| First Author | Aichler M | Year | 2017 |
| Journal | Cell Metab | Volume | 25 |
| Issue | 6 | Pages | 1334-1347.e4 |
| PubMed ID | 28591636 | Mgi Jnum | J:251858 |
| Mgi Id | MGI:6101784 | Doi | 10.1016/j.cmet.2017.04.012 |
| Citation | Aichler M, et al. (2017) N-acyl Taurines and Acylcarnitines Cause an Imbalance in Insulin Synthesis and Secretion Provoking beta Cell Dysfunction in Type 2 Diabetes. Cell Metab 25(6):1334-1347.e4 |
| abstractText | The processes contributing to beta cell dysfunction in type 2 diabetes (T2D) are uncertain, largely because it is difficult to access beta cells in their intact immediate environment. We examined the pathophysiology of beta 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 beta cells, leading to arrest of insulin synthesis and energy deficiency via excessive beta-oxidation and depletion of TCA cycle and oxidative phosphorylation metabolites. Acetylcarnitine and an accumulation of N-acyl taurines, a group not previously detected in beta cells, provoked insulin secretion. Thus, beta cell dysfunction results from enhanced insulin secretion combined with an arrest of insulin synthesis. |
