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The necessity for apical glucose transport is demonstrated in Sglt1 / mice, where glucose-stimulated GIP secretion is eliminated and levels rise only to the same extent as observed in the saline control ( ATP channels ( Kir6.2 / mice) significantly increases glucose absorption and glucose-stimulated GIP secretion, through a compensatory increase in duodenal Sglt1 mRNA expression (Ogata et al., 2014)

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Take the vial out of the fridge a few minutes before injecting

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To characterize the interaction between GLR3.3 and GSH, the predicted structure of GLR3.3 was used to perform molecular docking