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Aims/Introduction  Diabetes is a major health concern throughout the world because of its increasing prevalence in epidemic proportions. β‐Cell deterioration in the pancreas is a crucial factor for the progression of diabetes mellitus. Therefore, the restoration of β‐cell mass and its function is of vital importance for the development of effective therapeutic strategies and most accessible cell sources for the treatment of diabetes mellitus.    Materials and Methods  Human fetuses (12–20 weeks gestation age) were used to isolate human hepatic progenitor cells ( hHPC s) from fetal liver using a two‐step collagenase digestion method. Epithelial cell adhesion molecule‐positive (EpCAM+ve)‐enriched  hHPC s were cultured  in vitro  and induced with 5–30 mmol/L concentration of glucose for 0–32 h. Pdx‐1 expression and insulin secretion was analyzed using immunophenotypic and chemifluorescence assays, respectively. Relative gene expression was quantified in induced  hHPC s, and compared with uninduced and pancreatic cells to identify the activated transcription factors (Pdx‐1, Ngn‐3, Isl‐1, Pax‐4, Pax‐6 and Nkx‐6.1) involved in β‐cell production.    Results  EpCAM+ve cells derived from human fetal liver showed high  in vitro  trans‐differentiation potential towards the β‐cell phenotype with 23 mmol/L glucose induction after 24 h. The transcription factors showed eminent expression in induced cells. The expression level of transcription factors was found significantly high in 23 mmol/L‐induced  hHPC s as compared with the uninduced cells.    Conclusions  The present study has shown an exciting new insight into β‐cell development from  hHPC s trans‐differentiation. Relative quantification of gene expression in trans‐differentiated cells offers vast possibility for the production of a maximum number of functionally active pancreatic β‐cells for a future cure of diabetes.

journal of diabetes investigation

In vitro  quantitative and relative gene expression analysis of pancreatic transcription factors  P dx‐1,  N gn‐3,  I sl‐1,  P ax‐4,  P ax‐6 and  N kx‐6.1 in trans‐differentiated human hepatic progenitors