About 422 million people in the world are affected by diabetes mellitus. There are two major forms of diabetes, insulin-dependent diabetes (T1D) and non-insulin-dependent diabetes (T2D). Dysregulated glucose homeostasis is one of the main reasons behind diabetes. Blood glucose homeostasis is known to be regulated via glucose transporters (GLUTs). In the human pancreatic islet GLUT1/2 has a great role in the development of diabetes mellitus. The aim of this study: 1) To identify candidate proteins involved in GLUTs internalization. 2) To determine the effect of different glucose concentrations on GLUT transporter. 3) To verify the expression of these proteins involved in GLUT transporter in human pancreatic cells. 4) To understand how the expression of GLUT transporters involved in glucose transport is altered in type-2-diabetic cells. INS1 cells were tagged with GLUT1, GLUT2 GFP, Rab5, endophilin, and clathrin to study trafficking events at the plasma membrane and how the above-mentioned proteins are involved in the process. TIRF and confocal microscopy techniques were used for studying the trafficking of GLUTs. qPCR was performed to understand the relative expression of GLUTS in diabetic and non-diabetic conditions. The efficiency of tagged GLUT transporters was determined by following the photo-bleaching and fluorescence recovery after bleaching experiments. The tagged transporter was later found to co-localize with proteins such as Rab5, endophilin, and clathrin during the transporter trafficking process. The trafficking increased with glucose concentrations showing a higher number of GLUT1 and GLUT2 vesicles. This increase was coupled with increased co-localization of proteins involved in trafficking such as clathrin. Surpassingly, it was observed that expression of GLUT1 transporters was decreased in T2D human islets but not GLUT2 expression remained unaffected. Clathrin co-localized with GLUT2 in human T2D cells due to no decrease in their expression under such conditions. This shows the importance of GLUT transporter trafficking in maintaining glucose homeostasis and how it is affected in T2D.