Taurine rescues pancreatic β‐cell stress by stimulating α‐cell transdifferentiation

The semi‐essential ubiquitous amino acid taurine has been shown to alleviate obesity and hyperglycemia in humans; however, the pathways underlying the antidiabetic actions have not been characterized. We explored the effect of chronic taurine exposure on cell biology of pancreatic islets, in degenerative type 1‐like diabetes. The latter was modeled by small dose of streptozotocin (STZ) injection for 5 days in mice, followed by a 10‐day administration of taurine (2% w/v, orally) in the drinking water. Taurine treatment opposed the detrimental changes in islet morphology and β‐/α‐cell ratio, induced by STZ diabetes, coincidentally with a significant 3.9 ± 0.7‐fold enhancement of proliferation and 40 ± 5% reduction of apoptosis in β‐cells. In line with these findings, the treatment counteracted an upregulation of antioxidant (Sod1, Sod2, Cat, Gpx1) and downregulation of islet expansion (Ngn3, Itgb1) genes induced by STZ, in a pancreatic β‐cell line. At the same time, taurine enhanced the transdifferentiation of α‐cells into β‐cells by 2.3 ± 0.8‐fold, echoed in strong non‐metabolic elevation of cytosolic Ca2+ levels in pancreatic α‐cells. Our data suggest a bimodal effect of dietary taurine on islet β‐cell biology, which combines the augmentation of α‐/β‐cell transdifferentiation with downregulation of apoptosis. The dualism of action, stemming presumably from the intra‐ and extracellular modality of the signal, is likely to explain the antidiabetic potential of taurine supplementation.