4.7 Article

Subcutaneous Adipose Cell Size and Distribution: Relationship to Insulin Resistance and Body Fat

Journal

OBESITY
Volume 22, Issue 3, Pages 673-680

Publisher

WILEY
DOI: 10.1002/oby.20209

Keywords

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Funding

  1. National Institutes of Health/National Institute of Digestive Diseases and Diabetes [R01 DK080436, R01DK071309]

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Objective: Metabolic heterogeneity among obese individuals may be attributable to differences in adipose cell size. We sought to clarify this by quantifying adipose cell size distribution, body fat, and insulin-mediated glucose uptake in overweight to moderately-obese individuals. Methods: A total of 148 healthy nondiabetic subjects with BMI 25-38 kg/m(2) underwent subcutaneous adipose tissue biopsies and quantification of insulin-mediated glucose uptake with steady-state plasma glucose (SSPG) concentrations during the modified insulin suppression test. Cell size distributions were obtained with Beckman Coulter Multisizer. Primary endpoints included % small adipose cells and diameter of large adipose cells. Cell-size and metabolic parameters were compared by regression for the whole group, according to insulin-resistant (IR) and insulin-sensitive (IS) subgroups, and by body fat quintile. Results: Both large and small adipose cells were present in nearly equal proportions. Percent small cells was associated with SSPG (r = 0.26, P = 0.003). Compared to BMI-matched IS individuals, IR counterparts demonstrated fewer, but larger large adipose cells, and a greater proportion of small-to-large adipose cells. Diameter of the large adipose cells was associated with % body fat (r 0.26, P = 0.014), female sex (r = 0.21, P = 0.036), and SSPG (r = 0.20, P = 0.012). In the highest versus lowest % body fat quintile, adipose cell size increased by only 7%, whereas adipose cell number increased by 74%. Conclusions: Recruitment of adipose cells is required for expansion of body fat mass beyond BMI of 25 kg/m(2). Insulin resistance is associated with accumulation of small adipose cells and enlargement of large adipose cells. These data support the notion that impaired adipogenesis may underlie insulin resistance.

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