Context.—Posttransplant diabetes mellitus (PTDM) is a major complication after solid organ transplantation. The use of corticosteroids and calcineurin inhibitors, especially tacrolimus, are significant risk factors. However, it is not clear what genetic factors modify the risk. Evidence suggests vitamin D deficiency, perturbed glucose homeostasis, and increased inflammation all play roles in the development of diabetes.
Objective.—To investigate whether common vitamin D receptor (VDR), cytokine, and peroxisome proliferator–activated receptor γ (PPARγ) polymorphisms are correlated with the development of PTDM.
Design.—DNA was isolated from the peripheral blood of 51 kidney transplant recipients with PTDM and 72 patients without diabetes pretransplant or posttransplant at the time of follow-up. The genotypes for 5 polymorphisms, 1 each in VDR, PPARγ, INFγ, TGFβ1, and TNF, were determined using direct sequencing. Age, sex, number of acute rejection episodes, follow-up length, ethnicity, body mass index, and the frequency of alleles and genotypes for each polymorphism were compared between the 2 groups.
Results.—Body mass index was the only factor that was statistically different between the 2 groups (P = .001). The frequency of different alleles and genotypes for each of the 5 polymorphisms did not differ between the 2 groups.
Conclusions.—These results indicate that increased body mass index is a significant risk factor for the development of PTDM. However, none of the genetic polymorphisms studied confer predisposition to PTDM with the current sample size.
Maternal vitamin D deficiency during pregnancy affects expression of adipogenic-regulating genes peroxisome proliferator-activated receptor gamma (PPARγ) and vitamin D receptor (VDR) in lean male mice offspring
