Comparison of body fat composition and serum adiponectin levels in diabetic obesity and non-diabetic obesity
- PMID: 16899797
- DOI: 10.1038/oby.2006.133
Comparison of body fat composition and serum adiponectin levels in diabetic obesity and non-diabetic obesity
Abstract
Objective: Clinical aspects of diabetes and obesity are somewhat different, even at similar levels of insulin resistance. The purpose of this study was to determine differences in body fat distribution and serum adiponectin concentrations in diabetic and non-diabetic obese participants. We were also interested in identifying the characteristics of insulin resistance in these two groups, particularly from the standpoint of adiponectin.
Research methods and procedures: Adiponectin concentrations of 112 type 2 diabetic obese participants and 124 non-diabetic obese participants were determined. Abdominal adipose tissue areas and midthigh skeletal muscle areas were measured by computed tomography. A homeostasis model assessment of the insulin resistance score was calculated to assess insulin sensitivity. The relationships among serum adiponectin, body fat distribution, and clinical characteristics were also analyzed.
Results: Both abdominal subcutaneous and visceral fat areas were higher in the non-diabetic obese group, whereas midthigh low-density muscle area was higher in the diabetic obese group. The homeostasis model assessment of the insulin resistance score was similar between groups, whereas serum adiponectin was lower in the diabetic obese group. Abdominal visceral fat (beta = -0.381, p = 0.012) was a more important predictor of adiponectin concentration than low-density muscle (beta = -0.218, p = 0.026) in cases of non-diabetic obesity, whereas low-density muscle (beta = -0.413, p = 0.013) was a better predictor of adiponectin level than abdominal visceral fat (beta = - 0.228, p = 0.044) in diabetic obese patients.
Discussion: Therefore, factors involved in pathophysiology, including different serum adiponectin levels and body fat distributions, are believed to be responsible for differences in clinical characteristics, even at similar levels of insulin resistance in both diseases.
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