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In vitro data suggest that the primary route of metabolism of empagliflozin in humans is glucuronidation by the uridine 5-diphospho-glucuronosyltransferases UGT1A3, UGT1A8, UGT1A9, and UGT2B7

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Hyperglycaemia has been suggested to cause increased expression of inflammation-related genes in macrophages

These changes culminate in proliferative arrest and accumulation of senescence-associated -galactosidase (SA--gal) [51]

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As body weight decreases, some patients need lower levothyroxine doses because less hormone is needed to maintain metabolic function