The UKPDS (United Kingdom Prospective Diabetes Study) found that poor glycemic control in patients with type 2 diabetes is associated with an increased risk of cardiovascular complications, including coronary heart disease, myocardial infarction, and peripheral vascular disease, as well as microvascular complications and death.3 Figure 1 shows the relationship of hemoglobin A1C (HbA1C) to diabetes-related complications.4
The DCCT (Diabetes Control and Complications Trial) reported that maintaining fasting plasma glucose (FPG) between 70 and 120 mg/dL (3.89–6.67 mmol/L) and postprandial glucose (PPG) <180 mg/dL (10 mmol/L) helps sustain endogenous insulin secretion.5 Residual beta-cell function, in turn, is associated with better metabolic control and a lower risk of hypoglycemia and chronic complications, such as retinopathy and microalbuminuria.6
The EDIC (Epidemiology of Diabetes Interventions and Complications) study found that early glycemic control reduces the risk of cardiovascular events.7
The ARIC (Atherosclerosis Risk in Communities) study reported that elevated HbA1C leads to atherosclerosis and cardiovascular disease.8,9
The Steno-2 study found that intensive, multifactorial intervention reduced diabetes-related mortality and cardiovascular events.10
The ADVANCE (Action in Diabetes and Vascular Disease) study found that intensive glucose control reduced major macrovascular and microvascular events, primarily due to a 21% reduction in nephropathy.11
Li et al4,12 reported that short-term intensive insulin therapy titrated to maintain FPG <110 mg/dL (6.11 mmol/L) and PPG <160 mg/dL (8.89 mmol/L) prevented progression of beta-cell dysfunction and insulin resistance in newly diagnosed type 2 diabetic patients with severe hyperglycemia.
Weng et al3,13–17 found that hyperglycemia is brought under control more quickly, and the effects of insulin on beta-cell function are superior to those of oral hypoglycemic agents.
