Menzies Institute for Medical Research, University of Tasmania , Hobart, Tasmania , Australia.
Department of Health and Human Performance, College of Health Affairs, University of Texas Rio Grande Valley , Brownsville, Texas.
Am J Physiol Endocrinol Metab. 2018 Aug 1;315(2):E307-E315. doi: 10.1152/ajpendo.00448.2017. Epub 2018 May 15.
Skeletal muscle microvascular (capillary) blood flow increases in the postprandial state or during insulin infusion due to dilation of precapillary arterioles to augment glucose disposal. This effect occurs independently of changes in large artery function. However, acute hyperglycemia impairs vascular function, causes insulin to vasoconstrict precapillary arterioles, and causes muscle insulin resistance in vivo. We hypothesized that acute hyperglycemia impairs postprandial muscle microvascular perfusion, without disrupting normal large artery hemodynamics, in healthy humans. Fifteen healthy people (5 F/10 M) underwent an oral glucose challenge (OGC, 50 g glucose) and a mixed-meal challenge (MMC) on two separate occasions (randomized, crossover design). At 1 h, both challenges produced a comparable increase (6-fold) in plasma insulin levels. However, the OGC produced a 1.5-fold higher increase in blood glucose compared with the MMC 1 h postingestion. Forearm muscle microvascular blood volume and flow (contrast-enhanced ultrasound) were increased during the MMC (1.3- and 1.9-fold from baseline, respectively, P < 0.05 for both) but decreased during the OGC (0.7- and 0.6-fold from baseline, respectively, P < 0.05 for both) despite a similar hyperinsulinemia. Both challenges stimulated brachial artery flow (ultrasound) and heart rate to a similar extent, as well as yielding comparable decreases in diastolic blood pressure and total vascular resistance. Systolic blood pressure and aortic stiffness remained unaltered by either challenge. Independently of large artery hemodynamics, hyperglycemia impairs muscle microvascular blood flow, potentially limiting glucose disposal into skeletal muscle. The OGC reduced microvascular blood flow in muscle peripherally and therefore may underestimate the importance of skeletal muscle in postprandial glucose disposal.
骨骼肌微血管（毛细血管）血流在餐后状态或胰岛素输注期间增加，这是由于小动脉前血管扩张以增加葡萄糖的摄取。这种作用独立于大动脉功能的变化而发生。然而，急性高血糖会损害血管功能，导致胰岛素收缩小动脉前血管，并导致体内肌肉胰岛素抵抗。我们假设急性高血糖会损害健康人餐后肌肉微血管灌注，而不会破坏大动脉正常的血液动力学。15 名健康人（5 名女性，10 名男性）分别在两次不同时间接受口服葡萄糖挑战（OGC，50g 葡萄糖）和混合餐挑战（MMC）（随机交叉设计）。在 1 小时时，两种挑战都使血浆胰岛素水平增加了 6 倍。然而，OGC 在摄入后 1 小时使血糖升高了 1.5 倍，而 MMC 则升高了 1.5 倍。在 MMC 期间，前臂肌肉微血管血液体积和流量（对比增强超声）增加（分别比基线增加 1.3 倍和 1.9 倍，两者均 P < 0.05），但在 OGC 期间减少（分别比基线减少 0.7 倍和 0.6 倍，两者均 P < 0.05），尽管胰岛素水平相似。两种挑战都以相似的程度刺激肱动脉血流（超声）和心率，以及导致相似的舒张压和总血管阻力下降。收缩压和主动脉僵硬度不受任何一种挑战的影响。无论大动脉血液动力学如何，高血糖都会损害肌肉微血管血流，可能会限制葡萄糖进入骨骼肌的摄取。OGC 会减少肌肉外周的微血管血流，因此可能低估了骨骼肌在餐后葡萄糖摄取中的重要性。
