Increased hexosamine biosynthetic pathway flux alters cell-cell adhesion in INS-1E cells and murine islets.

ABSTRACT:

Purpose

In type 2 Diabetes, β-cell failure is caused by loss of cell mass, mostly by apoptosis, but also by simple dysfunction (dedifferentiation, decline of glucose-stimulated insulin secretion). Apoptosis and dysfunction are caused, at least in part, by glucotoxicity, in which increased flux of glucose in the hexosamine biosynthetic pathway plays a role. In this study, we sought to clarify whether increased hexosamine biosynthetic pathway flux affects another important aspect of β-cell physiology, that is β-cell-β-cell homotypic interactions.

Methods

We used INS-1E cells and murine islets. The expression and cellular distribution of E-cadherin and β-catenin was evaluated by immunofluorescence, immunohistochemistry and western blot. Cell-cell adhesion was examined by the ha

SUBMITTER: Lofrumento DD 

PROVIDER: S-EPMC10403402 | biostudies-literature | 2023 Sep

REPOSITORIES: biostudies-literature