Improved tolerance to sequential glucose loading (Staub-Traugott effect): size and mechanisms
Improved tolerance to sequential glucose loading (Staub-Traugott effect): size and mechanisms
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DOI：
10.1152/ajpendo.00127.2009
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发表时间：
2009-08-01
影响因子：
5.1
通讯作者：
Ferrannini, Ele
中科院分区：
文献类型：
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作者：
Bonuccelli, Sandra;Muscelli, Elza;Ferrannini, Ele
博努切利·S，穆斯塞利·E，加斯塔尔德利·A，巴索蒂·E，Astiarraga BD，Holst JJ，Mari A，Ferrannini E。改善对序贯葡萄糖负荷的耐受(Staub-Traugot效应)：大小和机制。AM J生理学内分泌代谢酶297：E532-E537,2009。2009年6月16日首次出版；DOI：10.1152/ajpendo.00127.2009。-对顺序葡萄糖负荷的葡萄糖耐受性提高(Staub-Traugot效应)是日常血糖暴露的一个重要决定因素。其机制尚未明确建立。我们招募了17名健康志愿者进行两次连续的口服葡萄糖耐量试验(OGTTS)，时间分别为0min和180min(研究I)。该方案在另一天重复(研究II)，只是在60到180分钟之间将血糖控制在8.3 mmol/L。通过C肽浓度的数学模型分析β细胞功能。在一个亚组中，通过三重示踪技术(输注[6，6-H-2(2)]葡萄糖并用[1-H-2]葡萄糖和[U-C-13]葡萄糖标记2个葡萄糖负荷)来测量葡萄糖动力学。在研究I和研究II中，对第二次口服葡萄糖耐量试验的血糖反应相当于第一次口服葡萄糖耐量试验的+/-2%(P=0.003)。胰岛素的绝对分泌量较低(37.8+/-4.3vs.42.8+/-5.1nmol/m(2)，P=0.02)，但葡萄糖增强(即在相同的血糖水平下较高的分泌量)较强(1.08+/-0.02vs.0.92+/-0.02倍，P=0.006)，增量(+36+/-5%)高于研究I(+19+/-6%，P<；0.05)。在合并数据中，第一次糖耐量试验中较高的葡萄糖区域与第二次糖耐量试验中较高的增强相关(Rho=0.6，P=0.002)。胰岛素清除量和葡萄糖清除量在不同负荷间无显著差异，首次负荷后3h出现的葡萄糖总量为60+/-6g，第二次负荷为52+/-5g(P=0.0 5)。空腹内源性葡萄糖产量[13.3+/-0.6mmol.min(-1).kg脱脂质量(-1)]在0~180min平均为6.0+/-3.8mmol.min(-1)，在180~360min平均为1.7+/-2.6(P<；0.03)。葡萄糖增强和对内源性葡萄糖释放的较强抑制是Staub-Traugot效应的主要机制。
Bonuccelli S, Muscelli E, Gastaldelli A, Barsotti E, Astiarraga BD, Holst JJ, Mari A, Ferrannini E. Improved tolerance to sequential glucose loading (Staub-Traugott effect): size and mechanisms. Am J Physiol Endocrinol Metab 297: E532-E537, 2009. First published June 16, 2009; doi:10.1152/ajpendo.00127.2009. - Improved glucose tolerance to sequential glucose loading (Staub-Traugott effect) is an important determinant of day-to-day glycemic exposure. Its mechanisms have not been clearly established. We recruited 17 healthy volunteers to receive two sequential oral glucose tolerance tests (OGTTs), at time 0 min and 180 min (Study I). The protocol was repeated on a separate day (Study II) except that plasma glucose was clamped at 8.3 mmol/l between 60 and 180 min. beta-Cell function was analyzed by mathematical modeling of C-peptide concentrations. In a subgroup, glucose kinetics were measured by a triple-tracer technique (infusion of [6,6-H-2(2)] glucose and labeling of the 2 glucose loads with [1-H-2] glucose and [U-C-13] glucose). In both Studies I and II, the plasma glucose response to the second OGTT equaled 84 +/- 2% (P = 0.003) of the response to the first OGTT. Absolute insulin secretion was lower (37.8 +/- 4.3 vs. 42.8 +/- 5.1 nmol/m(2), P = 0.02), but glucose potentiation (i. e., higher secretion at the same glycemia) was stronger (1.08 +/- 0.02 vs. 0.92 +/- 0.02-fold, P = 0.006), the increment being higher in Study II (+36 +/- 5%) than Study I (+19 +/- 6%, P < 0.05). In pooled data, a higher glucose area during the first OGTT was associated with a higher potentiation during the second OGTT (rho = 0.60, P = 0.002). Neither insulin clearance nor glucose clearance differed between loads, and appearance of glucose over 3 h totalled 60 +/- 6 g for the first load and 52 +/- 5 g for the second load (P = not significant). Fasting endogenous glucose production [13.3 +/- 0.6 mu mol.min(-1).kg fat-free mass (FFM)(-1)] averaged 6.0 +/- 3.8 mu mol.min(-1).kg FFM-1 between 0 and 180 min and 1.7 +/- 2.6 between 180 and 360 min (P < 0.03). Glucose potentiation and stronger suppression of endogenous glucose release are the main mechanisms underlying the Staub-Traugott effect.