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Assessment of Gastric Emptying in Non-obese Diabetic Mice Using a [13C]-octanoic Acid Breath Test
Published on: March 23, 2013
Impaired neural pathway in gastric muscles of patients with diabetes
Yang Won Min1, Eun-Ju Ko2, Ji-Yeon Lee2
1Department of Medicine, Sungkyunkwan University School of Medicine, Seoul, Korea.
Abstract:
To explore the pathogenic mechanism of diabetic gastropathy, we investigated differences in response to electrical field stimulation (EFS) of gastric muscles from diabetic and non-diabetic (control) patients. Gastric specimens were obtained from 34 patients and 45 controls who underwent gastrectomy for early gastric cancer. Using organ bath techniques, we examined peak and nadir values of contraction under EFS. To examine responses to purinergic and nitrergic inhibition without cholinergic innervation, atropine, MRS2500, and N-nitro-L-arginine (L-NNA) were added sequentially to the organ bath. Tetrodotoxin (TTX) was used to confirm that the responses to EFS were mediated via neural stimulation. In the absence of pharmacological agents, peak contraction amplitude was greater in non-diabetic controls compared to diabetics only in the distal longitudinal gastric muscles. However, the nadir was greater in controls than in patients in both proximal and distal gastric circular muscles. Addition of MRS2500 could not decrease the nadir in both controls and patients, both in the proximal and distal stomach. However, L-NNA completely reversed the relaxation. TTX had no further effect on nadir. In conclusion, impaired inhibitory nitrergic neural pathway in both proximal and distal stomach and impaired excitatory cholinergic neural pathway in the distal stomach may contribute to the pathogenic mechanism underlying diabetic gastropathy.
Insights
Diabetic gastropathy involves impaired stomach muscle function due to damaged nitrergic and cholinergic pathways. This study found reduced nerve-mediated contractions in diabetic patients, impacting gastric motility.
Area of Science:
- Gastroenterology
- Diabetology
- Neurogastroenterology
Background:
- Diabetic gastropathy is a complication of diabetes mellitus affecting gastric motility.
- The precise mechanisms underlying diabetic gastropathy remain incompletely understood.
- Gastric muscle dysfunction is a key feature, but neural pathway involvement needs further elucidation.
Purpose of the Study:
- To investigate the pathogenic mechanisms of diabetic gastropathy.
- To compare gastric muscle responses to electrical field stimulation (EFS) in diabetic and non-diabetic individuals.
- To elucidate the roles of nitrergic and cholinergic pathways in diabetic gastric dysfunction.
Main Methods:
- Gastric specimens from 34 diabetic patients and 45 controls were analyzed using organ bath techniques.
- Electrical field stimulation (EFS) assessed gastric muscle contraction.
- Pharmacological agents including atropine, MRS2500, N-nitro-L-arginine (L-NNA), and tetrodotoxin (TTX) were used to probe neural pathways.
Main Results:
- Diabetic patients exhibited impaired inhibitory nitrergic neural pathways in both proximal and distal stomach.
- An impaired excitatory cholinergic neural pathway was observed in the distal stomach of diabetic patients.
- Nadir contraction values were significantly greater in controls than diabetics in both proximal and distal gastric circular muscles.
Conclusions:
- Impaired inhibitory nitrergic pathways contribute to diabetic gastropathy.
- Impaired excitatory cholinergic pathways in the distal stomach also play a role.
- These neural deficits likely underlie the gastric motility disturbances seen in diabetic gastropathy.
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