Objective To investigate the effect of metformin (Met) on the epithelial interstitial transformation (EMT) of type Ⅱ alveolar epithelial cells in gestational diabetes mellitus (GDM) rats and its mechanism. Methods SD pregnant rats were randomly divided into Normal group and GDM group. Pregnant rats in GDM group were given high fat diet combined with low dose streptozotocin (STZ) to establish GDM model, and fasting blood glucose level (FBG) was measured. Lung tissues of fetal rats were collected under aseptic conditions, and alveolar epithelial cells were isolated. Cells were treated with different concentrations of Met for 48 h, and cell survival rate was detected by MTT method. Alveolar epithelial cells were randomly divided into Control group, GDM group and Met group. Met group was treated with 80 μmol/L Met for 48 h, and Control group and GDM group were not treated. Transwell assay were used to detect cell invasion. qRTPCR was used to detect mRNA relative expression levels of epithelial cadherin (E-cad), neurocadherin (N-cad) and Vimentin. The relative expression levels of phosphorylated nuclear factorκB (NFκB) and Twist1 protein were detected by Western blot. Results The FBG level in GDM group was significantly higher than that in Normal group (P＜0.05). The cell survival rate decreased with the increase of Met concentration in a dosedependent manner (P＜0.05). Compared with the Control group, the number of invasive cells, the mRNA relative expression levels of N-cad and Vimentin, the protein relative expression levels of p-NF-κB p65 and Twist1 in GDM group were increased, while the mRNA relative expression levels of E-cad were decreased (P＜0.05). Compared with GDM group, invasive cell number, mRNA relative expression levels of Ncad and Vimentin, protein relative expression levels of p-NF-κB p65 and Twist1 in Met group were decreased, while the mRNA relative expression levels of Ecad were increased (P＜0.05). Conclusion Met can inhibit the EMT process of type Ⅱ alveolar epithelial cells in GDM rats, possibly through inhibition of NFκB/Twist1 signaling pathway.