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低胰岛素血症对人体从低血糖中恢复血糖并不关键。

Hypoinsulinemia is not critical to glucose recovery from hypoglycemia in humans.

作者信息

Heller S R, Cryer P E

机构信息

Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110.

出版信息

Am J Physiol. 1991 Jul;261(1 Pt 1):E41-8. doi: 10.1152/ajpendo.1991.261.1.E41.

DOI:10.1152/ajpendo.1991.261.1.E41
PMID:1858873
Abstract

To test the hypothesis that glucose recovery from hypoglycemia can occur in the absence of decrements in insulin below baseline, we studied nine normal humans on six occasions. In a control study, saline was infused. In five experimental studies, insulin (0.6 mU.kg-1.min-1) was infused from 0 to 80 min, to produce hypoglycemia (approximately 3.3 mM). Then, from 80 to 180 min, insulin was not infused or was infused in four different doses 0.1, 0.2, 0.4, and 0.6 mU.kg-1.min-1), and glucose recovery was assessed. In the recovery periods, approximately fourfold peripheral with approximately twofold portal insulin elevations prevented glucose recovery (glucose = 3.6 +/- 0.1 mM, counter-regulatory hormone levels elevated throughout). However, biological glucose recovery, documented by increments to 4.3 +/- 0.1 mM and decrements in all counterregulatory hormones (glucagon, epinephrine, growth hormone, and cortisol) to control levels, occurred despite nearly twofold peripheral hyperinsulinemia (54 +/- 4 vs. 32 +/- 4 pM, P less than 0.01) in the absence of portal hypoinsulinemia (58 +/- 4 vs. 68 +/- 8 pM). Thus we conclude that, although dissipation of insulin normally plays an important role in the correction of hypoglycemia, biological glucose recovery from hypoglycemia to glucose levels more than sufficient to disengage glucose counterregulatory systems and well above those required to produce symptoms of hypoglycemia can occur in the absence of decrements in portal insulin below baseline and despite mild peripheral hyperinsulinemia.

摘要

为了验证在胰岛素水平不降至基线以下的情况下低血糖症的葡萄糖恢复是否能够发生这一假设,我们对9名正常人进行了6次研究。在一项对照研究中,输注生理盐水。在五项实验研究中,在0至80分钟内输注胰岛素(0.6 mU·kg⁻¹·min⁻¹)以产生低血糖(约3.3 mM)。然后,在80至180分钟内,不输注胰岛素或以四种不同剂量(0.1、0.2、0.4和0.6 mU·kg⁻¹·min⁻¹)输注胰岛素,并评估葡萄糖恢复情况。在恢复期,外周胰岛素升高约四倍而门静脉胰岛素升高约两倍阻止了葡萄糖恢复(葡萄糖 = 3.6 ± 0.1 mM,整个过程中反向调节激素水平升高)。然而,尽管外周胰岛素血症几乎增加了两倍(54 ± 4对32 ± 4 pM,P < 0.01)且门静脉无胰岛素血症(58 ± 4对68 ± 8 pM),但仍出现了生物学上的葡萄糖恢复,表现为葡萄糖增加至4.3 ± 0.1 mM且所有反向调节激素(胰高血糖素、肾上腺素、生长激素和皮质醇)降至对照水平。因此我们得出结论,虽然胰岛素的消散通常在低血糖的纠正中起重要作用,但在门静脉胰岛素不降至基线以下且尽管存在轻度外周高胰岛素血症的情况下,低血糖症的生物学葡萄糖恢复仍可发生,使葡萄糖水平升高到足以解除葡萄糖反向调节系统且远高于产生低血糖症状所需的水平。

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Hypoglycemia-associated autonomic failure in insulin-dependent diabetes mellitus. Recent antecedent hypoglycemia reduces autonomic responses to, symptoms of, and defense against subsequent hypoglycemia.胰岛素依赖型糖尿病中与低血糖相关的自主神经功能衰竭。近期发生的低血糖会降低自主神经对后续低血糖的反应、症状及防御能力。
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