Diabetes and the gut.

Progress report Diabetes and the gutThe pathophysiology of impaired gastrointestinal function in both chronic diabetes1' 2, and acute ketoacidosis3, remains undefined, although several mechanisms have been implicated.These include autonomic neuropathy4, microangiopathy5, changes in insulin and glucagon release, and acute metabolic disturbance.In recent years various new gastrointestinal hormones have been described6' 7, although their physiological importance remains to be determined8.It is likely that both the chronic, and acute, metabolic changes found in diabetes will modify the release of these hormones and alter their effects on the gut.However, at the present time there are no studies of gut hormone levels in diabetics with gastrointestinal complications and the pathophysiological significance of these substances remains ill-defined.This review will consider both the acute and chronic effects of diabetes mellitus on the gastrointestinal tract alone and will largely be confined to human data. Acute manifestationsAnorexia, nausea, and vomiting are common presenting features of diabetic ketoacidosis3'9.The aetiology of these symptoms is frequently attributed to acute gastric stasis and nasogastric suction has been advocated as a routine procedure in the emergency treatment of these patients10'11, although there is no general agreement on this12.The frequency of clinically significant gastric dilatation in such patients is unknown and there is no detailed study of gastric emptying during ketoacidosis.The aetiology of acute gastric dilatation during ketoacidosis is unknown, although acute metabolic changes including glucagon and insulin release have been implicated13 4. It has also been suggested that gastric atony results from an acute, reversible, autonomic disturbance'5.The effects of local gastrointestinal hormones on gastric motility have been incompletely studied and, to date, only motilin has been found to increase gastric emptying6"16, but has not been implicated in this context.Possibly the acute electrolyte changes of ketoacidosis, especially intracellular hypokalaemia, affect gastric motility.Acute gastroparesis has also been described in recent onset diabetics after sudden stress in whom there was no acute metabolic disturbance'7.Haematemesis as a complication of diabetic ketoacidosis is usually secondary to either acute erosive, or haemorrhagic, gastritis.It has been suggested that this results from an increased concentration of urea in the retained gastric fluid18.The incidence of duodenal ulceration is thought to be reduced among diabetics'920, although there is some conflicting evidence for this21, and it is rarely responsible for haematemesis in these subjects.Acute abdominal pain, in the absence of intra-abdominal disease, may occur in these patients and can be of sufficient severity to mimic an acute 1153