糖尿病酮酸血症（Diabetic ketoacidosis）為第1 型糖尿病（type 1 diabetes mellitus）常見的起始表現，但有部分病人的臨床表現及免疫學檢查卻和第2 型糖尿病類似。這些病人體型多較肥胖，有明顯家族史，但是沒有第1 型糖尿病常見的自體免疫抗體，或和第1 型糖尿病相關的HLA基因變化。這些病人被稱為「易酮病型第2 型糖尿病（Ketosis-prone type 2 diabetes）」。他們的的臨床表現為急性發作的多喝、多尿、及體重減輕，並且缺乏相關的誘發因子。在糖尿病酮酸血症發作的時候，這些病人的胰島素分泌下降，胰島素作用也不良。但經過胰島素治療後，b細胞的胰島素抗性會有明顯進步。因此，這些病人通常在治療數個月後可以停止胰島素注射，他們可以在使用口服藥物之下，甚至不需使用口服藥物來維持正常的血糖值。這段時期可以長達數個月到數年。在糖尿病酮酸血症時期的檢查，這些病人仍有胰島素分泌，且與第1 型糖尿病相關的自體免疫抗體呈現陰性。這群病人後續可能可以停用胰島素治療。對於造成這種暫時性的b細胞功能不良的機制目前不明。

Diabetic ketoacidosis (DKA) was regarded as an initial presentation of type 1 diabetes mellitus. However, a subgroup of patients with DKA shows clinical presentation similar to type 2 diabetes. These patients are obese and have strong family history of diabetes. No autoantibodies related to type 1 diabetes mellitus nor common HLA gene change is noted in these patients. They are now known as "Ketosis-prone type 2 diabetes".
Acute onset of polydipsia, polyuria, and body weight loss without obvious predisposing factor are typical presentations. During onset of DKA, decreasing secretion of insulin and insulin resistance were noted. b-cell
function improves after insulin therapy. Thus, these patients can aintain normo-glycemia without insulin injection after insulin therapy for a few months. The duration can last for weeks to months. Absence of autoantibodies and measurable insulin level can predict the probability of cessation of insulin injection in the future. Although glucose desentization was proposed, the mechanism of the transient dysfunction of b-cell is still unclear.