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They might be taking a high dose on paper, but only a small fraction is surviving the "first-pass metabolism" in the liver and digestive system

In normal repair, the hyperplastic type II cells die and the remaining cells spread and undergo a differentiation process to become type I cells

Given that EtOH-induced mitochondrial dysfunction and ER stress are intimately involved in the pathogenesis of ALD, future studies to examine these pathways under the current experimental setting will provide important mechanistic information underlying the protection seen in GCLM KO mice

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Supplementing with TUDCA improves liver cell function to help optimize the detoxification process and, subsequently, the gastrointestinal system.*1,2,3

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