Augmented gastrin responses in diabetic patients with vagal neuropathy

Kanatsuka, Azuma; Osegawa, Masaaki; An, Trusov; Suzuki, Tsuneo; Hashimoto, Naotake; Makino, Hideichi

doi:10.1007/bf00262219

Cited by 15 publications

(8 citation statements)

References 16 publications

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“…[13][14][15] Thus, when the branches of the vagus that innervate the heart are affected, the more distal branches of the vagus, such as the gastric nerve, are affected. [16][17][18][19][20] Cardio-vagal neuropathy was based on heart rate (HR) variability in response to deep breathing. Heart rate was recorded using a standard ECG monitor.…”

Section: Study Populationmentioning

confidence: 99%

Effects of glucagon‐like peptide‐1 and feeding on gastric volumes in diabetes mellitus with cardio‐vagal dysfunction

Delgado-Aros

Vella

Camilleri

et al. 2003

Neurogastroenterology Motil

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Glucagon-like peptide-1 (GLP-1) increases gastric volume in humans possibly through the vagus nerve. Gastric volume response to feeding is preserved after vagal denervation in animals. We evaluated gastric volume responses to GLP-1 and placebo in seven diabetic patients with vagal neuropathy in a crossover study. We also compared gastric volume response to feeding in diabetes with that in healthy controls. We measured gastric volume using SPECT imaging. Data are median (interquartile range). In diabetic patients, GLP-1 did not increase gastric volume during fasting [5 mL (-3; 30)] relative to placebo [4 mL (-14; 50) P = 0.5], or postprandially [Delta postprandial minus fasting volume 469 mL (383; 563) with GLP-1 and 452 mL (400; 493) with placebo P = 0.3]. Change in gastric volume over fasting in diabetic patients on placebo was comparable to that of healthy controls [452 mL (400; 493)], P = 0.5. In contrast to effects in health, GLP-1 did not increase gastric volume in diabetics with vagal neuropathy, suggesting GLP-1's effects on stomach volume are vagally mediated. Normal gastric volume response to feeding in diabetics with vagal neuropathy suggests that other mechanisms compensate for vagal denervation.

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Section: Study Populationmentioning

confidence: 99%

Effects of glucagon‐like peptide‐1 and feeding on gastric volumes in diabetes mellitus with cardio‐vagal dysfunction

Delgado-Aros

Vella

Camilleri

et al. 2003

Neurogastroenterology Motil

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“…tn the present study we have evaluated the integrity of the autonomic nervous system in gastroparesis in patients with type II diabetes using the aforementioned noninvasive methods, with a particular emphasis on gastric emptying rate and plasma concentrations of gastrin after a standard solid and liquid labeled with radionuclide meal to see whether the response of this substance may serve as a simple test to distinguish between patients with diabetes with AN and those without AN [10,11] …”

mentioning

confidence: 99%

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

Migdalis

Thomaides

Chairopoulos

et al. 2001

Clinical Autonomic Research

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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.

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“…The elevated gastrin concentrations cannot be explained by atrophic gastritis in this study since only one subject had this condition. However, the elevation could be a result of a disturbed feedback mechanism due to neuropathy in the stomach [6], vagal neuropathy [16,17], an increased quantity of gastrin cells in the stomach [43], reduced number of somatostatin cells [44], or hyperglycaemia [45]. …”

Section: Resultsmentioning

confidence: 99%

“…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].…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2009

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BackgroundGastrointestinal (GI) dysmotility and autonomic neuropathy are common problems among diabetics with largely unknown aetiology. Many peptides are involved in the autonomic nervous system regulating the GI tract. The aim of this study was to examine if concentrations of oxytocin, cholecystokinin (CCK), gastrin and vasopressin in plasma differ between diabetics with normal function and dysfunction in GI motility.MethodsNineteen patients with symptoms from the GI tract who had been examined with gastric emptying scintigraphy, oesophageal manometry, and deep-breathing test were included. They further received a fat-rich meal, after which blood samples were collected and plasma frozen until analysed for hormonal concentrations.ResultsThere was an increase in postprandial oxytocin plasma concentration in the group with normal gastric emptying (p = 0.015) whereas subjects with delayed gastric emptying had no increased oxytocin secretion (p = 0.114). Both CCK and gastrin levels increased after the meal, with no differences between subjects with normal respective delayed gastric emptying. The concentration of vasopressin did not increase after the meal. In patients with oesophageal dysmotility the basal level of CCK tended to be higher (p = 0.051) and those with autonomic neuropathy had a higher area under the curve (AUC) of gastrin compared to normal subjects (p = 0.007).ConclusionReduced postprandial secretion of oxytocin was found in patients with delayed gastric emptying, CCK secretion was increased in patients with oesophageal dysmotility, and gastrin secretion was increased in patients with autonomic neuropathy. The findings suggest that disturbed peptide secretion may be part of the pathophysiology of digestive complications in diabetics.

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Augmented gastrin responses in diabetic patients with vagal neuropathy

Cited by 15 publications

References 16 publications

Effects of glucagon‐like peptide‐1 and feeding on gastric volumes in diabetes mellitus with cardio‐vagal dysfunction

Effects of glucagon‐like peptide‐1 and feeding on gastric volumes in diabetes mellitus with cardio‐vagal dysfunction

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

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

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