Mechanism of Insulin Action

Insulin is a small 51 residue hormone synthesized and secreted by ß cells in the pancreas. Insulin is central to lowering blood glucose and maintaining metabolic function. Diabetes Educators and healthcare providers use this set of 3D printed models to explain how insulin binds the insulin receptor, calls up Glucose Transporters to the plasma membrane so that Glucose molecules can then flow through to the inside the cell.

Following meals when blood glucose levels begin to rise, our stomachs signal the pancreas to express the hormone called insulin. Insulin travels the blood stream to various tissue destinations like muscle, liver, and fat. Insulin initiates its mechanism of action after binding to the insulin receptor on the surface of these cells. Once at insulin reaches its target destination, it binds to the Insulin Receptor on the surface of cells. Upon binding the Insulin Receptor, an intracellular chemical cascade signals for glucose transporter 4 (GLUT4) to come up to the surface of the cell.




The Insulin Receptor consists of an alpha-subunit, which binds the hormone, and am intracellular beta-subunit, which is an insulin-stimulated, tyrosine-specific protein kinase.  Activation of this kinase is believed to generate a signal that eventually results in the disposal of glucose. The Insulin signal for GLUT4 begins when it binds to the insulin receptor on the surface of cells throughout the body. Insulin Receptors are membrane glycoproteins composed of two separate extracellular ectodomains and two intracellular tyrosine kinases. Conformational changes in the kinase allows  for adenosine triphosphate (ATP) to bind and begins downstream processes associated with insulin expression.


Stored inside the cell transport vesicles are spheres phospholipids holding GLUT4. Upon insulin stimulation, these lipid spheres fuse with the extracellular membrane and insert glucose transporters on the external membrane of the cell. At the completion of the insulin stimulated chemical cascade, GLUT4 vesicles quickly begin transporting glucose from the extracellular space into cells where it can then be used for fuel. 


Through activation of these signaling pathways, insulin acts as a powerful regulator of metabolic function. In patients that develop pancreatic dysfunction, insulin insufficiency develops into the chronic disease Type 1 Diabetes Mellitus. Insulin insufficiency must be addressed in order to prevent systemic organ failure and eventual death. Like Type 1 Diabetes, people that experience Type 2 Diabetes may also require the use of exogenous insulin, not because they do not express insulin, but rather because of insulin resistance when the body no longer recognizes endogenous insulin. Insulin resistance can be caused by both metabolic and genetic abnormalities. Pharmaceutical insulin supplementation is required to treat both Type 1 and 2 Diabetes Mellitus.


Regulation and usage can be difficult for many patients. This 3D printed model set includes an Insulin Receptor, Insulin, Glucose transporter, and multiple pieces of glucose. This articulating model set was designed to help Diabetes Educators and Healthcare professionals explain how Insulin signals the body to lower blood glucose.