shown that genetic variation in the genes for glucokinase (GCK), glucokinase regulatory protein (GCKR), islet-specific glucose 6 phosphatase catalytic subunit-related protein (G6PC2) and melatonin receptor type 1B (MTNR1B) is associated with FPG. In this study we examined whether these loci also contribute to type 2 diabetes  ...[more]

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