Meal feeding improves oral glucose tolerance in male rats and causes adaptations in postprandial islet hormone secretion that are independent of plasma incretins or glycemia.
Meal feeding improves oral glucose tolerance in male rats and causes adaptations in postprandial islet hormone secretion that are independent of plasma incretins or glycemia.
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DOI：
10.1152/ajpendo.00339.2014
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发表时间：
2014-11
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通讯作者：
T. Vahl;B. Aulinger;Eric P. Smith;D. L. Drazen;Yve Ulrich-Lai;R. Seeley;S. Woods;D. D’Alessio
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作者：
T. Vahl;B. Aulinger;Eric P. Smith;D. L. Drazen;Yve Ulrich-Lai;R. Seeley;S. Woods;D. D’Alessio
在光周期期间仅连续4小时获得食物的进食（MF）大鼠学会吃大餐以保持能量平衡。MF动物发生行为和内分泌变化，允许葡萄糖耐量，尽管增加膳食量。我们假设MF期间肠胰岛轴活性增强介导葡萄糖稳态。将大鼠队列分配至MF或随意（AL）方案2-4周。在口服碳水化合物和腹膜内（ip）和静脉内（iv）葡萄糖后测定胰岛素分泌和葡萄糖耐量。MF大鼠在第一周吃得比AL少，但此后保持了相当的体重轨迹。MF大鼠在液体混合餐后血糖波动减少（AUC：MF 75 ± 7，AL 461 ± 28 mmol·l·min，P < 0.001），胰岛素分泌左移（AUC（0-15）：MF 31.0 ± 4.9，AL 9.6 ± 4.4 pM·min，P < 0.02），在血糖显著升高之前达到峰值。两组的空腹胰高血糖素水平相当，但MF组的餐后反应较低。然而，MF组和AL组之间的proGIP和胰高血糖素原mRNA的肠表达和血浆肠促胰岛素水平均无差异。MF和AL大鼠对ip或iv葡萄糖的胰岛素反应无差异。这些发现表明，MF改善口服葡萄糖耐量，并与餐后胰岛激素分泌的显着变化。由于MF在口服而非胃肠外碳水化合物给药期间增强了β细胞功能，并且不受循环肠促胰岛素变化的影响，因此这些结果支持适应性胰岛素分泌的神经机制。
Meal-fed (MF) rats with access to food for only 4 consecutive hours during the light cycle learn to eat large meals to maintain energy balance. MF animals develop behavioral and endocrine changes that permit glucose tolerance despite increased meal size. We hypothesized that enhanced activity of the enteroinsular axis mediates glucose homeostasis during MF. Cohorts of rats were allocated to MF or ad libitum (AL) regimens for 2-4 wk. Insulin secretion and glucose tolerance were determined after oral carbohydrate and intraperitoneal (ip) and intravenous (iv) glucose. MF rats ate less than AL in the first week but maintained a comparable weight trajectory thereafter. MF rats had decreased glucose excursions after a liquid mixed meal (AUC: MF 75 ± 7, AL 461 ± 28 mmol·l⁻¹·min, P < 0.001), with left-shifted insulin secretion (AUC(0-15): MF 31.0 ± 4.9, AL 9.6 ± 4.4 pM·min, P < 0.02), which peaked before a significant rise in blood glucose. Both groups had comparable fasting glucagon levels, but postprandial responses were lower with MF. However, neither intestinal expression of proGIP and proglucagon mRNA nor plasma incretin levels differed between MF and AL groups. There were no differences in the insulin response to ip or iv glucose between MF and AL rats. These findings demonstrate that MF improves oral glucose tolerance and is associated with significant changes in postprandial islet hormone secretion. Because MF enhanced β-cell function during oral but not parenteral carbohydrate administration, and was not accounted for by changes in circulating incretins, these results support a neural mechanism of adaptive insulin secretion.