The role of β-catenin in glucose metabolism

Type 2 diabetes (T2D) is characterized by the impaired ability for insulin to stimulate the transport of glucose into the cell (insulin resistance) and failure of the pancreatic β-cells to secrete sufficient insulin to maintain normal blood glucose levels. The mechanisms regulating glucose transport and β-cell insulin secretion, and how they are modified by metabolic imbalance leading to the development of T2D are not well understood. However, it is known that intracellular vesicles need to insert and be maintained at the cell membrane for glucose to be transported into the cell, and for β-cells to release insulin. This process is impaired during the development of T2D.

This project will investigate whether the protein β-catenin is involved in facilitating glucose transport and insulin release, and whether its dysregulation contributes to impairments in muscle insulin sensitivity and β-cell function associated with T2D. To do this both cell culture and mouse models will be utlised.