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Background  Recent data indicate that loss-of-function mutation in the gene encoding the facilitative glucose transporter GLUT10 ( SLC2A10 ) causes arterial tortuosity syndrome via upregulation of the TGF-β pathway in the arterial wall, a mechanism possibly causing vascular changes in diabetes.    Methods  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.    Results  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.    Conclusion  Our data demonstrate that genetic polymorphism of the  SLC2A10  gene is an independent risk factor for PAD in type 2 diabetes.

SLC2A10 genetic polymorphism predicts development of peripheral arterial disease in patients with type 2 diabetes. SLC2A10and PAD in type 2 diabetes