N-acyl Taurines and Acylcarnitines Cause an Imbalance in Insulin Synthesis and Secretion Provoking β Cell Dysfunction in Type 2 Diabetes

Cell Metab. 2017 Jun 6;25(6):1334-1347.e4. doi: 10.1016/j.cmet.2017.04.012.


The processes contributing to β cell dysfunction in type 2 diabetes (T2D) are uncertain, largely because it is difficult to access β cells in their intact immediate environment. We examined the pathophysiology of β cells under T2D progression directly in pancreatic tissues. We used MALDI imaging of Langerhans islets (LHIs) within mouse tissues or from human tissues to generate in situ-omics data, which we supported with in vitro experiments. Molecular interaction networks provided information on functional pathways and molecules. We found that stearoylcarnitine accumulated in β cells, leading to arrest of insulin synthesis and energy deficiency via excessive β-oxidation and depletion of TCA cycle and oxidative phosphorylation metabolites. Acetylcarnitine and an accumulation of N-acyl taurines, a group not previously detected in β cells, provoked insulin secretion. Thus, β cell dysfunction results from enhanced insulin secretion combined with an arrest of insulin synthesis.

Keywords: Langerhans islets; MALDI imaging mass spectrometry; MALDI-FT-ICR; N-acyl taurines; acylcarnitines; diabetes type 2; pathophysiology; β cells.

MeSH terms

  • Animals
  • Carnitine / adverse effects
  • Carnitine / analogs & derivatives*
  • Carnitine / pharmacology
  • Diabetes Mellitus, Type 2* / chemically induced
  • Diabetes Mellitus, Type 2* / metabolism
  • Diabetes Mellitus, Type 2* / pathology
  • Humans
  • Insulin / metabolism*
  • Insulin Secretion
  • Insulin-Secreting Cells / metabolism*
  • Insulin-Secreting Cells / pathology
  • Mice
  • Taurine / adverse effects*
  • Taurine / pharmacology


  • Insulin
  • acylcarnitine
  • Taurine
  • Carnitine