Hypoglycaemia and Gastric Emptying

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.