In vivo measurements of brain glucose transport using the reversible Michaelis-Menten model and simultaneous measurements of cerebral blood flow changes during hypoglycemia
In vivo measurements of brain glucose transport using the reversible Michaelis-Menten model and simultaneous measurements of cerebral blood flow changes during hypoglycemia
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DOI：
10.1097/00004647-200106000-00003
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发表时间：
2001-06-01
影响因子：
6.3
通讯作者：
Gruetter, R
中科院分区：
文献类型：
--
作者：
Choi, IY;Lee, SP;Gruetter, R
葡萄糖是维持正常大脑功能的主要底物。当大脑葡萄糖浓度接近零时，葡萄糖跨血脑屏障的运输成为代谢过程中的速率限制。例如，代谢活动增加和低血糖。稳态脑葡萄糖浓度：在α-氯醛糖麻醉的大鼠中，非侵入性测量作为血糖的函数。脑内血糖与血糖的关系在4.50~30 mm ol/L范围内呈线性关系，符合可逆米氏模型。当模型用于脑葡萄糖测量时，表观米氏常数K-t为3.3+/-1.0 mmol/L，最大转运速率与CMRglc的比值T-max/CMRglc为2.7+/-0.1，与作者以前的人体数据相当。这表明葡萄糖在人和大鼠体内的转运动力学是相似的。同时测定脑血流量，血糖控制在2 mmol/L以上，血糖浓度为73+/-6mL100g(-1)min(-1)。通过对低血糖的可逆Michaelis-Menten模型的外推，正确地预测了脑内葡萄糖浓度趋近于零的血糖浓度(2.1+/-0.6 mmol/L)。在这一点上，CBF大幅增加了57%+/-22%。这表明，大脑葡萄糖浓度是触发防御机制的信号，目的是在低血糖期间改善葡萄糖向大脑的输送。
Glucose is the major substrate that sustains normal brain function. When the brain glucose concentration approaches zero, glucose transport across the blood-brain barrier becomes rate limiting for metabolism during. for example, increased metabolic activity and hypoglycemia. Steady-state brain glucose concentrations: in alpha -chloralose anesthetized rats were measured noninvasively as a function of plasma glucose. The relation between brain and plasma glucose was linear at 4.5 to 30 mmol/L plasma glucose, which is consistent with the reversible Michaelis-Menten model. When the model was fitted to the brain glucose measurements, the apparent Michaelis-Menten constant, K-t, was 3.3 +/- 1.0 mmol/L, and the ratio of the maximal transport rate relative to CMRglc, T-max/CMRglc, was 2.7 +/- 0.1, This K-t is comparable to the authors' previous human data. suggesting that glucose transport kinetics in humans and rats are similar. Cerebral blood flow (CBF) was simultaneously assessed and constant above 2 mmol/L plasma glucose at 73 +/- 6 mL 100 g(-1) min(-1). Extrapolation of the reversible Michaelis-Menten model to hypoglycemia correctly predicted the plasma glucose concentration (2.1 +/- 0.6 mmol/L) at which brain glucose concentrations approached zero. At this point, CBF increased sharply by 57% +/- 22%. suggesting that brain glucose concentration is the signal that triggers defense mechanisms aimed at improving glucose delivery to the brain during hypoglycemia.