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included 101 prediabetic T2D patients with MASH and randomized them to pioglitazone or placebo groups

The key mechanistic concept derived from these mouse studies was that the cellular toxicity was caused by a cytochrome P450-derived reactive metabolite, which was typically detoxified by GSH, but after the depletion of cellular GSH levels during an overdose, the reactive metabolite binds to cellular proteins thereby causing cell death [79]

In an in vitro investigation, Kerry et al