Department of Internal Medicine, Maastricht University Medical Centre and Cardiovascular Research Institute Maastricht, P.O. Box 5800, 6202 AZ Maastricht, The Netherlands.
Microvasc Res. 2011 Nov;82(3):423-9. doi: 10.1016/j.mvr.2011.08.006. Epub 2011 Aug 22.
Adequate microvascular perfusion is essential for the regulation of tissue metabolism. Therefore, defects in microvascular function may play a role in obesity-associated insulin resistance. Steady-state hyperinsulinemia during a euglycemic hyperinsulinemic clamp stimulates endothelium-dependent vasodilation and capillary recruitment, which contribute to increased glucose uptake. These phenomena have been shown to be blunted in obesity. If insulin's effects on microcirculatory function indeed play a physiological role in regulating insulin-mediated glucose uptake, such effects should be demonstrable not only during steady-state hyperinsulinemia, but also after meal ingestion. We investigated whether similar responses occur after ingestion of a glucose load or a mixed meal. We examined the effects of a glucose drink, a mixed meal drink, or a control drink (water) on skin capillary density (i.e. baseline capillary density, hyperemic capillary recruitment, and density during venous congestion, using capillaroscopy) and skin endothelium-(in)dependent vasodilation (using laser-Doppler flowmetry with iontophoresis of acetylcholine and sodium nitroprusside) in 20 lean and 19 obese individuals. In lean individuals, neither the glucose nor the mixed meal drink induced a significant effect on capillary density or endothelium-(in)dependent vasodilation. Possibly this is related to the modest plasma insulin levels as compared to the insulin clamp. In obese individuals, the mixed meal drink, compared to the control drink, decreased baseline skin perfusion (P<0.05) and acetylcholine-mediated vasodilation (P<0.05), while no effect of the drinks on capillary density was found. Compared to lean individuals, obese individuals had impaired acetylcholine-mediated vasodilation after meal ingestion (P=0.02). The latter findings are consistent with impaired postprandial microvascular function in obesity.
足够的微血管灌注对于组织代谢的调节至关重要。因此，微血管功能的缺陷可能在肥胖相关的胰岛素抵抗中发挥作用。在正常血糖高胰岛素钳夹期间，稳态高胰岛素血症刺激内皮依赖性血管舒张和毛细血管募集，从而促进葡萄糖摄取增加。这些现象在肥胖中已经被证明是减弱的。如果胰岛素对微循环功能的影响确实在调节胰岛素介导的葡萄糖摄取中发挥生理作用，那么这种作用不仅应该在稳态高胰岛素血症期间表现出来，而且在餐后也应该表现出来。我们研究了在摄入葡萄糖负荷或混合餐后是否会出现类似的反应。我们检查了葡萄糖饮料、混合餐饮料或对照饮料（水）对皮肤毛细血管密度（即基线毛细血管密度、充血性毛细血管募集和静脉充血期间的密度，使用毛细血管镜）和皮肤内皮（非）依赖性血管舒张（使用激光多普勒流量测量仪，通过乙酰胆碱和硝普钠离子电渗进行）的影响在 20 名瘦人和 19 名肥胖者中。在瘦人中，葡萄糖或混合餐饮料都没有对毛细血管密度或内皮（非）依赖性血管舒张产生显著影响。这可能与与胰岛素钳夹相比，血浆胰岛素水平适中有关。在肥胖者中，与对照饮料相比，混合餐饮料降低了基础皮肤灌注（P<0.05）和乙酰胆碱介导的血管舒张（P<0.05），但饮料对毛细血管密度没有影响。与瘦人相比，肥胖者在餐后摄入时乙酰胆碱介导的血管舒张受损（P=0.02）。后一种发现与肥胖餐后微血管功能受损一致。
