The Concept of CMR

Abdominal obesity

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Type 2 diabetes is recognized as a significant cardiovascular disease (CVD) risk factor, but the independent contribution of type 2 diabetic hyperglycemia to CVD risk is rather weak. It has been proposed that this hyperglycemic state is only the tip of a huge dysmetabolic iceberg, mostly resulting from a combination of factors found in overweight and obese patients with excess abdominal fat and insulin resistance (1).

Abdominal obesity is associated with a cluster of atherogenic metabolic abnormalities that are now often referred to as the metabolic syndrome. These abnormalities include atherogenic dyslipidemia, insulin resistance, and a pro-thrombotic and pro-inflammatory state. The simultaneous presence of all these risk factors is known to increase the risk of type 2 diabetes and CVD (2). At specific fault is excess intra-abdominal adipose tissue (visceral adipose tissue), which is more closely associated with a detrimental metabolic profile than excess subcutaneous adipose tissue (3). This observation has led to the widespread use of waist circumference (a surrogate measure of intra-abdominal adipose tissue) in epidemiological analyses and as a metabolic syndrome identification criterion (4, 5). In the Insulin Resistance in Atherosclerosis Study (IRAS), high waist circumference predicted the incidence of metabolic syndrome more accurately than directly measured insulin resistance (6). Moreover, a prospective study has been published on the predictive power of high initial levels of intra-abdominal fat as a type 2 diabetes risk factor (7). Intervention trials have also confirmed the strong association between excess body fat and type 2 diabetes found in observational studies. These trials have shown that reducing body weight in overweight and obese subjects at high risk of developing diabetes could substantially reduce the incidence of diabetes (8-10).

Reference

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1. Després JP and Lemieux I. Abdominal obesity and metabolic syndrome. Nature 2006; 444: 881-7

2. Lakka HM, Laaksonen DE, Lakka TA, et al. The metabolic syndrome and total and cardiovascular disease mortality in middle-aged men. JAMA 2002; 288: 2709-16.

3. Gasteyger C and Tremblay A. Metabolic impact of body fat distribution. J Endocrinol Invest 2002; 25: 876-83.

4. Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA 2001; 285: 2486-97.

5. Lemieux I, Pascot A, Couillard C, et al. Hypertriglyceridemic waist: A marker of the atherogenic metabolic triad (hyperinsulinemia; hyperapolipoprotein B; small, dense LDL) in men? Circulation 2000; 102: 179-84.

6. Palaniappan L, Carnethon MR, Wang Y, et al. Predictors of the incident metabolic syndrome in adults: the Insulin Resistance Atherosclerosis Study. Diabetes Care 2004; 27: 788-93.

7. Bergstrom RW, Newell-Morris LL, Leonetti DL, et al. Association of elevated fasting C-peptide level and increased intra- abdominal fat distribution with development of NIDDM in Japanese- American men. Diabetes 1990; 39: 104-11.

8. Lean ME, Powrie JK, Anderson AS, et al. Obesity, weight loss and prognosis in type 2 diabetes. Diabet Med 1990; 7: 228-33.

9. Knowler WC, Barrett-Connor E, Fowler SE, et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002; 346: 393-403.

10. Tuomilehto J, Lindstrom J, Eriksson JG, et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med 2001; 344: 1343-50.

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