Sitagliptin Might Be a Favorable Antiobesity Drug For New Onset Diabetes After a Renal Transplant

Abstract

Objectives: The aim of this study was to evaluate the effectiveness of sitagliptin, alone or in combination with metformin, in kidney transplant patients with newly diagnosed new-onset diabetes mellitus after transplant who had inadequate glycemic control, compared with a group of patients receiving insulin glargine with special emphasis on weight gain. Materials and Methods: Newly diagnosed renal transplant patients with new-onset diabetes mellitus after a transplant was defined by a blood glucose ≥ 11.1 mmol/L after an oral glucose tolerance test were examined. They were treated with standard immunosuppression composed of triple therapy with tacrolimus or cyclosporine, mycophenolate mofetil or azathioprine, and prednisone. They had stable graft function for more than 6 months after the transplant. Results: Patients with new-onset diabetes mellitus after transplant (n=28) whose glycemia was not controlled adequately with oral hypoglycemic agents (either alone or in combination) received oral sitagliptin 100 mg once daily in addition to existing therapy for 12 weeks. Patients who received insulin glargine as add-on therapy (n=17) served as the control group. Data analyses included glycated hemoglobin, fasting plasma glucose, lipid profile, body weight, and the occurrence of hypoglycemia. We found significant reductions in glycated hemoglobin and fasting plasma glucose values after 12 weeks of additional sitagliptin therapy that were comparable to those with insulin glargine. While the addition of stagliptin resulted in a small weight loss (0.4 kg), the addition of insulin glargine resulted in a weight gain (0.8 kg). The overall incidence of adverse experiences was low and generally mild in both groups. Conclusions: In a group of renal transplant recipients with new-onset diabetes mellitus after a transplant in whom glycemia was not controlled adequately by oral hypoglycemic agents, the addition of sitagliptin helped to achieve glycemic control similar to insulin glargine but with a marginal weight advantage.

Review of Newer Antidiabetic Agents for Diabetes Management in Kidney Transplant Recipients

“…25 The combination of metformin and sitagliptin led to greater weight reductions than with metformin and insulin glargine (−0.4 vs +0.8 kg; P < 0.05) at 12 weeks. 30 Reductions in BMI were observed after 12 months of treatment (−0.8 kg/m 2 ; P < 0.05). 28 As for safety, DPP-4 inhibitors are well tolerated, with mild GI AEs.…”

New onset diabetes after kidney transplantation is associated with increased mortality—A retrospective cohort study

“…1 Even though insulin has been considered the treatment of choice in transplanted patients first presenting with hyperglycemia, 12 oral antidiabetic drugs are used frequently in NODAT. In 1 study, there was no difference in glycemic control when adding an oral agent such as sitagliptin as compared with insulin glargine, 13 and another recent randomized study showed that DPP-4 inhibition in kidney transplant recipients with overt NODAT was safe and efficient. 14 In this retrospective cohort study in kidney-transplanted patients with NODAT, we aim to better define the association between fasting plasma glucose/HbA1C values and patient/graft survival and cardiovascular outcome and to examine glucose control of different treatment modalities in NODAT.…”

An Analysis of Regularity in Fasting Blood Sugar Variations and Influence Factors After Kidney Transplantation

“…The pathogenesis of PTDM has been reported different in the literature. The majority of the scholars have opined that the potential low insulin secretion of PTDM patients are aggravated by the immunosuppressor and their B cells are susceptible to anti-rejection medicines [20][21][22]. Research has also indicated that the state of insulin resistance is present in patients with terminal kidneydiseases; application of hormones further lowers the sensitivity of the peripheral insulin following transplantation; in addition, the insulin secretion defect caused by calcineurin inhibitor also accelerates the progression of PTDM [23][24].…”