Glucose metabolism is an important part of animal homeostasis and, when dysregulated, results in significant dysfunction. Diabetes is broken down into type I and type II. Type I diabetes is characterized by the elimination of pancreatic β-cells. Pancreatic β-cells are responsible for the synthesis, storage, and release of insulin. Type II diabetes is characterized by the tissues effect becoming resistant to a high level of insulin and causing pancreatic β-cells to overwork. The overworked pancreatic β-cells start to fail which causes a loss of insulin production. For the body to have glucose homeostasis the glucose transporters must facilitate the diffusion of glucose into cells. There are two types of glucose transporters, insulin independent and insulin dependent. Insulin independent glucose transporters do not require the presence of insulin to allow glucose into cells. Insulin dependent glucose transporters require insulin to be present to accept glucose into the cell. The insulin independent glucose transporters are glucose transporter 1, 2, 3, 9, 10, and 12. The insulin dependent glucose transporters are glucose transporter 5, 8, 11, and 14. Together all these transporters keep glucose homeostasis in an organism’s body. In this research we use broiler chickens to model glucose transporters. Since chickens are a natural model of insulin resistance and rarely get diabetes. They use glucose independently of insulin. By studying their glucose transporters, we can evaluate why they use glucose independently and see if we can translate our findings to human diseases. Using rt-qPCR we measured the amounts of glucose transporters in different skeletal muscles of chickens. We found that leg muscles have an upregulation of insulin independent glucose transporters 1 and 3 and the pectoralis muscle has an upregulation of insulin dependent glucose transporters 5 and 8. These findings suggest that varied locations of skeletal muscles utilize different glucose transporters. Further, these findings can assist in determining preferred sites for specific insulin usage and delineate mechanisms for resistance to insulin in diabetes.