-
Views
-
Cite
Cite
Susan Bonner-Weir, Perspective: Postnatal Pancreatic β Cell Growth, Endocrinology, Volume 141, Issue 6, June 2000, Pages 1926–1929, https://doi.org/10.1210/endo.141.6.7567
Close - Share Icon Share
Extract
Even 15 years ago, the accepted concept was that one was born with all the pancreatic β cells one ever had. Many thought that insulin resistance would lead to diabetes without change in the β cells. However, now the concept that diabetes only results when there is an inadequate functional mass of β cells has gained general acceptance. The more obvious lack of β cells is seen in type 1 diabetes as the result of autoimmune destruction of β cells. The lack in type 2 diabetes with its hallmark of peripheral insulin resistance has been less obvious to many, yet the inability of the β cells to match the increased demand for insulin can be seen as a lack of adequate functional mass. The evidence over the past decade has been compelling that in most cases the β cells can, and do, compensate for added demand, resulting from pregnancy, obesity, or insulin resistance. It is important to remember that only 15–20% of people with obesity or severe insulin resistance become diabetic; the others maintain normoglycemia due to β cell compensation.
