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Impaired methionine metabolism is a major contributor to hepatic GSH dysfunction in liver disease patients, and rodents naturally express higher levels of betaine-homocysteine methyltransferase, an enzyme which maintains proper hepatic methionine function [86]

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Glu8.0 and Glu8.2 mapped to distinct previously annotated mouse NTS neuronal populations, GLU2 and GLU11, respectively

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