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Nearly two years after Robert F

doi: 10.3109/03639045.2011.569934

Cc axit amin ny sau c hp th qua rut hoc vn chuyn vo t bo qua cc cht vn chuyn (transporter) c hiu

While these metabolic effects were likely to have been mediated by compensatory upregulation of FGF19 and/or FGF21 (308), they were clearly independent of FGFR4 agonism, instead being mediated by agonism of FGFR1c, 2c or 3c