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A Polymorphism in the Zinc Transporter Gene SLC30A8 Confers Resistance Against Posttransplantation Diabetes Mellitus in Renal Allograft Recipients

¹ Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea
² Institute of Endocrine Research, Yonsei University College of Medicine, Seoul, Korea
³ Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea
⁴ Department of Surgery, Yonsei University College of Medicine, Seoul, Korea
⁵ The Research Institute for Transplantation, Yonsei University College of Medicine, Seoul, Korea
⁶ Department of Pharmacology, Yonsei University College of Medicine, Seoul, Korea
⁷ Department of Preventive Medicine and Public Health, Yonsei University College of Medicine, Seoul, Korea

Address correspondence and reprint requests to Hyun Chul Lee, MD, PhD, Department of Internal Medicine, Yonsei University College of Medicine, 134 Shinchon-Dong Seodaemun-Gu, Seoul, Korea 120-752; or to Soon Il Kim, MD, PhD, Department of Surgery, Yonsei University College of Medicine, 134 Shinchon-Dong Seodaemun-Gu, Seoul, Korea 120-752. E-mail: endohclee{at}yumc.yonsei.ac.kr and soonkim{at}yumc.yonsei.ac.kr

Abbreviations: FPG, fasting plasma glucose; HOMA, homeostasis model assessment; PTDM, posttransplantation diabetes mellitus; SNP, single nucleotide polymorphism; ZnT, zinc transporter

OBJECTIVE—Posttransplantation diabetes mellitus (PTDM) is a major metabolic complication in renal transplant recipients, and insulin secretory defects play an important role in the pathogenesis of PTDM. The R325W (rs13266634) nonsynonymous polymorphism in the islet-specific zinc transporter protein gene, SLC30A8, has been reported to be associated with type 2 diabetes and possibly with a defect in insulin secretion. This study investigated the association between genetic variations in the SLC30A8 gene and PTDM in renal allograft recipients.

RESEARCH DESIGN AND METHODS—A total of 624 unrelated renal allograft recipients without previously diagnosed diabetes were enrolled. Rs13266634 was genotyped in the cohort, which consisted of 174 posttransplantation diabetic patients and 450 non-posttransplantation diabetic subjects. The genotyping of the SLC30A8 polymorphism was performed using real-time PCR.

RESULTS—The prevalence of PTDM was 33.8% in patients carrying the R/R genotype, 26.8% in patients with the R/W genotype, and 19.8% in patients with the W/W genotype. There was a strong association between the number of W-alleles and PTDM risk reduction (P for trend = 0.007). Patients with at least one T-allele showed a decreased risk of PTDM compared with those with the R/R genotype (R/W, risk ratio [RR] 0.78, P = 0.126; W/W, RR 0.52, P = 0.007). The effect of the SLC30A8 genotype remained significant after adjustments for age, sex, body weight gain, and type of immunosuppressant (R/W, hazard ratio [HR] 0.77, P = 0.114; W/W, HR 0.58, P = 0.026).

CONCLUSIONS—These data provide evidence that the SLC30A8 rs13266634 gene variation is associated with protection from the development of PTDM in renal allograft recipients.

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