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In parallel, hepatocyte-directed PPAR gene therapy has been shown to enhance systemic -hydroxybutyrate availability, providing a neuroprotective energy substrate during cerebral metabolic crisis [128, 284, 285]

PMID: 20590847

This glycolytic exhaustion, intertwined with lipid toxicity, coalesces into a self-reinforcing metabolic vortex that etches both the penumbras fate and the patients long-term functional identity, directly linking metabolic collapse to neuropsychiatric sequelae like post-stroke depression and anxiety [19, 20]

In addition, ChREBP is required for fructose to exert its effects on hepatic gene expression (160)