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SLC2A10 genetic polymorphism predicts development of peripheral arterial disease in patients with type 2 diabetes. SLC2A10 and PAD in type 2 diabetes

DOI: 10.1186/1471-2350-11-126

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Abstract:

We genotyped 10 single nucleotide polymorphisms and one microsatellite spanning 34 kb across the SLC2A10 gene in a prospective cohort of 372 diabetic patients. Their association with the development of peripheral arterial disease (PAD) in type 2 diabetic patients was analyzed.At baseline, several common SNPs of SLC2A10 gene were associated with PAD in type 2 diabetic patients. A common haplotype was associated with higher risk of PAD in type 2 diabetic patients (haplotype frequency: 6.3%, P = 0.03; odds ratio [OR]: 14.5; 95% confidence interval [CI]: 1.3- 160.7) at baseline. Over an average follow-up period of 5.7 years, carriers with the risk-conferring haplotype were more likely to develop PAD (P = 0.007; hazard ratio: 6.78; 95% CI: 1.66- 27.6) than were non-carriers. These associations remained significant after adjustment for other risk factors of PAD.Our data demonstrate that genetic polymorphism of the SLC2A10 gene is an independent risk factor for PAD in type 2 diabetes.Peripheral arterial disease (PAD), defined as lower extremity arterial atherosclerosis, is one of most common diseases of the arteries and is a major complication of type 2 diabetes [1]. Conventional cardiovascular risk factors such as aging, smoking, hyperglycemia, hypertension and dyslipidemia have been shown to be associated with PAD [1]. However, the increased risk for atherosclerotic diseases in diabetic patients can be only partially explained by the conventional risk factors [2]. In fact, a high heritability for ankle-brachial blood pressure index (ABI), an index of PAD, has been obtained in Twin studies in Caucasians [3], indicating that additional genetic factors might be involved in the pathogenesis of PAD. In this respect, the search for genetic causes of PAD remains limited [4].Recently, a genetic form of arterial tortuosity syndrome (ATS; OMIM 208050) was reported to be caused by loss-of-function mutations in the SLC2A10 gene encoding the facilitative glucose transporter GLUT10. A

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