Type 2 Diabetes (T2D) is characterised by loss of pancreatic beta cell function, defective glucose induced insulin secretion (GSIS) and degranulation of insulin secretory granules (ISG). Recently, proposed models of “newcomer” ISG that are rapidly fused and secreted challenge the conventional paradigm that pre-docked pools of ISG at the plasma membrane govern the first phase insulin secretion. Instead, newly formed ISG are preferentially secreted upon glucose stimulation regardless of proximity to the plasma membrane, while older ISG are prioritised for lysosomal degradation. As such, decreased newcomer ISG number is found to be associated with blunted first phase GSIS in T2D. Here, using a syncollin adenoviral dsRed-E5 TIMER construct that targets to ISG and then alters its fluorescence properties over time, we show that we can label ISG within primary murine beta cells in normal and T2D islets and segregate them by age. We demonstrate in preliminary data that after 72 hours of transduction, ISG in beta cells can be sorted into “young” and “old” pools from which we can quantify insulin by ELISA. Additionally, while insulin is expressed in both young and old granules, we find that newcomer granule-associated SNARE proteins such as VAMP8, and the SG sorting protein sortilin, are almost exclusively expressed in young granules. Thus, we hypothesise that these temporal pools of ISG exhibit distinct physical and molecular properties which determine their fate within the beta cell. Furthermore, that these properties may offer insight into ISG behaviour and a target for improving beta cell function in T2D.