부산대학교 도서관

We previously reported that the canonical Wnt signaling pathway is activated during compensatory islet hyperplasia in prediabetic mice. Here, we aimed to expand our knowledge concerning the Wnt signaling partners and modulators involved in this process. We report here that Axin1, Axin2, and DACT1, inhibitors of the canonical Wnt signaling pathway, displayed no change in their expression, while GSK-3β, a multi-functional kinase that acts as a negative regulator of this pathway as well as affects insulin secretion/action, was up-regulated in hyperplastic islets of prediabetic mice. We also observed that COUP-TFII, a protein that acts positively on Wnt-target genes related to cell proliferation, displays a significant increase in gene expression and protein content and is highly immunolabeled in islet cell nuclei of prediabetic mice compared to control islets. These findings suggest that GSK-3β and COUP-TFII may play a role in beta-cell dysfunction and hyperplasia during type 2 prediabetes. • GSK-3β and COUP-TFII are up-regulated in hyperplastic islets during type 2 prediabetes. • Axin1, Axin2, and DACT1 expression does not change in mouse hyperplastic islets. • GSK-3β and COUP-TFII may play a role in type 2 prediabetes-associated beta-cell dysfunction and hyperplasia. [ABSTRACT FROM AUTHOR]