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The presence of higher quantities of lactate in SC-islets than human islets could be consistent with previous observations of defects in glycolytic flux, an inability to silence lactate metabolism due to expression of disallowed genes (such as LDHA ), or due to the inability to switch from primarily glycolytic to oxidative metabolism in immature cells, all of which have been reported previously 5,6,10,18,19

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In all three cases, liver injury was fully reversible normalization occurred within 7 weeks to 3 months after stopping