Enteroendocrine signaling in irritable bowel syndrome: beyond cell counts toward stimulus-responsive physiological profiling
- 1College of Traditional Chinese Medicine, Changchun University of Chinese Medicine, Changchun, Jilin, China
- 2The Affiliated Hospital of Changchun University of Chinese Medicine, Changchun, Jilin, China
Abstract
Meals are a major symptom trigger in irritable bowel syndrome (IBS), yet the endocrine steps linking luminal nutrients to pain, bloating, urgency, and altered bowel habits remain poorly defined. Early studies relied heavily on mucosal enteroendocrine cell (EEC) counts. Those observations remain informative, particularly in post-infectious IBS, but findings vary with intestinal site, bowel-habit phenotype, staining, and morphometry, and cell abundance does not measure secretory function. Human meal-challenge studies distinguish circulating concentrations from stimulus-evoked responses. In IBS with diarrhea, higher fasting and fed plasma 5-hydroxytryptamine (serotonin, 5-HT) may reflect altered handling more than a uniformly exaggerated postprandial response, whereas IBS with constipation can show impaired stimulus-evoked release. Cholecystokinin, peptide YY, motilin, ghrelin, and related peptides also vary with sex, bowel habit, and visceral sensitivity. Recent human organoid and transcriptomic studies identify distinct nutrient-sensing programs among EEC subtypes and provide a cellular framework for this heterogeneity. We integrate these findings across luminal sensing, secretion, metabolism, receptor responsiveness, and motor or sensory output. The evidence does not support a single IBS endocrine signature. Standardized nutrient challenges linked to serial hormone measurements, mucosal molecular data, and objective physiological readouts are more likely to yield reproducible and clinically testable response patterns.
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BibTeX
@article{han2026enteroendocrine,
title = {{Enteroendocrine signaling in irritable bowel syndrome: beyond cell counts toward stimulus-responsive physiological profiling}},
author = {Jiayi Han and Yixuan Lang and Kangmeng Yao and Jia Mi},
journal = {Frontiers in Medicine},
year = {2026},
month = oct,
doi = {10.3389/fmed.2026.1992567},
url = {https://doi.org/10.3389/fmed.2026.1992567},
note = {CC BY},
}
RIS
TY - JOUR
TI - Enteroendocrine signaling in irritable bowel syndrome: beyond cell counts toward stimulus-responsive physiological profiling
AU - Jiayi Han
AU - Yixuan Lang
AU - Kangmeng Yao
AU - Jia Mi
PY - 2026
DA - 2026/10/23
JO - Frontiers in Medicine
DO - 10.3389/fmed.2026.1992567
UR - https://doi.org/10.3389/fmed.2026.1992567
AB - Meals are a major symptom trigger in irritable bowel syndrome (IBS), yet the endocrine steps linking luminal nutrients to pain, bloating, urgency, and altered bowel habits remain poorly defined. Early studies relied heavily on mucosal enteroendocrine cell (EEC) counts. Those observations remain informative, particularly in post-infectious IBS, but findings vary with intestinal site, bowel-habit phenotype, staining, and morphometry, and cell abundance does not measure secretory function. Human meal-challenge studies distinguish circulating concentrations from stimulus-evoked responses. In IBS with diarrhea, higher fasting and fed plasma 5-hydroxytryptamine (serotonin, 5-HT) may reflect altered handling more than a uniformly exaggerated postprandial response, whereas IBS with constipation can show impaired stimulus-evoked release. Cholecystokinin, peptide YY, motilin, ghrelin, and related peptides also vary with sex, bowel habit, and visceral sensitivity. Recent human organoid and transcriptomic studies identify distinct nutrient-sensing programs among EEC subtypes and provide a cellular framework for this heterogeneity. We integrate these findings across luminal sensing, secretion, metabolism, receptor responsiveness, and motor or sensory output. The evidence does not support a single IBS endocrine signature. Standardized nutrient challenges linked to serial hormone measurements, mucosal molecular data, and objective physiological readouts are more likely to yield reproducible and clinically testable response patterns.
SN - 2296-858X
ER -