The Potential Influence of Inflammation and Insulin Resistance on the Pathogenesis and Treatment of Atherosclerosis-Related Complications in Type 2 Diabetes

Abstract

The rationale for the treatment of diabetes has hitherto been directed to the correction of hyperglycemia because hyperglycemia is known to be responsible for the symptoms of polyuria and polydipsia in the short term and microangiopathic complications of diabetes in the long term. The correction of hyperglycemia leads to immediate resolution of polydipsia and polyuria and the prevention of microvascular complications in the long term (1, 2). The relationship between the decline in glycosylated hemoglobin (HbA_1c) and the reduction in the rate of complications is well established, and a fall in HbA_1c can reasonably predict a fall in the rate of microangiopathic complications (1, 2). In view of this close relationship between glycemia and the microangiopathic complications of diabetes, it is now accepted that any means used to decrease blood glucose concentrations will result in a reduction in microangiopathic complications. Thus, glycemic control is the cardinal measure required to prevent microangiopathic complications.