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Acute hypoxic hypoxia leads to increased glucose formation by rat liver slices from pyruvate,α-glycerophosphate,α-ketoglutarate, and fructose. During exposure to hypoxia after prolonged administration of hydrocortisone acetate, increasing gluconeogenesis from the above-mentioned substances and also from alanine, lactate, and glycerol, the rate of glucose synthesis in liver slices was higher than in the control but lower than after the action of hydrocortisone alone.