The prognosis of<unk>  combines aspects of both Type 1 and Type 2 diabetes. While the presentation mimics type 1 diabetes with its<unk> nsity for DKA, patients with<unk>  can regain pancreatic beta cell function over time. Specifically patients who have beta cell reserve at the onset of the disease (the β+ subtype) have around a 50% chance to regain full beta cell function and become insulin independent. These cases do make a minority of<unk>  patients however, and insulin dependence is an expected outcome for most patients. In these cases insulin dependence will reflect that of type 2 diabetes with increased insulin dependence reflecting lifestyle choices and diabetic management. Education for these patients should reflect the education for patients presenting with regular type 2 diabetes. The presence of beta cell function restoration seems to come down to how much beta cell reserve the patient has at onset but also the presence of autoantibodies. Patients with autoantibodies at presentation have a lower likelihood of having beta cell function restored, a fact that holds true even when the type of<unk>  is not distinguished by the traditional Aβ subtype system. Lifestyle changes that worsen regular type 2 diabetes are still associated with insulin dependence, such as patients who do not make effective diet and lifestyle changes. An important factor for beta cell functionality is<unk> r glycemic control, a factor it shares with type 2 diabetes. Patients who maintain<unk> r glycemic control to<unk> ct their functioning beta cells exhibited lesser disease courses and regained beta cell functionality at a much higher rate than patients who had looser or less stringent glucose control.
Ketosis-prone diabetes
Diabetic hypoglycemia
Lifestyle causes of type 2 diabetes
Idiopathic hypoglycemia
Steroid diabetes
Lipoatrophic diabetes
Non-islet cell tumor hypoglycemia
Reactive hypoglycemia