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Circulating metabolic molecules are either shortacting (e.g., amino acids, fatty acids, gastrointestinal peptide hormones) or longacting (e.g., leptin, insulin)

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Since GSH is the final product of the homocysteine metabolism in the transsulfuration pathway by transferring sulfur from homocysteine to cysteine, a deficiency in transsulfuration pathway leads to excessive homocysteine production (hyperhomocysteinemia) and reduced GSH synthesis (159, 160)