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01,P<0.01, respectively), suppressed the mRNA level of PCK1 (P<0.01), and increased the mRNA level of GCK(P<0.01). In addition,miR-106b mimic or antagomiR-106b significantly reduced or enhanced the protein levels of signal transducer and activator of transcription 3 (STAT3)(P<0.01,P<0.01, respectively).The inhibition of STAT3 by its specific inhibitor abolished the inhibitory effects of antagomiR-106b on hepatic gluconeogenesis. Conclusion miR-106b increases hepatic gluconeogenesis by inhibiting the STAT3 signaling pathway.Objective To i