Meneilly G S, Cheung E, Tuokko H
Department of Medicine, University of British Columbia, Vancouver.
J Clin Endocrinol Metab. 1994 Jun;78(6):1341-8. doi: 10.1210/jcem.78.6.8200936.
Many elderly people are treated with medications or are subjected to diseases which can cause hypoglycemia. We conducted the following studies to assess whether alterations in counterregulatory hormone release, decreased awareness of warning symptoms or alterations in psychomotor performance might increase the susceptibility of the elderly to hypoglycemia. Healthy, nonobese young (n = 10, age < 30) and old (n = 9, age > 65) subjects underwent paired hyperinsulinaemic clamp studies (insulin infusion rate 60 mU/m2.min). In the control study, glucose was kept at 5.0 mmol/L for 5 h. In the hypoglycemic study, glucose was kept at 5 mmol/L for 1 h and was lowered in stepwise fashion to 4.4, 3.8, 3.3, and 2.8 mmol/L in each subsequent hour. Subjects were blinded as to which study they were undergoing. Counterregulatory hormones were measured and a hypoglycemic symptom checklist was administered every 15 min in each study. Neuropsychological tests were performed at regular intervals. The glucose threshold for release of counterregulatory hormones was defined as the glucose level at which the values during the hypoglycemic study first exceeded values during the control study by 2 SD. The glucose threshold for glucagon and epinephrine release was higher in the young (approximately 3.3 mmol/L) than the old (approximately 2.8 mmol/L) and the epinephrine responses to hypoglycemia were also greater in the young. The threshold for release of GH (approximately 3.3 mmol/L) and norepinephrine and cortisol (approximately 2.8 mmol/L) was similar in each age group, as was the magnitude of release of these hormones. Although the variance in symptoms scores was large, the elderly appeared to have reduced awareness of the autonomic but not neuroglycopenic symptoms of hypoglycemia. There was no difference between young and old in the effect of hypoglycemia on neuropsychologic tests. We conclude that healthy elderly people may have impaired release of glucagon and epinephrine in response to hypoglycemia and reduced awareness of the autonomic symptoms of hypoglycemia.
许多老年人接受药物治疗或患有可导致低血糖的疾病。我们进行了以下研究，以评估反调节激素释放的改变、对警告症状的意识降低或精神运动表现的改变是否会增加老年人对低血糖的易感性。健康、非肥胖的年轻受试者（n = 10，年龄<30岁）和老年受试者（n = 9，年龄>65岁）接受了配对的高胰岛素钳夹研究（胰岛素输注速率为60 mU/m2.min）。在对照研究中，血糖维持在5.0 mmol/L 5小时。在低血糖研究中，血糖先维持在5 mmol/L 1小时，随后每小时逐步降至4.4、3.8、3.3和2.8 mmol/L。受试者对自己所参与的研究不知情。在每项研究中，每15分钟测量一次反调节激素，并发放一份低血糖症状清单。定期进行神经心理学测试。反调节激素释放的血糖阈值定义为低血糖研究期间的值首次超过对照研究期间的值2个标准差时的血糖水平。年轻受试者中胰高血糖素和肾上腺素释放的血糖阈值（约3.3 mmol/L）高于老年受试者（约2.8 mmol/L），并且年轻受试者对低血糖的肾上腺素反应也更大。生长激素（约3.3 mmol/L）、去甲肾上腺素和皮质醇（约2.8 mmol/L）释放的阈值在每个年龄组中相似，这些激素的释放幅度也相似。尽管症状评分的差异很大，但老年人似乎对低血糖的自主神经症状而非神经低血糖症状的意识降低。低血糖对神经心理学测试的影响在年轻人和老年人之间没有差异。我们得出结论，健康的老年人在低血糖反应时可能胰高血糖素和肾上腺素释放受损，并且对低血糖的自主神经症状意识降低。
