The multiphasic profile of free fatty acids during the intravenous glucose tolerance test is unresponsive to exogenous insulin.

The multiphasic profile of free fatty acids during the intravenous glucose tolerance test is unresponsive to exogenous insulin.
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静脉内葡萄糖耐量试验期间游离脂肪酸的多相特征对外源性胰岛素没有反应。

DOI:
10.1016/j.metabol.2004.03.020
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发表时间:
2004
期刊:
Metabolism: clinical and experimental
影响因子:
--
通讯作者:
Boston,RC
Boston,RC
中科院分区:
--
文献类型:
--
作者:
Sumner,AE;Bergman,RN;Vega,GL;Genovese,DJ;Cochran,CS;Pacak,K;Watanabe,RM;Boston,RC

文献摘要

相似文献

由于胰岛素浓度的小幅增加对脂肪分解有深远的影响,我们的目标是描述在频繁采样的静脉葡萄糖耐量试验(FSIGT)中的游离脂肪酸(FFA)谱,并确定内源性和外源性胰岛素是否影响FFA谱。13名受试者同时接受了单纯葡萄糖(GO-FSIGT)和胰岛素修饰的FSIGT(IM-FSIGT)。两种方案均持续6小时。基线时静脉注射葡萄糖(0.3g/kg)。在IM-FSIGT中,胰岛素输注时间为20~25min(4mU/kg·min)。另外6名受试者同时接受IM-FSIGT和生理盐水研究(NS-研究)。在NS研究中,注入的是生理盐水,而不是葡萄糖和胰岛素。所有测试的空腹血糖、胰岛素、游离脂肪酸和肾上腺素浓度都是相似的。两组FSIGT内源性胰岛素峰值均为4±1分钟。IM-FSIGT计算的外源性胰岛素峰值时间为26±1分钟。IM-FSIGT的血糖浓度低于GO-FSIGT,肾上腺素浓度高于GO-FSIGT。在FSIGT期间,FFA时间进程显示了四个不同的阶段,这在不同的协议之间没有什么不同。在第I期(0~11min),游离脂肪酸水平维持在接近基础水平(491±183minFFA)水平;在第II期(11~79min),游离脂肪酸水平下降至最低点,达139.63μ/L;在第III期(79~188min),游离脂肪酸水平直线上升,并恢复到基础水平;在第IV期(188~360分钟),游离脂肪酸水平升至基础水平以上,并稳定在732±214μμ/L(P;.001)。在NS研究中,游离脂肪酸水平一直维持在接近基线水平(388±118mEq/L)直到180分钟,然后在360分钟上升至618±258μ/L。在IM-FSIGT和NS-研究中,180到360分钟的FFA浓度没有差异。由于4个FFA时相在不同方案之间没有差异,胰岛素对FSIGT中FFA水平的影响可归因于内源性胰岛素。但IM-FSIGT和NS-Study的FFA水平从180分钟到360分钟的相似性表明,昼夜变化与胰岛素或FSIGT方案最终的基础上FFA平台期无关。
As small increments in insulin concentration profoundly affect lipolysis, our goal was to describe the free fatty acid (FFA) profile during the frequently sampled intravenous glucose tolerance test (FSIGT) and determine if both endogenous and exogenous insulin influenced the FFA profile. Thirteen subjects had both a glucose-only (GO-FSIGT) and insulin-modified FSIGT (IM-FSIGT). Both protocols were of 6 hours duration. At baseline an intravenous glucose bolus (0.3 g/kg) was given. In the IM-FSIGT, insulin was infused from 20 to 25 minutes (4 mU/kg · min). Six additional subjects had both an IM-FSIGT and a normal saline study (NS-Study). For the NS-Study, normal saline solution was infused instead of glucose and insulin. Fasting glucose, insulin, FFA and epinephrine concentrations were similar for all tests. Endogenous insulin peaked at 4 ± 1 minute in both FSIGTs. The mean calculated peak time of exogenous insulin in the IM-FSIGT was 26 ± 1 minute. Glucose concentrations were lower and epinephrine concentrations higher in the IM-FSIGT versus GO-FSIGT. During the FSIGTs, the FFA time course revealed four distinct phases, which did not differ between protocols. In phase I (0 to 11 minutes), FFA levels remained near basal (491 ± 183 μmol/L); in phase II (11 to 79 minutes), FFA levels declined achieving a nadir of 139 ± 63 μmol/L; in phase III (79 to 188 minutes), FFA levels rose linearly and reattained basal levels; and in phase IV (188 to 360 minutes), FFA levels rose above basal and plateaued at 732 ± 214 μmol/L (P < .001). In the NS-Study, FFA levels remained near baseline (388 ± 118 mEq/L) until 180 minutes and then trended upward to 618 ± 258 μmol/L at 360 minutes. FFA concentrations from 180 to 360 minutes did not differ in the IM-FSIGT versus NS-Study. As the 4 FFA phases did not differ between protocols, the insulin effect on FFA levels in the FSIGT can be attributed to endogenous insulin. But the similarity in FFA levels from 180 to 360 minutes in the IM-FSIGT and NS-Study suggests diurnal variation and not a dynamic related to insulin or the FSIGT protocol is responsible for the final suprabasal FFA plateau.