An initial deficit in beta cell mass could thus play a key role in the development of T2D. Patients with a history of GDM have a significantly increased risk of developing T2D. While an increase in beta cell mass has been found in healthy women during pregnancy, it is not yet known whether patients with GDM have a deficit in beta cell mass. While little is known about beta cell mass in women with a history of GDM, it is well recognized that these women have a chronic defect in beta cell function that progressively worsens in the years after the pregnancy and mediates their high risk of progression to T2D. This deterioration of beta cell function begins as early as the first year after delivery, is partly driven by hepatic insulin resistance, takes place in the presence of initial normal glucose tolerance, and precedes the development of abnormal glucose tolerance. Accordingly, women with a recent history of GDM represent a patient population in which there is beta cell dysfunction without the potential confounding effect of hyperglycemia (and resultant glucotoxicity).