N-acyl taurines and acylcarnitines cause an imbalance in insulin synthesis and secretion provoking β cell dysfunction in type 2 diabetes.
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Beta cells under fire
||Dr. Michaela Aichler||
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The processes contributing to ß-cell dysfunction in type 2 diabetes (T2D) are uncertain, largely because it is difficult to access ß-cells in their intact immediate environment. We examined the pathophysiology of ß-cells under T2D progression directly in pancreatic tissues. We used MALDI imaging of Langerhans islets (LHI) 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 accumulates in ß-cells, leading to arrest of insulin synthesis and energy deficiency via excessive ß-oxidation and depletion of TCA cycle and oxidative phosphorylation metabolites. Acetlycarnitine and an accumulation of N-acyl taurines, a group not previously detected in ß-cells, provoke insulin secretion. Thus, ß-cell dysfunction results from enhanced insulin secretion combined with an arrest of insulin synthesis.
Core statement Pressemitteilung:
Type 2 diabetes causes pathological changes in the beta cells. Scientists have successfully depicted the processes on the basis of the metabolome and proteome for the first time. Their work has been published in Cell Metabolism.
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