Obesity and Diabetes Clinical Research Section, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Phoenix, AZ 85016, USA.
Metabolism. 2010 Oct;59(10):1396-401. doi: 10.1016/j.metabol.2010.01.006. Epub 2010 Feb 12.
In the fasting state, approximately 83% of glucose uptake occurs via non-insulin-mediated mechanisms. A widely accepted static rate for NIMGU is 1.62 mg kg(-1)·min(-1). To investigate the variability of NIMGU, we examined differences by glucose tolerance, sex, age, race (American Indian/African American/Caucasian), and adiposity in 616 volunteers (including individuals with normal glucose regulation [NGR] and impaired glucose regulation [IGR] and diabetes mellitus [DM]) using data from euglycemic-hyperinsulinemic clamp experiments. NIMGU was determined by plotting basal glucose output and insulin action against fasting and steady-state clamp insulin. The intercept with the y-axis after extrapolation was interpreted as NIMGU at zero insulin. Body composition was determined by dual-energy x-ray absorptiometry; and glucose regulation, by a 75-g oral glucose tolerance test. Energy expenditure was measured by indirect calorimetry in a metabolic chamber. In individuals with NGR (n = 385), NIMGU was 1.63 mg kg(estimated metabolic body size (fat free mass + 17.7 kg))(-1) min(-1) (95% confidence interval, 1.59-1.66). NIMGU increased with IGR and DM (IGR: n = 189, 1.67 [1.62-1.72]; DM: n = 42, 2.39 [2.29-2.49]; P < .0001 across groups). NIMGU did not differ by sex (P = .13), age (P = .22), or race (P = .06); however, NIMGU was associated with percentage body fat (r(2) = 0.04, P < .0001). Furthermore, NIMGU was positively associated with 24-hour and sleep energy expenditure (r(2) = 0.002, P = .03; r(2) = 0.01, P < .01). Extrapolated NIMGU in individuals with NGR is remarkably consistent with previously published data. Our results indicate that NIMGU is associated with adiposity. NIMGU increases with declining glucose tolerance perhaps to preserve glucose uptake during increased insulin resistance.
在禁食状态下,约 83%的葡萄糖摄取通过非胰岛素介导的机制发生。普遍接受的 NIMGU 静态率为 1.62mg/kg·min(-1)。为了研究 NIMGU 的变异性,我们检查了 616 名志愿者(包括血糖调节正常(NGR)、葡萄糖调节受损(IGR)和糖尿病(DM)患者)的葡萄糖耐量、性别、年龄、种族(美洲印第安人/非裔美国人/高加索人)和肥胖程度的差异,使用的是正葡萄糖高胰岛素钳夹实验的数据。通过绘制基础葡萄糖输出和胰岛素作用与空腹和稳态钳夹胰岛素的关系来确定 NIMGU。外推后的 y 轴截距被解释为零胰岛素时的 NIMGU。身体成分通过双能 X 射线吸收法确定;葡萄糖调节通过 75g 口服葡萄糖耐量试验确定。能量消耗通过代谢室内的间接热量法测量。在 NGR 个体(n=385)中,NIMGU 为 1.63mg/kg(估计代谢体型大小(去脂体重+17.7kg))(-1)min(-1)(95%置信区间,1.59-1.66)。NIMGU 随着 IGR 和 DM 而增加(IGR:n=189,1.67[1.62-1.72];DM:n=42,2.39[2.29-2.49];P<.0001 组间)。NIMGU 与性别(P=0.13)、年龄(P=0.22)或种族(P=0.06)无关;然而,NIMGU 与体脂百分比相关(r(2)=0.04,P<.0001)。此外,NIMGU 与 24 小时和睡眠能量消耗呈正相关(r(2)=0.002,P=0.03;r(2)=0.01,P<.01)。NGR 个体的外推 NIMGU 与先前发表的数据非常一致。我们的结果表明,NIMGU 与肥胖有关。随着葡萄糖耐量的下降,NIMGU 增加,可能是为了在胰岛素抵抗增加时保持葡萄糖摄取。