...
首页> 外文期刊>Obesity >Subcutaneous adipose cell size and distribution: Relationship to insulin resistance and body fat
【24h】

Subcutaneous adipose cell size and distribution: Relationship to insulin resistance and body fat

机译:皮下脂肪细胞的大小和分布:与胰岛素抵抗和体内脂肪的关系

获取原文
获取原文并翻译 | 示例

摘要

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/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. 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/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.
机译:肥胖个体之间的客观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,体脂和胰岛素介导的葡萄糖摄取来阐明这一点。方法在改良的胰岛素抑制试验中,对148例BMI 25-38 kg / m2的健康非糖尿病受试者进行皮下脂肪组织活检,并用稳态血浆葡萄糖(SSPG)浓度对胰岛素介导的葡萄糖摄取进行定量。用Beckman Coulter Multisizer获得细胞大小分布。主要终点包括小脂肪细胞百分比和大脂肪细胞直径。根据胰岛素抵抗(IR)和胰岛素敏感性(IS)亚组,通过对整个组的回归,以及通过身体脂肪五分位数,比较细胞大小和代谢参数。结果大和小的脂肪细胞均以几乎相等的比例存在。小细胞百分比与SSPG相关(r = 0.26,P = 0.003)。与BMI匹配的IS个体相比,IR对应者显示出较少但较大的大型脂肪细胞,而较大比例的小至大型脂肪细胞。大脂肪细胞的直径与%体脂肪(r = 0.26,P = 0.014),女性(r = 0.21,P = 0.036)和SSPG(r = 0.20,P = 0.012)相关。在最高百分比与最低百分比的人体脂肪五分位数中,脂肪细胞大小仅增加7%,而脂肪细胞数量增加74%。结论脂肪细胞的增加需要补充脂肪细胞,以使体脂超过25 kg / m2的BMI。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。这些数据支持受损的脂肪生成可能是胰岛素抵抗的基础。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号