Briscoe Vanessa Jones, Tate Donna Bowman, Davis Stephen Neil
Division of Diabetes, Endocrinology, and Metabolism, Vanderbilt University Medical Center, 715 Preston Research Building, Nashville, TN 37232-6303, USA.
Appl Physiol Nutr Metab. 2007 Jun;32(3):576-82. doi: 10.1139/H07-025.
The Diabetes Control and Complications Trial demonstrated that tight control of diabetes management greatly reduces the risk of microvascular complications of diabetes. Unfortunately, tight control of blood glucose can also result in hypoglycemia, especially in patients with type 1 diabetes mellitus (T1DM). It is now widely recognized that antecedent hypoglycemia can blunt neuroendocrine, autonomic nervous system (ANS), and metabolic counterregulatory responses to subsequent hypoglycemia. Thus, blunted counterregulatory defenses against falling plasma glucose levels are a major risk factor for hypoglycemia in people with diabetes. This risk is also complicated by a difference in responses between males and females. Because of the qualitative similarity of neuroendocrine, ANS, and metabolic responses to hypoglycemia and exercise, we developed studies to determine whether neuroendocrine and ANS counterregulatory dysfunction play a role in the pathogenesis of exercise-related hypoglycemia in T1DM. Results from these studies have shown that neuroendocrine (catecholamine and glucagon), ANS (muscle sympathetic nerve activity), and metabolic (lipolysis and glucose kinetics) responses are blunted during exercise after antecedent hypoglycemia, and that there is a sexual dimorphism in responses. Similarly, antecedent episodes of exercise can blunt counterregulatory responses during subsequent hypoglycemia, thereby creating reciprocal feed-forward vicious cycles that increase the risk of hypoglycemia during either stress.
糖尿病控制与并发症试验表明，严格控制糖尿病管理可大大降低糖尿病微血管并发症的风险。不幸的是，严格控制血糖也可能导致低血糖，尤其是在1型糖尿病（T1DM）患者中。现在人们普遍认识到，先前发生的低血糖会削弱神经内分泌、自主神经系统（ANS）以及对后续低血糖的代谢反调节反应。因此，针对血浆葡萄糖水平下降的反调节防御能力减弱是糖尿病患者发生低血糖的主要危险因素。男性和女性在反应上的差异也使这种风险变得更加复杂。由于神经内分泌、ANS和对低血糖及运动的代谢反应在性质上具有相似性，我们开展了研究，以确定神经内分泌和ANS反调节功能障碍是否在T1DM患者运动相关低血糖的发病机制中起作用。这些研究的结果表明，在先前发生低血糖后的运动过程中，神经内分泌（儿茶酚胺和胰高血糖素）、ANS（肌肉交感神经活动）和代谢（脂肪分解和葡萄糖动力学）反应均减弱，并且反应存在性别差异。同样，先前的运动发作也会削弱后续低血糖期间的反调节反应，从而形成相互促进的恶性循环，增加两种应激状态下发生低血糖的风险。
