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Radiosynthesis of 1-2-[18F]Fluoroethyl-L-Tryptophan using a One-pot, Two-step Protocol
Published on: September 21, 2021
Tryptophan Metabolites in Irritable Bowel Syndrome: An Overnight Time-course Study
Robert L Burr1,2, Haiwei Gu3, Kevin Cain2,4
1Department of Biobehavioral Nursing and Health Informatics, University of Washington, Seattle, WA, USA.
Poor sleep in irritable bowel syndrome (IBS) may be linked to altered tryptophan metabolites. Specific metabolites like nicotinamide and indole-3-lactic acid differed between IBS patients and healthy controls, suggesting a role in sleep disturbances.
Area of Science:
- Gastroenterology
- Neuroscience
- Metabolomics
Background:
- Irritable bowel syndrome (IBS) is frequently associated with poor sleep quality.
- The relationship between sleep disturbances and tryptophan (Trp) metabolites in IBS remains largely unexplored.
Purpose of the Study:
- To compare serum Trp metabolite profiles in women with IBS and healthy controls (HCs).
- To investigate associations between Trp metabolites, IBS symptoms, sleep indices, and stress markers (cortisol, ACTH) in IBS patients.
Main Methods:
- Targeted liquid chromatography mass spectrometry (LC-MS) profiling of serum Trp metabolites.
- Blood samples collected over 80-minute intervals during a sleep laboratory protocol following a stressor in 38 IBS subjects and 21 HCs.
- Analysis of metabolite levels across different sleep stages and correlation with symptom diaries, sleep measures, and hormonal data.
Main Results:
- Significant differences in Trp metabolite profiles were observed between IBS patients and HCs (P = 0.014).
- IBS patients exhibited higher nicotinamide and lower indole-3-lactic acid levels compared to HCs.
- Melatonin and indole-3-acetic acid levels correlated with sleep measures, while kynurenine and kynurenic acid showed associations with ACTH and cortisol/ACTH ratios.
Conclusions:
- Nighttime tryptophan metabolite patterns may offer insights into the interplay of poor sleep and stress in IBS.
- Further research into the mechanistic roles of these metabolites in IBS pathophysiology is warranted.
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