负的动脉-门静脉葡萄糖梯度在运动后状态中的作用。

P Galassetti, Y Koyama, R H Coker, D B Lacy, A D Cherrington, D H Wasserman
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引用次数: 12

摘要

未标示:先前的运动刺激肌肉和肝脏葡萄糖摄取。负的动脉-门静脉葡萄糖梯度(A -pv grad)刺激静息净肝葡萄糖摄取(NHGU),但减少肌肉葡萄糖摄取。本研究探讨了a-pv负梯度对狗运动后葡萄糖给药的影响。实验方案:运动(-180 ~ -30分钟)、过渡(-30 ~ -20分钟)、基础期(-20 ~ 0分钟)、实验期(0 ~ 100分钟)。实验期间通过腔静脉(Pe, n = 6)或门静脉(Po, n = 6)输注葡萄糖诱导130 mg/dl动脉性高血糖。胰岛素和胰高血糖素的替换率是基础和基础比率的四倍。在试验期间,Pe的a-pv梯度(mg/dl)为3 +/- 1,Po为-10 +/- 2。两组动脉胰岛素和胰高血糖素相似。在Pe中,净肝脏葡萄糖平衡(mg x kg(-1) x min(-1),阴性=摄取)为4.2 +/- 0.3(基础期)和-1.2 +/- 0.3(葡萄糖输注);Po分别为4.1 +/- 0.5和-3.2 +/- 0.4 (P < 0.005 vs. Pe)。Po组总葡萄糖输注量(mg × kg(-1) × min(-1))为11 +/- 1,Pe组为8 +/- 1 (P < 0.05)。后肢净摄糖量与全身非肝摄糖量相似。结论:运动后门静脉信号独立刺激NHGU。相反,先前的运动消除了门脉信号对非肝组织葡萄糖摄取的抑制作用。因此,门脉信号增加了运动后的全身葡萄糖处理,其量等于NHGU的增加。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Role of a negative arterial-portal venous glucose gradient in the postexercise state.

Unlabelled: Prior exercise stimulates muscle and liver glucose uptake. A negative arterial-portal venous glucose gradient (a-pv grad) stimulates resting net hepatic glucose uptake (NHGU) but reduces muscle glucose uptake. This study investigates the effects of a negative a-pv grad during glucose administration after exercise in dogs.

Experimental protocol: exercise (-180 to -30 min), transition (-30 to -20 min), basal period (-20 to 0 min), and experimental period (0 to 100 min). In the experimental period, 130 mg/dl arterial hyperglycemia was induced via vena cava (Pe, n = 6) or portal vein (Po, n = 6) glucose infusions. Insulin and glucagon were replaced at fourfold basal and basal rates. During the experimental period, the a-pv grad (mg/dl) was 3 +/- 1 in Pe and -10 +/- 2 in Po. Arterial insulin and glucagon were similar in the two groups. In Pe, net hepatic glucose balance (mg x kg(-1) x min(-1), negative = uptake) was 4.2 +/- 0.3 (basal period) and -1.2 +/- 0.3 (glucose infusion); in Po it was 4.1 +/- 0.5 and -3.2 +/- 0.4, respectively (P < 0.005 vs. Pe). Total glucose infusion (mg x kg(-1) x min(-1)) was 11 +/- 1 in Po and 8 +/- 1 in Pe (P < 0.05). Net hindlimb and whole body nonhepatic glucose uptakes were similar.

Conclusions: the portal signal independently stimulates NHGU after exercise. Conversely, prior exercise eliminates the inhibitory effect of the portal signal on glucose uptake by nonhepatic tissues. The portal signal therefore increases whole body glucose disposal after exercise by an amount equal to the increase in NHGU.

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