Berne C
Department of Internal Medicine, University Hospital, Uppsala, Sweden.
Diabet Med. 1996 Sep;13(9 Suppl 5):S28-30.
The following studies show that insulin-induced hypoglycaemia increases the gastric emptying rate for both liquids and solid food in healthy volunteers and in patients with IDDM of short duration. This response to low blood glucose concentrations may help protect against sustained hypoglycaemia by increasing the uptake of ingested carbohydrates. The results suggest that gastric emptying in patients with diabetes should be examined under conditions that are standardized with respect to blood glucose concentration. The finding that cholinergic muscarinic blockade with atropine inhibited the hypoglycaemia-induced acceleration of gastric emptying indicates that vagal stimulation plays an important role in this mechanism. The fact that plasma pancreatic polypeptide concentrations were unchanged during hypoglycaemic episodes in the presence of atropine indicates that complete inhibition of the cholinergic transmission was achieved. It is not yet established whether hypoglycaemia directly stimulates vagal activity or whether this is achieved through the activation of hormones or other second messengers. It is likely, however, that vagal activity is an important determinant of the varying rate of gastric emptying at different glycaemic levels. The pancreatic polypeptide response in the atropine-treated subjects resembles that seen in diabetic patients with autonomic neuropathy when exposed to insulin-induced hypoglycaemia. Disturbances of vagal function are frequent in diabetic patients with autonomic neuropathy, and can lead to a reduction in the stimulated gastric output. A failure to increase gastric emptying in response to hypoglycaemia would be disadvantageous when ingestion of oral carbohydrates is used to restore normoglycaemia, and diabetic patients with autonomic neuropathy could therefore be at increased risk for severe hypoglycaemia. The influence of glycaemia on vagal activity and gastric emptying rate probably alters the optimal time interval between insulin injections and postprandial increases in the blood glucose concentration in patients treated with short-acting insulin administered at mealtimes. This may cause variations in blood glucose concentrations. Furthermore, it is possible that drugs that have anticholinergic effects (such as tricyclic antidepressants) may deleteriously decrease the gastric emptying rate during hypoglycaemia in diabetic patients.
以下研究表明,胰岛素诱导的低血糖会增加健康志愿者和病程较短的胰岛素依赖型糖尿病(IDDM)患者液体和固体食物的胃排空率。这种对低血糖浓度的反应可能通过增加摄入碳水化合物的吸收来帮助预防持续性低血糖。结果表明,糖尿病患者的胃排空应在血糖浓度标准化的条件下进行检查。用阿托品进行胆碱能毒蕈碱阻断可抑制低血糖诱导的胃排空加速,这一发现表明迷走神经刺激在该机制中起重要作用。在存在阿托品的低血糖发作期间血浆胰多肽浓度未发生变化,这一事实表明实现了胆碱能传递的完全抑制。低血糖是否直接刺激迷走神经活动,或者这是否通过激素或其他第二信使的激活来实现,目前尚未确定。然而,迷走神经活动很可能是不同血糖水平下胃排空率变化的重要决定因素。阿托品治疗的受试者的胰多肽反应类似于患有自主神经病变的糖尿病患者在接受胰岛素诱导的低血糖时所观察到的反应。自主神经病变的糖尿病患者经常出现迷走神经功能障碍,并可能导致刺激的胃输出减少。当使用口服碳水化合物来恢复血糖正常时,未能因低血糖而增加胃排空将是不利的,因此患有自主神经病变的糖尿病患者发生严重低血糖的风险可能会增加。血糖对迷走神经活动和胃排空率的影响可能会改变在用餐时注射短效胰岛素治疗的患者中胰岛素注射与餐后血糖浓度升高之间的最佳时间间隔。这可能会导致血糖浓度的变化。此外,具有抗胆碱能作用的药物(如三环类抗抑郁药)可能会在糖尿病患者低血糖期间有害地降低胃排空率。