© 2003 by the American Diabetes Association, Inc.
Type 1 Diabetes Is Not Associated With Increased Central Abdominal ObesityResponse to SobelFrom the Diabetes and Obesity Research Program, Garvan Institute of Medical Research, Sydney, Australia Address correspondence to Professor Donald Chisholm, Diabetes and Obesity Research Program, Garvan Institute of Medical Research, 384 Victoria St., Darlinghurst NSW 2010, Sydney, Australia. E-mail: d.chisholm{at}garvan.org.au We read with interest the recent editorial by Sobel (1), wherein it is asserted that "intensive treatment of type 1 diabetes appears to increase central obesity." We agree with Sobel that "the insulin resistance underlying type 2 diabetes and frequently manifested in those with type 1 diabetes may be the most powerful determinant of coronary disease" (1), but argue that insulin resistance in type 1 diabetes is unrelated to increased central abdominal adiposity. Attention should be directed to our recent study (2), which examined the relationships between insulin sensitivity (glucose infusion rate [GIR] measured during euglycemic-hyperinsulinemic clamp), abdominal fat, lipid levels, blood pressure, and androgens in 10 premenopausal women with type 1 diabetes (HbA1c 8.1 ± 1% and diabetes duration 24 ± 10 years) and 10 nondiabetic BMI-matched control subjects. We found that GIR was lower in subjects with type 1 diabetes than in control subjects (49.3 ± 14.8 vs. 73.2 ± 21.6 µmol · min-1 · kg fat-free mass-1 respectively, P = 0.01), indicating greater insulin resistance in the former (2). However, we found no difference between control and type 1 diabetic subjects in central abdominal adiposity (measured directly by dual-energy X-ray absorptiometry) and intra-abdominal fat (measured by four-slice computed tomography) (2). Furthermore, unlike control subjects, we found that GIR was unrelated to abdominal obesity in type 1 diabetes (2). The finding that women with type 1 diabetes do not have greater central abdominal fat than nondiabetic control subjects confirms one of the few reports (3) that directly quantified abdominal adiposity in type 1 diabetes. Although a previous study of men found that waist-to-hip ratios were greater in men with type 1 diabetes than control subjects (4), this study relied on indirect and imperfect anthropometric surrogates (5). We echo Sobels conclusion that targeting insulin resistance may reduce excess coronary risk in type 1 diabetes. Although insulin "sensitizers" traditionally used in the treatment of type 2 diabetes, such as metformin, have been reported to improve insulin action in small studies of type 1 diabetes (6), it is not known whether this improvement translates into lower rates of coronary artery disease and whether newer agents, the thiazolidinediones, have a similar effect. We believe this to be an important question, especially due to the excess rates of coronary disease associated with type 1 diabetes and failure of traditional vascular risk factors to fully explain this excess risk. References
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