UPTAKE AND RELEASE OF GLUCOSE BY THE HUMAN KIDNEY - POSTABSORPTIVE RATES AND RESPONSES TO EPINEPHRINE
UPTAKE AND RELEASE OF GLUCOSE BY THE HUMAN KIDNEY - POSTABSORPTIVE RATES AND RESPONSES TO EPINEPHRINE
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DOI：
10.1172/jci118314
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发表时间：
1995-11-01
影响因子：
15.9
通讯作者：
GERICH, J
中科院分区：
文献类型：
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作者：
STUMVOLL, M;CHINTALAPUDI, U;GERICH, J
尽管有充分的证据表明肾脏可以产生和使用可观数量的葡萄糖，但人类肾脏通常被认为在葡萄糖稳态中起次要作用。该观点基于动脉-肾静脉葡萄糖浓度的测量，表明葡萄糖的净释放很少或没有，然而，从净平衡测量的推断没有考虑肾脏同时释放和摄取葡萄糖。因此，为了评估人体肾脏葡萄糖的释放和摄取对血浆葡萄糖总体进入和清除的贡献，我们使用平衡和同位素技术相结合的方法，在基础吸收后条件下和3小时肾上腺素输注期间，测量10名正常志愿者的肾脏葡萄糖净平衡、部分提取、摄取酸释放以及总体血浆葡萄糖外观和处置。在基础吸收后状态下，肾脏有少量但显著的葡萄糖净输出（66 +/- 22 μ mol . min（-1），P = 0.016）。然而，由于肾脏葡萄糖提取分数平均为2.9 +/-0.3%，因此存在相当大的肾脏葡萄糖摄取（2.3 +/- 0.2 μ mol . kg（-1）。min（-1）），占全身葡萄糖处置（11.4 +/- 0.5 μ mol . kg（-1）。min（-1））。肾脏葡萄糖释放（3.2 +/- 0.2 μ mol . kg（-1）。min（-1））占全身葡萄糖出现的27.8 ± 2.1%（11.4 ± 0.5 μ mol- . kg（-1）。min（-1））。肾上腺素输注使血浆肾上腺素增加到低血糖期间观察到的水平（3722 +/- 453 pmol/L），使肾脏葡萄糖释放增加近两倍（5.2 +/- 0.5 vs 2.8 +/- 0.1 mol）。kg（-1）。min（-1），P = 0.01），因此在输注结束时，肾葡萄糖释放占全身葡萄糖出现的40.3 +/-5.5%，并且基本上占全身葡萄糖出现的所有增加。这些观察结果表明，人类肾脏在葡萄糖稳态中起着重要作用。
Despite ample evidence that the kidney can both produce and use appreciable amounts of glucose, the human kidney is generally regarded as playing a minor role in glucose homeostasis. This view is based on measurements of arterio-renal vein glucose concentrations indicating little or no net release of glucose, However, inferences from net balance measurements do not take into consideration the simultaneous release and uptake of glucose by the kidney. Therefore, to assess the contribution of release and uptake of glucose by the human kidney to overall entry and removal of plasma glucose, we used a combination of balance and isotope techniques to measure renal glucose net balance, fractional extraction, uptake acid release as well as overall plasma glucose appearance and disposal in 10 normal volunteers under basal postabsorptive conditions and during a 3-h epinephrine infusion. In the basal postabsorptive state, there was small but significant net output of glucose by the kidney (66 +/- 22 mu mol . min(-1), P = 0.016). However, since renal glucose fractional extraction averaged 2.9 +/- 0.3%, there was considerable renal glucose uptake (2.3 +/- 0.2 mu mol . kg(-1) . min(-1)) which accounted for 20.2 +/- 1.7% of systemic glucose disposal (11.4 +/- 0.5 mu mol . kg(-1) . min(-1)). Renal glucose release (3.2 +/- 0.2 mu mol . kg(-1) . min(-1)) accounted for 27.8 +/- 2.1% of systemic glucose appearance (11.4 +/- 0.5 mu mol- . kg(-1) . min(-1)). Epinephrine infusion, which increased plasma epinephrine to levels observed during hypoglycemia (3722 +/- 453 pmol/liter) increased renal glucose release nearly twofold (5.2 +/- 0.5 vs 2.8 +/- 0.1 mol . kg(-1) . min(-1), P = 0.01) so that at the end of the infusion, renal glucose release accounted for 40.3 +/- 5.5% of systemic glucose appearance and essentially all of the increase in systemic glucose appearance. These observations suggest an important role for the human kidney in glucose homeostasis.