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Associations of common polymorphisms in GCKR with type 2 diabetes and related traits in a Han Chinese population: a case-control study

DOI: 10.1186/1471-2350-12-66

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Abstract:

We investigated the association of polymorphisms in the GCKR gene with type 2 diabetes by employing a case-control study design (1118 cases and 1161 controls). Four tag SNPs (rs8179206, rs2293572, rs3817588 and rs780094) with pairwise r2 > 0.8 and minor allele frequency > 0.05 across the GCKR gene and its flanking regions were studied and haplotypes were constructed. Genotyping was performed by matrix-assisted laser desorption/ionization time-of-flight mass spectroscopy using a MassARRAY platform.The G alleles of GCKR rs3817588 and rs780094 were associated with an increased risk of type 2 diabetes after adjustment for year of birth, sex and BMI (OR = 1.24, 95% CI 1.08-1.43, p = 0.002 and OR = 1.22, 95% CI 1.07-1.38, p = 0.002, respectively). In the non-diabetic controls, the GG carriers of rs3817588 and rs780094 were nominally associated with a lower plasma triglyceride level compared to the AA carriers after adjustment for year of birth, sex and BMI (p for trend = 0.00004 and 0.03, respectively). Furthermore, the association of rs3817588 with plasma triglyceride level was still significant after correcting for multiple testing.The rs3817588 A/G polymorphism of the GCKR gene was associated with type 2 diabetes and plasma triglyceride level in the Han Chinese population.Glucokinase (GCK) is the key glucose phosphorylation enzyme responsible for the first rate-limiting step in the glycolysis pathway. GCK regulates glucose metabolism in the liver and glucose-stimulated insulin secretion from pancreatic beta cells [1]. GCK activity is closely regulated by the glucokinase regulatory protein (GCKR), a process depending on fructose 6-phosphate and fructose 1-phosphate [2,3]. Gckr-deficient mice display reduced GCK protein levels and activity in the liver and exhibit impaired postprandial glycemic control [4,5]. In a previous study, adenoviral-mediated hepatic overexpression of GCKR significantly improved insulin sensitivity and glucose tolerance in mice and resulted in dec

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