Department of Medicine, Stanford University School of Medicine, Stanford, California, USA.
Obesity (Silver Spring). 2014 Mar;22(3):673-80. doi: 10.1002/oby.20209. Epub 2013 Dec 17.
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.
A total of 148 healthy nondiabetic subjects with BMI 25-38 kg/m2 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.
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%.
Recruitment of adipose cells is required for expansion of body fat mass beyond BMI of 25 kg/m2 . 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.
肥胖个体之间的代谢异质性可能归因于脂肪细胞大小的差异。我们试图通过量化超重至中度肥胖个体的脂肪细胞大小分布、体脂肪和胰岛素介导的葡萄糖摄取来阐明这一点。
共有 148 名健康的非糖尿病 BMI 为 25-38kg/m2 的个体接受了皮下脂肪组织活检,并在改良胰岛素抑制试验期间使用稳态血浆葡萄糖(SSPG)浓度量化胰岛素介导的葡萄糖摄取。使用贝克曼库尔特 Multisizer 获得细胞大小分布。主要终点包括小脂肪细胞的%和大脂肪细胞的直径。根据胰岛素抵抗(IR)和胰岛素敏感(IS)亚组以及体脂肪五分位数,通过回归比较整个组的细胞大小和代谢参数。
大脂肪细胞和小脂肪细胞几乎以相等的比例存在。小脂肪细胞的%与 SSPG 相关(r = 0.26,P = 0.003)。与 BMI 匹配的 IS 个体相比,IR 对应个体表现出较少但更大的大脂肪细胞,以及更大比例的小到大脂肪细胞。大脂肪细胞的直径与体脂肪%相关(r = 0.26,P = 0.014),与女性性别相关(r = 0.21,P = 0.036),与 SSPG 相关(r = 0.20,P = 0.012)。在最高与最低体脂肪五分位数相比,脂肪细胞大小仅增加 7%,而脂肪细胞数量增加 74%。
在 BMI 超过 25kg/m2 的情况下,脂肪细胞的募集对于体脂肪量的扩张是必需的。胰岛素抵抗与小脂肪细胞的积累和大脂肪细胞的增大有关。这些数据支持了胰岛素抵抗可能是由于脂肪生成受损的观点。