Abdominal Obesity and Type 2 Diabetes

Upper Body Fat Distribution: the Importance of Intra-abdominal Adipose Tissue

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Evidence is mounting in support of the notion that it is not excess body fat but rather high intra-abdominal adiposity that increases the risk of type 2 diabetes and CVD (30). For a given amount of total body fat, individuals with more intra-abdominal—or visceral— adipose tissue are at substantially greater risk of being insulin resistant and developing atherogenic and diabetogenic complications (30, 31). It has been shown that intra-abdominal adipose tissue is more metabolically active and more closely tied to metabolic abnormalities than subcutaneous adipose tissue (32, 33). In 1987, Fujioka et al. (34) were the first to propose that a preferential accumulation of intra-abdominal adipose tissue could explain the deterioration in glucose and lipid metabolism observed in obese patients. They found that subjects with large amounts of intra-abdominal adipose tissue had higher fasting plasma triglyceride levels and higher plasma glucose responses following an oral glucose challenge than subjects who had the same total body fat mass (as measured by BMI) but a preferential accumulation of abdominal subcutaneous adipose tissue. Pouliot et al. (35) later quantified the respective contributions of subcutaneous and intra-abdominal fat to glucose intolerance and hyperinsulinemia in obese individuals. Two groups of obese patients were carefully matched for the same amount of total body fat but had either low or high amounts of  intra-abdominal adipose tissue. The authors found that obese individuals with low levels of intra-abdominal adipose tissue had normal glucose tolerance when compared to lean controls. However, obese subjects with high levels of intra-abdominal adipose tissue showed an increase in their glycemic and insulinemic responses to an oral glucose challenge. Additional studies by Ross et al. (36, 37) further explored the relationship between intra-abdominal adipose tissue and metabolic risk in men and women. When individuals who were matched for similar abdominal subcutaneous adipose tissue but had different levels of intra-abdominal adipose tissue were compared, it was revealed that subjects with high intra-abdominal adipose tissue had higher glucose values following an OGTT and lower glucose disposal values compared to subjects with low intra-abdominal adipose tissue. These results lend weight to the idea that obese individuals with excess intra-abdominal adipose tissue display alterations in indices of plasma glucose-insulin homeostasis and are therefore at increased risk of developing type 2 diabetes.

Reference

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31. Després JP. Is visceral obesity the cause of the metabolic syndrome? Ann Med 2006; 38: 52-63.

32. Frayn KN, Karpe F, Fielding BA, et al. Integrative physiology of human adipose tissue. Int J Obes Relat Metab Disord 2003; 27: 875-88.

33. Wajchenberg BL. Subcutaneous and visceral adipose tissue: their relation to the metabolic syndrome. Endocr Rev 2000; 21: 697-738.

34. Fujioka S, Matsuzawa Y, Tokunaga K, et al. Contribution of intra-abdominal fat accumulation to the impairment of glucose and lipid metabolism in human obesity. Metabolism 1987; 36: 54-9.

35. Pouliot MC, Després JP, Nadeau A, et al. Visceral obesity in men. Associations with glucose tolerance, plasma insulin, and lipoprotein levels. Diabetes 1992; 41: 826-34.

36. Ross R, Aru J, Freeman J, et al. Abdominal adiposity and insulin resistance in obese men. Am J Physiol Endocrinol Metab 2002; 282: E657-63.

37. Ross R, Freeman J, Hudson R, et al. Abdominal obesity, muscle composition, and insulin resistance in premenopausal women. J Clin Endocrinol Metab 2002; 87: 5044-51.

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