beta cell
A beta cell is the body's blood-sugar thermostat sensor and responder rolled into one. It constantly tastes the glucose flowing past it, and when sugar rises after a meal, it pumps out insulin to bring it back down. Beta cells are the most abundant cell type in each islet, typically making up the majority of its mass.
Mechanistically, glucose enters the beta cell through the GLUT2 transporter and is metabolized to make ATP. Rising ATP closes ATP-sensitive potassium channels, the cell membrane depolarizes, voltage-gated calcium channels open, and the calcium influx triggers fusion of insulin-containing secretory granules with the membrane. The same granules also release C-peptide and amylin alongside insulin.
Beta cells are remarkably plastic but also vulnerable. They can expand in number and output when demand rises, for instance in pregnancy or early insulin resistance. But chronic overwork, lipotoxicity, glucotoxicity, and in type 1 diabetes autoimmune attack can exhaust or destroy them, and the resulting beta-cell failure is central to both major forms of diabetes.
In type 1 diabetes, T cells selectively attack and destroy beta cells, so by diagnosis a person may have lost most of their insulin-producing capacity and require lifelong insulin therapy.
Beta-cell loss is the defining lesion of type 1 diabetes.
Sulfonylurea drugs treat type 2 diabetes by directly closing the beta cell's ATP-sensitive potassium channels, forcing insulin release independent of glucose — which is why they can cause hypoglycemia if a meal is missed.