Biphasic Insulin Aspart 30: Premix Analogue for Initiating Insulin Therapy in Type 2 Diabetes

Introduction T he last two decades have seen an explosive increase in the number of people with diabetes globally due to changes in lifestyle and genetic predisposition 1,2 Patients with diabetes mellitus have an impaired capacity to regulate blood glucose. In type 1 diabetes, autoimmune destruction of pancreatic beta cells results in a diminished and rapidly absent ability to produce insulin. With type 2 diabetes, the disease is progressive, typically starting with peripheral insulin resistance. In the early disease state, the first phase of the prandial insulin response is lost, resulting in hyperglycaemia. A compensatory mechanism may be initiated in the form of increased insulin production during the second stage of the prandial insulin response. This hyperinsulinaemia, however, serves only to exacerbate insulin resistance. The inability of beta cells to maintain this overproduction of insulin results in a reduced prandial insulin response and subsequent postprandial hyperglycaemia,3.4 a pre-diabetic state called impaired glucose tolerance (IGT). Many of these patients will develop clinical diabetes, in which fasting blood glucose becomes chronically raised, and postprandial glucose (PPG) becomes elevated to as much as three-times normal values.5 The percentage of glycated haemoglobin type A1c (% HbA1c) represents a 2–3 month average of overall blood glucose control, which is a reflection of both fasting and prandial blood glucose. There is growing evidence that hyperglycaemia is associated with microvascular & macrovascular complications,6–8 and tight glycaemic control has been shown in type 1 and type 2 diabetes to significantly reduce the risk of microvascular complications, including neuropathy, nephropathy and retinopathy.9,10 The recommended HbA1c goals are <7% (American Diabetes Association [ADA]) and <6.5% (American College of endocrinologists [ACe] and International Diabetes Federation [IDF]). ACe also recommends that fasting and postprandial blood glucose should not exceed 110 mg/dl (6.1 mmol/l) and 140 mg/dl (7.8 mmol/l), respectively. Thus, aggressive therapy is becoming the standard of care to prevent long-term complications of DM.