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首页> 外文期刊>Diabetes >Effect of Antecedent Hypoglycemia on Counterregulatory Responses to Subsequent Euglycemic Exercise in Type 1 Diabetes
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Effect of Antecedent Hypoglycemia on Counterregulatory Responses to Subsequent Euglycemic Exercise in Type 1 Diabetes

机译：前期低血糖对1型糖尿病患者随后进行的正常血糖运动反调节反应的影响

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Exercise-related hypoglycemia is common in intensively treated patients with type 1 diabetes. The underlying mechanisms are not clearly defined. In nondiabetic subjects, hypoglycemia blunts Counterregulatory re-sponses to subsequent exercise. It is unknown whether this also occurs in type 1 diabetes. Therefore, the goal of this study was to test the hypothesis that prior hypoglycemia could result in acute Counterregulatory failure during subsequent exercise in type 1 diabetes. A total of 16 type 1 diabetic patients (8 men and 8 women, HbA_(1c) 7.8 +- 0.3%) were investigated during 90 min of euglycemic cycling exercise, following either two 2-h periods of previous-day hypoglycemia (2.9 mmol/1) or previous-day euglycemia. Patients' Counterregulatory responses (circulating levels of Counterregulatory hor-mones, intermediary metabolites, substrate flux via indirect calorimetry, tracer-determined glucose kinetics, and cardiovascular measurements) were comprehen-sively assessed during exercise. Identical euglycemia and basal insulin levels were successfully maintained during all exercise studies, regardless of blood glucose levels during the previous day. After resting euglycemia, patients displayed normal Counterregulatory responses to exercise. Conversely, when identical exercise was repeated after hypoglycemia, the glucagon response to exercise was abolished, and the epinephrine, norepi-nephrine, cortisol, endogenous glucose production, and lipolytic responses were reduced by 40-80%. This resulted in a threefold increase in the amount of exogenous glucose needed to maintain euglycemia during exercise. Our results demonstrate that antecedent hypoglycemia, in type 1 diabetes, can produce acute Counterregulatory failure during a subsequent episode of prolonged moderate-intensity exercise. The metabolic consequence of the blunted neuroendocrine and autonomic nervous system Counterregulatory responses was an acute failure of endogenous glucose production to match the increased glucose requirements during exer- cise. These data indicate that counterregulatory failure may be a significant in vivo mechanism responsible for exercise-associated hypoglycemia in type 1 diabetes.
机译：与运动有关的低血糖在1型糖尿病的强化治疗患者中很常见。尚无明确的基本机制。在非糖尿病患者中，低血糖会减弱对后续运动的反调节反应。目前尚不清楚这是否也会在1型糖尿病中发生。因此，本研究的目的是检验以下假设：先前的低血糖症可能导致1型糖尿病患者随后的运动期间出现急性反调节功能衰竭。在前两天的低血糖（2.9 mmol / L）的两个2小时周期内，共进行了90分钟的正常血糖循环运动，共研究了16名1型糖尿病患者（8名男性和8名女性，HbA_（1c）7.8±0.3％）。 / 1）或前一天的血糖正常。在运动过程中，全面评估了患者的反调节反应（反调节激素的循环水平，中间代谢物，间接量热法测定的底物通量，示踪剂测定的葡萄糖动力学和心血管测量结果）。在所有运动研究中，无论前一天血糖水平如何，均能成功维持相同的正常血糖和基础胰岛素水平。静息血糖正常后，患者对运动表现出正常的反调节反应。相反，当低血糖后重复相同的运动时，胰高血糖素对运动的反应被取消，肾上腺素，去甲肾上腺素，皮质醇，内源性葡萄糖生成和脂解反应降低了40-80％。这导致运动期间维持正常血糖所需的外源葡萄糖量增加了三倍。我们的结果表明，在1型糖尿病患者中，先前的低血糖症可在随后的中度长时间运动后发作，引起急性反调节功能衰竭。神经内分泌和自主神经系统钝化的代谢后果反调节反应是内源性葡萄糖产生的急性衰竭，无法适应运动中增加的葡萄糖需求。这些数据表明，反调节失败可能是导致1型糖尿病运动相关性低血糖的重要体内机制。

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