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Results Despite impaired cardiolipin remodelling, pancreatic islets from Taz-KD mice maintained insulin secretion, supported by compensatory mechanisms such as increased glucose uptake, expanded mitochondrial volume and increased metabolic parameters

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Finally, we highlight directions for future research to target L-serine as a promising therapeutic strategy.

Cells lacking ETT are more susceptible to oxidative stress, resulting in increased mitochondrial DNA damage, protein oxidation and lipid peroxidation

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