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Effect of Empagliflozin on Tacrolimus-Induced Pancreas Islet Dysfunction and Renal Injury

J Jin1,2, L Jin1,2, K Luo1,2

  • 1Transplantation Research Center, Department of Internal Medicine, Seoul St. Mary's Hospital, The Catholic University of Korea, Seoul, South Korea.

American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons
|April 20, 2017
PubMed

Insights

Empagliflozin effectively manages hyperglycemia and protects against pancreatic and kidney damage in tacrolimus-induced diabetes. This sodium glucose co-transporter type 2 inhibitor shows promise for patients with this specific condition.

Area of Science:

  • Endocrinology
  • Nephrology
  • Pharmacology

Background:

  • Tacrolimus (TAC) can induce type 2 diabetes mellitus (DM), a condition where the efficacy of sodium glucose co-transporter type 2 (SGLT-2) inhibitors remains unclear.
  • Understanding the impact of SGLT-2 inhibition on TAC-induced metabolic and organ damage is crucial for patient management.

Purpose of the Study:

  • To investigate the effects of empagliflozin (Em), an SGLT-2 inhibitor, on pancreatic islet dysfunction and renal injury in a model of TAC-induced DM.
  • To assess the direct cellular effects of empagliflozin on pancreatic beta-cells and kidney cells exposed to TAC.

Main Methods:

  • Utilized an experimental model of TAC-induced DM to evaluate empagliflozin's effects on glycemic control, insulin secretion, and pancreatic and renal histology.
  • Conducted in vitro studies using INS-1 (beta-cell) and HK-2 (kidney) cell lines to assess cell viability and oxidative stress markers.

Main Results:

  • Empagliflozin reduced hyperglycemia, increased plasma insulin levels, and improved glucose-stimulated insulin secretion in the TAC-induced DM model.
  • Empagliflozin alleviated TAC-induced renal dysfunction, decreased albuminuria, and mitigated histological damage, while also reducing oxidative stress and apoptosis in pancreatic and renal tissues.
  • In vitro, empagliflozin enhanced cell viability and reduced reactive oxygen species (ROS) in kidney cells (HK-2) but not in beta-cells (INS-1) exposed to TAC.

Conclusions:

  • Empagliflozin is effective in controlling hyperglycemia associated with TAC-induced diabetes.
  • Empagliflozin demonstrates a direct protective effect on renal injury induced by TAC, suggesting potential therapeutic benefits beyond glycemic control.
Keywords:
basic (laboratory) research/sciencecalcineurin inhibitor: tacrolimusdiabetes: new onset/posttransplantimmunosuppressantkidney transplantation/nephrology

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