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Combining the therapeutic approaches of GLP-1 agonists (which target extrahepatic mechanisms for metabolic disorders) with resmetirom (which target intrahepatic mechanisms for MASH and liver fibrosis) seems like a promising strategy for addressing fat accumulation, inflammation, and fibrosis associated with MASH

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Eventually, GABA is removed from the system by converting it into succinate, which is then used in the Krebs cycle in the mitochondria to make ATP.[ref] The enzyme succinic semialdehyde dehydrogenase ( ALDH5A1 gene) is needed to convert GABA into succinate.[ref] Rare genetic mutations in the ALDH5A1 gene cause succinic semialdehyde dehydrogenase deficiency, which decreases the breakdown of GABA