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& u shown to be highly correlated with waist-hip ratio, hypertension, and HbAlc level (24). These three parameters can be used to clinically estimate insulin resistance in type 1 diabetic patients.

In summary, the available data suggest that the major factors responsible for CHD and CVD in type 1 diabetic patients are nephropathy, the development of the insulin resistance syndrome or poor glycemic control (Fig. 5). Based on current data, one can speculate that maintaining near-normoglycemia without the development of central obesity from the onset of type 1 diabetes should eliminate the excessive CVD risk as well as microvascular risk. In the event that near-normoglycemia cannot be achieved, aggressive management of blood pressure (systolic <120 mmHg and diastolic <80 mmHg), plasma lipids (LDL cholesterol <100 mg/dL; HDL cholesterol >45 mg/dL; and triglycerides <150 mg/dL), as

Figure 5 A hypothesis for the pathogenesis of macrovascular disease in type 1 diabetic patients. Absent beta-cell function leads to fasting and postprandial hyperglycemia. If inadequately controlled, hyperglycemia leads to microvascular disease (nephropathy) and biochemical abnormalities such as formation of AGEs, excessive activation of protein kinase C, oxidative stress, etc., which accelerate atherosclerosis. If the hyperglycemia is intensively but not physiologically controlled, visceral obesity develops and, with it, the insulin resistance syndrome that can itself accelerate atherosclerosis.

Figure 5 A hypothesis for the pathogenesis of macrovascular disease in type 1 diabetic patients. Absent beta-cell function leads to fasting and postprandial hyperglycemia. If inadequately controlled, hyperglycemia leads to microvascular disease (nephropathy) and biochemical abnormalities such as formation of AGEs, excessive activation of protein kinase C, oxidative stress, etc., which accelerate atherosclerosis. If the hyperglycemia is intensively but not physiologically controlled, visceral obesity develops and, with it, the insulin resistance syndrome that can itself accelerate atherosclerosis.

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