Frier B M, Fisher B M, Gray C E, Beastall G H
Diabetic Department, Western Infirmary, Glasgow, UK.
Diabetologia. 1988 Jul;31(7):421-9. doi: 10.1007/BF00271586.
Acute insulin-induced hypoglycaemia in humans provokes autonomic neural activation and counterregulatory hormonal secretion mediated in part via hypothalamic stimulation. Many patients with Type 1 (insulin-dependent) diabetes have acquired deficiencies of counterregulatory hormonal release following hypoglycaemia. To study the integrity of the hypothalamic-pituitary and the sympatho-adrenal systems, the responses of pituitary hormones, beta-endorphin, glucagon and adrenaline to acute insulin-induced hypoglycaemia (0.2 units/kg) were examined in 16 patients with Type 1 diabetes who did not have autonomic neuropathy. To examine the effect of duration of diabetes these patients were subdivided into two groups (Group 1: 8 patients less than 5 years duration; Group 2: 8 patients greater than 15 years duration) and were compared with 8 normal volunteers (Group 3). The severity and time of onset of hypoglycaemia were similar in all 3 groups, but mean blood glucose recovery was slower in the diabetic groups (p less than 0.01). The mean responses of glucagon, adrenaline, adrenocorticotrophic hormone, prolactin and beta-endorphin were similar in all 3 groups, but the mean responses of growth hormone were lower in both diabetic groups than in the normal group (p less than 0.05). The mean increments of glucagon and adrenaline in the diabetic groups were lower than the normal group, but these differences did not achieve significance; glucagon secretion was preserved in several diabetic patients irrespective of duration of disease. Various hormonal responses to hypoglycaemia were absent or diminished in individual diabetic patients, and multiple hormonal deficiencies could be implicated in delaying blood glucose recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
人体急性胰岛素诱导的低血糖会引发自主神经激活和反调节激素分泌,部分是通过下丘脑刺激介导的。许多1型(胰岛素依赖型)糖尿病患者在低血糖后出现了反调节激素释放不足的情况。为了研究下丘脑 - 垂体和交感 - 肾上腺系统的完整性,对16例无自主神经病变的1型糖尿病患者进行了垂体激素、β - 内啡肽、胰高血糖素和肾上腺素对急性胰岛素诱导的低血糖(0.2单位/千克)反应的研究。为了研究糖尿病病程的影响,这些患者被分为两组(第1组:8例病程小于5年;第2组:8例病程大于15年),并与8名正常志愿者(第3组)进行比较。三组患者低血糖的严重程度和发作时间相似,但糖尿病组的平均血糖恢复较慢(p < 0.01)。三组中胰高血糖素、肾上腺素、促肾上腺皮质激素、催乳素和β - 内啡肽的平均反应相似,但两组糖尿病患者生长激素的平均反应均低于正常组(p < 0.05)。糖尿病组中胰高血糖素和肾上腺素的平均增量低于正常组,但这些差异无统计学意义;无论病程长短,部分糖尿病患者的胰高血糖素分泌仍得以保留。个别糖尿病患者对低血糖的各种激素反应缺失或减弱,多种激素缺乏可能与血糖恢复延迟有关。(摘要截取自250词)