Changes of gastric emptying rate and gastrin levels are early indicators of autonomic neuropathy in type II diabetic patients

Abstract

The authors investigated the effect of a balanced meal on gastric emptying rate and gastrin plasma concentrations in patients with type II diabetes and autonomic neuropathy, in diabetic patients without autonomic neuropathy, and in healthy subjects (controls). Before food the gastrin plasma concentrations were higher in patients with diabetes with autonomic neuropathy. After food, gastric emptying rate was slower in patients with diabetes with autonomic neuropathy, whereas gastrin plasma concentrations increased in 30 minutes in all groups but to a greater extent in patients with diabetes with autonomic neuropathy. Sixty minutes after food, there was a significant decrease in gastrin plasma concentrations in patients with diabetes with autonomic neuropathy, compared with the other two groups. These data suggest that in patients with type II diabetes with autonomic neuropathy, food causes slower gastric emptying and different plasma gastrin level responses from those in patients with type II diabetes without autonomic neuropathy and controls. There are therefore differences in the responses to food ingestion between these groups because of vagal denervation induced by autonomic neuropathy. These tests should be reserved for patients with symptoms suggestive of disturbed gastric emptying, or for patients with autonomic neuropathy without symptoms of gastroparesis.

Gastroparesis is associated with oxytocin deficiency, oesophageal dysmotility with hyperCCKemia, and autonomic neuropathy with hypergastrinemia

“…This process is regulated by a negative feedback mechanism to prevent excessive acid secretion. In accordance with earlier studies we found that patients with autonomic neuropathy have significantly higher concentrations of gastrin in plasma [16-18,20]. The elevated gastrin concentrations cannot be explained by atrophic gastritis in this study since only one subject had this condition.…”

“…Cholecystokinin (CCK) and gastrin are released from endocrine cells in the upper GI tract in response to food, and they influence relaxation of the lower oesophageal sphincter (LOS), gastric acid secretion, gastric emptying, growth of gastric mucosa, contraction of the gallbladder, pancreatic growth, enzyme secretion, and intestinal motility [14,15]. Earlier studies have reported increased CCK and gastrin concentrations in plasma from diabetics with autonomic neuropathy [16-20], whereas patients without neuropathy showed normal concentrations, irrespective of GI function [17,19-21]. Recently, receptors for vasopressin, a peptide hormone homologous to oxytocin, have also been found in the GI tract [22], and vasopressin has been shown to affect the electrical rhythm in the human stomach [23,24].…”

Gastroparesis in type 2 diabetes mellitus: Prevalence, etiology, diagnosis, and treatment

“…In 34 individuals with T2DM, the gastric emptying rate was slower in the group with CAN (n=16) compared to the group without CAN (n=18) and the control subjects (n=18) [37]. Furthermore, a positive correlation was found between degree of autonomic dysfunction and gastric emptying rate for both solids and liquids.…”

Unanticipated full stomach at anesthesia induction in a type I diabetic patient with asymptomatic gastroparesis

“…In our case, the patient had none of these symptoms and hence had never been diagnosed as having diabetic gastroparesis. However, recent studies have suggested that slowed gastric emptying is present in patients with autonomic neuropathy without any symptoms of gastroparesis [3]. Furthermore, the relation between symptoms and the rate of gastric emptying is weak, and the mechanisms by which abnormal motility causes symptoms are unclear [4][5][6].…”