Type 2 diabetes (T2D) is a metabolic disease that negatively impacts the health of many individuals worldwide. It accounts for roughly 95% of diabetes cases and was found to be responsible for 6.7 million diabetes related deaths in 2021, with approximately 536.6 million people suffering from this disease globally. Despite the advancements that have been made in our understanding of T2D, the molecular mechanisms underlying this disease remain poorly understood. Therefore, it is necessary to investigate the cellular mechanisms underlying conditions such as insulin resistance and T2D to understand the extent of the metabolic dysfunction. There are three main tissues implicated in T2D; skeletal muscle, adipocytes and the liver. Among these, skeletal muscle is responsible for 75% of insulin-dependent glucose uptake and is therefore important for maintaining glucose homeostasis.
Core mathematical models were constructed for the insulin signalling pathway, glucose transport and glucose metabolism to simulate insulin dependent glucose metabolism in control C2C12 skeletal muscle cells, and in insulin insensitive cells. The model parameters were fitted to experimental data for dose and time dependent data for insulin addition and removal. Analysis of the individual models and their interactions will reveal the effected points leading to insulin insensitivity. Although the mouse cell model might not accurately reflect the T2D disease state in patients, the concept to analyse the point(s) of interference is still applicable.