The conference opened with the clinical presentation of a 50-year-old male with fasting hyperglycemia (296 mg per cent) and hypertriglyceridemia (2736 mg per cent). The discussion began with a summary of current concepts regarding the manner in which chylomicra (intestine) and very low density lipoproteins (intestine and liver) are formed, transported into the plasma, and removed from the circulation. This was followed by a consideration of diabetic hypertriglyceridemia in which this syndrome was subdivided into two categories. The first form is seen in patients with severe fasting hyperglycemia, and is characterized by marked insulin deficiency, decreased very low density lipoprotein production, a fall in the activity of lipoprotein lipase, and hypertriglyceridemia secondary to a defect in removal of lipoproteins from the plasma. In contrast the other form of diabetic hypertriglyceridemia is seen in patients with minimal abnormalities of carbohydrate tolerance, and in this instance insulin resistance, not insulin lack, seems to play the pivotal role. In these patients, the rise in plasma triglyceride levels seems to be secondary to increased production of very low density lipoproteins, presumably as a result of the hyperinsulinemia associated with the insulin resistance. The conference ended with an attempt to relate the patient presented to the models of diabetic hypertriglyceridemia that had been defined.