Obesity is common in African-American patients with newly diagnosed diabetes who present with diabetic ketoacidosis (DKA).1 Despite the presentation with severe symptoms of insulinopenia and ketoacidosis, clinical and immunogenetic observations indicate that most obese AA patients with DKA have type 2 diabetes. In such patients, our previous studies reveal: a) at presentation, obese AA patients with DKA have markedly de-creased pancreatic insulin secretion, lower than in obese non-DKA patients admitted with comparable hyperglycemia, but significantly greater than in lean patients with DKA;2 b) aggressive diabetic management results in significant improvement in b-cell function and insulin sensitivity sufficient to allow discontinuation of insulin therapy within 3 months of follow-up.2, 3 Based on these observations we conclude that similar to obese patients with hyperglycemia, most obese AA with DKA have type 2 diabetes, and that although defects in both insulin secretion and insulin action are present, transient b-cell failure is the primary defect in the development of ketoacidosis.