Diabetes mellitus and the stomach

Abstract

Many patients with diabetes mellitus complain of early satiety and postprandial gastric fullness. In 1945, these symptoms were first found to result from a gastric motor dysfunction which makes the delivery of ingesta into the small intestine, the time of their absorption and the related blood-glucose rise unpredictable. Consequently, insulin or hypoglycaemic agents are administered at inappropriate time points and poor glycaemic control ensues. About 50% of patients with Type I (insulin-dependent) and Type II (non-insulin-dependent) diabetes mellitus are affected. Hyperglycaemia may play an important role in the disorder: gastric emptying was found to be slower in states of induced hyperglycaemia than in euglycaemia. However, significantly reduced blood-glucose concentrations after therapy readjustment were not associated with an increase in emptying rate. Prolonged hyperglycaemia could alter nerve metabolism and contribute to the development of neuropathy. Severity of cardiovascular autonomic neuropathy, but not actual blood-glucose and glycated haemoglobin level, has been found to correlate with the degree of emptying impairment. Drugs enhancing gastric emptying could improve the coordination between insulin administration and the onset of nutrient absorption and thus glycaemic control. Disappointingly, trials to study the long-term effects of such drugs are scarce and their results predominantly negative. In conclusion, many diabetic patients have impaired gastric motor function 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 topics.