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首页> 外文期刊>American Journal of Physiology >Counterregulatory deficits occur within 24 h of a single hypoglycemic episode in conscious, unrestrained, chronically cannulated mice.
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Counterregulatory deficits occur within 24 h of a single hypoglycemic episode in conscious, unrestrained, chronically cannulated mice.

机译：在有意识的，不受约束的，慢性插管的小鼠中，单次降血糖发作后24小时内就会出现反调节缺陷。

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Hypoglycemia-induced counterregulatory failure is a dangerous complication of insulin use in diabetes mellitus. Controlled hypoglycemia studies in gene knockout models, which require the use of mice, would aid in identifying causes of defective counterregulation. Because stress can influence counterregulatory hormones and glucose homeostasis, we developed glucose clamps with remote blood sampling in conscious, unrestrained mice. Male C57BL/6 mice implanted with indwelling carotid artery and jugular vein catheters were subjected to 2 h of hyperinsulinemic glucose clamps 24 h apart, with a 6-h fast before each clamp. On day 1, blood glucose was maintained (euglycemia, 178 +/- 4 mg/dl) or decreased to 62 +/- 1 mg/dl (hypoglycemia) by insulin (20 mU x kg(-1) x min(-1)) and variable glucose infusion. Donor blood was continuously infused to replace blood sample volume. Baseline plasma epinephrine (32 +/- 8 pg/ml), corticosterone (16.1 +/- 1.8 microg/dl), and glucagon (35 +/- 3 pg/ml) were unchanged during euglycemia but increased significantly during hypoglycemia, with a glycemic threshold of approximately 80 mg/dl. On day 2, all mice underwent a hypoglycemic clamp (blood glucose, 64 +/- 1 mg/dl). Compared with mice that were euglycemic on day 1, previously hypoglycemic mice had significantly higher glucose requirements and significantly lower plasma glucagon and corticosterone (n = 6/group) on day 2. Epinephrine tended to decrease, although not significantly, in repeatedly hypoglycemic mice. Pre- and post-clamp insulin levels were similar between groups. We conclude that counterregulatory responses to acute and repeated hypoglycemia in unrestrained, chronically cannulated mice reproduce aspects of counterregulation in humans, and that repeated hypoglycemia in mice is a useful model of counterregulatory failure.
机译：低血糖引起的反调节衰竭是糖尿病患者使用胰岛素的危险并发症。需要使用小鼠的基因敲除模型中的对照低血糖研究将有助于确定不良调控的原因。由于压力会影响调节激素和葡萄糖稳态，因此我们开发了葡萄糖钳夹，可以对有意识且不受约束的小鼠进行远程血液采样。植入有留置颈动脉和颈静脉导管的雄性C57BL / 6小鼠每隔24小时接受2小时的高胰岛素葡萄糖钳夹，每个钳夹之前禁食6小时。在第1天，通过胰岛素（20 mU x kg（-1）x min（-1）维持血糖（血糖正常，178 +/- 4 mg / dl）或降至血糖62 +/- 1 mg / dl（低血糖） ））和可变葡萄糖输注。连续注入捐献者血液以代替血液样本量。基线血浆肾上腺素（32 +/- 8 pg / ml），皮质酮（16.1 +/- 1.8 microg / dl）和胰高血糖素（35 +/- 3 pg / ml）在正常血糖期间不变，但在低血糖期间显着增加。血糖阈值约为80 mg / dl。在第2天，所有小鼠均进行降血糖钳制（血糖为64 +/- 1 mg / dl）。与在第1天正常血糖的小鼠相比，以前的低血糖小鼠在第2天的葡萄糖需求量显着更高，而血浆胰高血糖素和皮质酮的水平则显着降低（n = 6 /组）。两组之间的钳夹前后胰岛素水平相似。我们得出结论，在不受约束的慢性插管小鼠中，对急性和反复性低血糖的反调节反应在人类中再现了反调节的方面，并且在小鼠中反复的低血糖是反调节失败的有用模型。

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