Editing Beta cell (section)

=== Medications ===
Many drugs to combat diabetes are aimed at modifying the function of the beta cell.

* Sulfonylureas are insulin secretagogues that act by closing the ATP-sensitive potassium channels, thereby causing insulin release.<ref>{{cite journal | vauthors = Bolen S, Feldman L, Vassy J, Wilson L, Yeh HC, Marinopoulos S, Wiley C, Selvin E, Wilson R, Bass EB, Brancati FL | title = Systematic review: comparative effectiveness and safety of oral medications for type 2 diabetes mellitus | journal = Annals of Internal Medicine | volume = 147 | issue = 6 | pages = 386–399 | date = September 2007 | pmid = 17638715 | doi = 10.7326/0003-4819-147-6-200709180-00178 | doi-access = free }}</ref><ref name="Inzucchi_2012">{{cite journal | vauthors = Inzucchi SE, Bergenstal RM, Buse JB, Diamant M, Ferrannini E, Nauck M, Peters AL, Tsapas A, Wender R, Matthews DR | title = Management of hyperglycaemia in type 2 diabetes: a patient-centered approach. Position statement of the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD) | journal = Diabetologia | volume = 55 | issue = 6 | pages = 1577–1596 | date = June 2012 | pmid = 22526604 | doi = 10.1007/s00125-012-2534-0 | doi-access = free }}</ref> These drugs are known to cause hypoglycemia and can lead to beta-cell failure due to overstimulation.<ref name="Chen_2017" /> Second-generation versions of sulfonylureas are shorter acting and less likely to cause hypoglycemia.<ref name="Inzucchi_2012" />
* GLP-1 receptor agonists stimulate insulin secretion by simulating activation of the body's endogenous incretin system.<ref name="Inzucchi_2012" /> The incretin system acts as an insulin secretion amplifying pathway.<ref name="Inzucchi_2012" />
* DPP-4 inhibitors block DPP-4 activity which increases postprandial incretin hormone concentration, therefore increasing insulin secretion.<ref name="Inzucchi_2012" />