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Related Experiment Video

Updated: Mar 3, 2026

Quantification of the Immunosuppressant Tacrolimus on Dried Blood Spots Using LC-MS/MS
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Deciphering Tacrolimus-Induced Toxicity in Pancreatic β Cells.

J Triñanes1,2, A E Rodriguez-Rodriguez3, Y Brito-Casillas4

  • 1Centre for Biomedical Research of the Canary Islands (CIBICAN), University of La Laguna, La Laguna, Tenerife, Spain.

American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons
|April 23, 2017
PubMed
Summary

Tacrolimus (TAC) worsens type 2 diabetes mellitus (T2DM) by increasing pancreatic beta cell dysfunction, unlike cyclosporine A (CsA). This TAC-induced beta cell damage is potentially reversible, offering hope for transplant patients.

Keywords:
animal modelsbasic (laboratory) research/sciencecalcineurin inhibitor (CNI)cellular biologyclinical research/practicediabetes: new onset/posttransplantdrug toxicityimmunosuppressantislets of Langerhanskidney transplantation/nephrologymolecular biology

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Area of Science:

  • Endocrinology
  • Immunology
  • Molecular Biology

Background:

  • Type 2 diabetes mellitus (T2DM) involves dysfunctional beta cell transcription factors like FoxO1 and MafA.
  • Posttransplant diabetes mellitus shares similarities with T2DM, arising from insulin resistance and immunosuppressants, particularly calcineurin inhibitors (CNIs).

Purpose of the Study:

  • To investigate the impact of tacrolimus (TAC), cyclosporine A (CsA), and metabolic stressors on beta cell function.
  • To compare the effects of TAC and CsA on beta cell transcription factors and insulin secretion in vitro and in vivo.

Main Methods:

  • Insulinoma beta cells and pancreata from Zucker rats were exposed to glucose, palmitate, TAC, and CsA.
  • Changes in nuclear transcription factors (FoxO1, MafA), insulin content, insulin secretion, calcineurin, and NFAT were analyzed.

Main Results:

  • Glucose plus palmitate increased nuclear FoxO1 and decreased nuclear MafA; TAC exacerbated these changes.
  • Both TAC and CsA reduced insulin content, but TAC also affected insulin secretion.
  • TAC withdrawal or switching to CsA reversed TAC-induced changes; TAC potentiates glucolipotoxicity more than CsA.

Conclusions:

  • Tacrolimus potentiates glucolipotoxicity in beta cells, likely through shared pathways of dysfunction, leading to more severe beta cell impairment than CsA.
  • The diabetogenic effect of CNIs may involve calcineurin-NFAT pathway inhibition, but this doesn't fully explain TAC's stronger impact.
  • TAC-induced beta cell dysfunction appears to be potentially reversible.