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Duration of Follow-up (yrs)

Figure 4 The comparable coronary heart disease mortality in women from the study described in Figure 3. (Reproduced with permission from Ref. 14.)

Duration of Follow-up (yrs)

Figure 4 The comparable coronary heart disease mortality in women from the study described in Figure 3. (Reproduced with permission from Ref. 14.)

The inconsistency of the results of the studies that have examined the relationship between glycemic control and CVD in type 1 diabetic patients is difficult to reconcile with other data. Type 1 diabetic patients do not have an increase in the traditional CV risk factors, either proceeding or in the first few years after the onset of their diabetes. CVD occurs only in type 1 diabetics with a long duration of diabetes. These observations indicate that either CV risk factors increase during the course of type 1 diabetes or type 1 diabetes is associated with previously unknown CV risk factors. Considerable circumstantial data support the hypothesis that type 1 diabetic patients develop an increase in cardiovascular risk factors during the course of their disease. The most likely causes of the increase in CV risk are poor glycemic control or treatment-induced obesity (11,12,20,21). Patients with poor glycemic control have a rise in plasma free fatty acids and an increase in VLDL particle synthesis, and a decrease in clearance of chylomicrons and VLDL particles as a result of diminished lipoprotein lipase activity. These alterations lead to elevated plasma triglycerides. Poor glycemic control also results in increases in protein glycosylation and formation of AGEs (advanced glycosylation end products), activation of PKC (protein kinase C), -o endothelial dysfunction, and increased oxidative stress, all of which increase car- |

diovascular risk (13,22). On the other hand, patients who are intensively treated £

with insulin are at significant risk to develop central obesity and the insulin resistance syndrome (12,23,24). 5

The type 1 diabetic patients in the DCCT (Diabetes Control and Complications Trial) after 6.5 years of treatment had a prevalence of obesity of 33.1% in J the intensively treated cohort and 19.1% in the conventionally treated cohort. a

Obesity was defined as a BMI > 27.8 kg/m2 for men and >27.3 kg/m2 for women (11). The patients were identified at the conclusion of the study by the magnitude of their weight gain and metabolic effects were analyzed by quartiles of weight gain (Table 5) (12). The conventionally treated patients had a mean change in BMI from baseline that ranged from a 4% loss in the lowest quartile to a 13% increase in the highest quartile. The highest quartile had a 3 mmHg rise in mean systolic and diastolic blood pressure and about a 10% increase in plasma triglycerides and total and LDL cholesterol levels. These changes in metabolic parameters occurred with no significant change in HbA1c. The intensively treated patients had an increase in BMI that ranged from no increase in the lowest quartile to a mean 29% increase in the highest quartile. The highest quartile had an absolute 1.9% mean decrease in HbA1c, a 6 mmHg rise in systolic and a 4 mmHg rise in diastolic BP, a 7 to 8% rise in plasma triglycerides and LDL cholesterol levels, and a 4% decrease in plasma HDL cholesterol levels. These data indicate that insulin treatment of type 1 diabetic patients creates the insulin resistance syndrome in a significant number of patients.

The data from the DCCT are not unexpected, as a number of previous studies had reported the development of insulin resistance in treated type 1 diabetic patients. Several reports from the Pittsburgh Epidemiology of Diabetic Complications Study provide additional new information. A family history of type 2 diabetes gave an odds ratio of 1.45 for the presence of CAD in their type 1 cohort (23). The presence of insulin resistance in type 1 diabetic patients was

Table 5 The Effect of Insulin Treatment on Body Weight and Lipid Profiles in Patients with Type 1 Diabetes
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