FTZ promotes islet β-cell regeneration in T1DM mice via the regulation of nuclear proliferation factors

The aim is to investigate the role of FTZ in promoting β-cell regeneration in T1DM mice, and to further explore its mechanism. Materials and

FTZ can restore the insulin-secreting function of the impaired pancreatic islet, improve blood glucose level, possibly via the enhancing β cell regeneration via upregulation of PDX-1, MAFA, and NGN3 in T1DM mice, and may be a potential therapeutic drug for T1DM.

C57BL/6 mice were used as control. NOD/LtJ mice were divided into the Model group and FTZ group. Oral glucose tolerance, fasting blood glucose, and fasting insulin level were measured. Immunofluorescence staining was used to detect the level of β-cell regeneration and the composition of α-cells and β-cells in islets. Hematoxylin and eosin staining was used to detect the infiltration degree of inflammatory cells. The apoptosis of islet cells was detected by terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling. Western blotting was used to detect the expression levels of Pancreas/duodenum homeobox protein 1 (PDX-1), V-maf musculoaponeurotic fibrosarcoma oncogene homolog A (MAFA), and Neurogenin-3 (NGN3).

FTZ could increase insulin levels and reduce the glucose level of T1DM mice and promote β-cell regeneration. FTZ also inhibited the invasion of inflammatory cells and the islet cell apoptosis, and maintained the normal composition of islet cells, thus preserving the quantity and quality of β-cells. Furthermore, FTZ promoting β-cell regeneration was accompanied by increasing the expression of PDX-1, MAFA, and NGN3.