In vivo kinetics of islet compensation and dysfunction in a mouse model of diet-induced obesity and insulin resistance

Abstract

Aims: Pancreatic islets have been shown to compensate in function and mass during the development of obesity and insulin resistance (IR). However, the transition of successful islet compensation to islet cell dysfunction, which results in the development of type 2 diabetes (T2D), is largely unknown. In this study we aimed to assess the adaptation of islet cell mass and function during obesity induced IR in vivo to correlate these changes with systemic physiological parameters.