Diabetes mellitus and the stomach

Many patients with diabetes mellitus complain of early satiety and postpran dial gastric fullness. In 1945, these symptoms were first found to result f rom a gastric motor dysfunction which makes the delivery of ingesta into th e small intestine, the time of their absorption and the related blood-gluco se rise unpredictable. Consequently, insulin or hypoglycaemic agents are ad ministered at inappropriate time points and poor glycaemic control ensues. About 50 % of patients with Type I (insulin-dependent) and Type II(non-insu lin-dependent) diabetes mellitus are affected. Hyperglycaemia may play an i mportant role in the disorder: gastric emptying was found to be slower in s tates of induced hyperglycaemia than in euglycaemia. However, significantly reduced blood-glucose concentrations after therapy readjustment were not a ssociated with an increase in emptying rate. Prolonged hyperglycaemia could alter nerve metabolism and contribute to the development of neuropathy. Se verity of cardiovascular autonomic neuropathy, but not actual blood-glucose and glycated haemoglobin level, has been found to correlate with the degre e of emptying impairment. Drugs enhancing gastric emptying could improve th e coordination between insulin administration and the onset of nutrient abs orption and thus glycaemic control. Disappointingly, trials to study the lo ng-term effects of such drugs are scarce and their results predominantly ne gative. In conclusion, many diabetic patients have impaired gastric motor f unction which could contribute to poor glycaemic control. Evidence suggests that autonomic neuropathy is the main underlying factor. This review aims to offer a critical survey of all the data available at present on these to pics.