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Urea cycle induction and increased Put-GABA synthesis in glia is associated with AD pathology, and blockade of ornithine decarboxylase to force nitrogen stress away from oxidative Put-GABA synthesis and into the urea cycle attenuates AD-like pathology and behavioral defects in AD animal models (Bensemain et al., 2009

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In vivo studies in humans have shown that skeletal muscle insulin resistance fuels hepatic lipid accumulation by causing the diversion of substrates from ingested carbohydrates away from skeletal muscle glycogen synthesis toward hepatic DNL (102, 103)