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Additionally, inhibition of CD36 effectively decreased ceramide-induced JNK and p66Shc serine 36 phosphorylation, preserving mitochondrial function, enhancing antioxidant defenses (thioredoxin-2 and peroxiredoxin-3), and restoring GSIS, suggesting CD36 as a potential therapeutic target to mitigate ceramide-induced β-cell dysfunction [9]

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mTORC1 also regulates lipid and nucleotide synthesis through the sterol responsive element binding protein (SREBP) transcription factors and the activation of the transcription factor 4 (ATF4), respectively [4,5]