Abstract

Ketosis prone type 2 diabetes mellitus which was once described as “atypical diabetes” is being recognized increasingly worldwide; being originally described in African population has been seen in multiple ethnic groups, especially in urban areas. These patients are typically obese, middle-aged men with a strong family history of type 2 diabetes. The pathophysiologic mechanisms involved in its cause are unknown, but preliminary evidence suggests that patients with ketosis-prone type 2 diabetes have a unique propensity to glucose desensitization. These individuals have negative autoantibodies associated with type 1 diabetes but frequently HLA class II DRB1*03 and/or DRB1*04 are detected. Severe impairment of both insulin secretion and insulin action are found at presentation. Aggressive diabetes management results in marked improvement in beta cell function and insulin sensitivity sufficient to allow discontinuation of insulin therapy within a few months of treatment. In the long run, insulin can be substituted with oral hypoglycemic agents in most of these patients under careful supervision and close follow up. Molecular investigations into KPD syndromes utilizing multiple approaches (genomic, metabolic, proteomic) to generate etiological hypotheses can help us understand the underlying defects of insulin secretion and sensitivity in these and other types of diabetic patients.

Key words: Diabetesis mellitus (DM), ketosis prone diabetes (KPD), diabetic ketoacidosis (DKA), latent auto-immune diabetes of adults (LADA).