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IL-6 Promoter Polymorphism –174 Is Associated with New-Onset Diabetes after Transplantation

Jamal Bamoulid^*,, Cécile Courivaud^*,, Marina Deschamps^*,, Patricia Mercier^*,, Christophe Ferrand^*,, Alfred Penfornis, Pierre Tiberghien^*,,||, Jean-Marc Chalopin^*,,||, Philippe Saas^*, and Didier Ducloux^*,,||

^* INSERM, U645, University Besançon, and IFR133, CHU Saint Jacques, Department of Nephrology, Dialysis, and Renal Transplantation, EFS Bourgogne Franche-Comté, Plateforme de Biomonitoring, CHU Jean Minjoz, Department of Endocrinology, and ^|| CHU Saint Jacques, CIC Biothérapie, Besançon, France

Address correspondence to: Dr. Didier Ducloux, CHU St. Jacques, 2 Place Saint Jacques, Besançon 25000, France. Phone: +33-38-121-8782; Fax: +33-38-121-8781; E-mail: dducloux{at}chu-besancon.fr

Received for publication January 29, 2006. Accepted for publication May 29, 2006.

New-onset diabetes after transplantation (NODAT) is a serious complication of transplantation. This study tested whether IL-6 production capacity may influence the development of NODAT in two different groups of patients. The occurrence of NODAT was analyzed with respect to IL-6 gene promoter polymorphism at position –174 (GC) and other relevant risk factors retrospectively in 217 renal transplant recipients and prospectively in 132. A linear increase in both circulating IL-6 (P = 0.09) and C-reactive protein (an indicator of basal IL-6 secretion; P = 0.03) concentrations from the CC genotype to the GG genotype was observed. In the multivariate model, the CC genotype was associated with a decreased risk for NODAT compared with the GG genotype in the two cohorts. Homeostasis Model Assessment for Insulin Resistance also revealed lesser insulin sensitivity in the GG carriers than in the CC carriers (2.15 ± 2 versus 1.32 ± 1.03; P = 0.03). Subgroup analysis showed that the influence of IL-6 gene promoter polymorphism on the development of NODAT was restricted mostly to overweight patients. These results highly suggest that IL-6 production capacity influences the development of NODAT and that diabetes-inducing drug administration should be limited in overweight patients who carry the GG genotype.

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