Editing Beta cell (section)

=== Type 2 diabetes ===
[[Type 2 diabetes]], also known as non insulin dependent diabetes and as chronic hyperglycemia, is caused primarily by genetics and the development of metabolic syndrome.<ref name="Chen_2017" /><ref name="Fu_2013" /> The beta cells can still secrete insulin but the body has developed a resistance and its response to insulin has declined.<ref name="Boland_2017" /> It is believed to be due to the decline of specific receptors on the surface of the [[liver]], [[Adipose tissue|adipose]], and [[muscle cells]] which lose their ability to respond to insulin that circulates in the blood.<ref>{{cite journal | vauthors =  | title = U.K. prospective diabetes study 16. Overview of 6 years' therapy of type II diabetes: a progressive disease. U.K. Prospective Diabetes Study Group | journal = Diabetes | volume = 44 | issue = 11 | pages = 1249–1258 | date = November 1995 | pmid = 7589820 | doi = 10.2337/diabetes.44.11.1249 }}</ref><ref>{{cite journal | vauthors = Rudenski AS, Matthews DR, Levy JC, Turner RC | title = Understanding "insulin resistance": both glucose resistance and insulin resistance are required to model human diabetes | journal = Metabolism | volume = 40 | issue = 9 | pages = 908–917 | date = September 1991 | pmid = 1895955 | doi = 10.1016/0026-0495(91)90065-5 }}</ref> In an effort to secrete enough insulin to overcome the increasing insulin resistance, the beta cells increase their function, size and number.<ref name="Boland_2017" /> Increased insulin secretion leads to hyperinsulinemia, but blood glucose levels remain within their normal range due to the decreased efficacy of insulin signaling.<ref name="Boland_2017" /> However, the beta cells can become overworked and exhausted from being overstimulated, leading to a 50% reduction in function along with a 40% decrease in beta-cell volume.<ref name="Fu_2013" /> At this point, not enough insulin can be produced and secreted to keep blood glucose levels within their normal range, causing overt type 2 diabetes.<ref name="Fu_2013" />