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Peer-reviewedCC BYFrontiers in physiology

Transcriptomic insights into loperamide-induced gastric dysmotility: RNA-seq analysis of a mouse model.

  • Chunggeon Lee1,2
  • Seung-Ju Hwang3
  • Young-Su Yang4
  • Bokyung Kim5
  • Dong-Seon Kim6
  • Daeui Park1,2
  • Chang-Woo Song2,5
  • Chang-Gue Son3
6 affiliations
  1. 1Center for National Toxicology AI and Data, Korea Institute of Toxicology, Daejeon, Republic of Korea.
  2. 2School of Korea Institute of Toxicology, University of Science and Technology, Daejeon, Republic of Korea.
  3. 3Institute of Bioscience & Integrative Medicine, Daejeon University, Daejeon, Republic of Korea.
  4. 4Division of Jeonbuk Advanced Bio Research, Korea Institute of Toxicology, Jeongeup, Republic of Korea.
  5. 5Translational Toxicology Technical Research Team, Division of Jeonbuk Advanced Bio Research, Korea Institute of Toxicology, Jeongeup, Republic of Korea.
  6. 6Korean Medicine Science Research Division, Korea Institute of Oriental Medicine, Daejeon, Republic of Korea.
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Abstract

Background

Loperamide, a μ-opioid receptor agonist that slows gastrointestinal transit, is widely used as an antidiarrheal agent and an experimental model of gastric dysmotility and functional dyspepsia (FD). However, transcriptomic alterations associated with loperamide-induced delayed gastric emptying remain poorly characterized. This study aimed to investigate gastric gene-expression profiles associated with loperamide-induced gastric dysmotility using RNA sequencing.Methods

Male BALB/c mice were intraperitoneally injected with loperamide after 20 h of fasting. Delayed gastric emptying was assessed in one cohort, while gastric antrum tissues from a separate cohort were collected for RNA sequencing. Differentially expressed genes (DEGs) were identified using fold change ≥1.5 and false discovery rate (FDR) <0.01. Gene set enrichment analysis (GSEA) and pathway-network analysis were conducted to characterize biological pathways associated with loperamide treatment.Results

Loperamide significantly delayed gastric emptying, as demonstrated by increased gastric retention of phenol red. Transcriptomic analysis identified 1,356 DEGs, including 553 upregulated and 803 downregulated genes. GSEA revealed enrichment of inflammatory response-related pathways among upregulated genes, whereas synaptic transmission- and calcium signaling-related pathways were predominantly downregulated. Representative genes involved in cholinergic signaling (Chrm2 and Chrna9), glutamatergic signaling (Grm7), and calcium-channel function (Cacna1a) showed reduced expression, while Il33 was increased.Conclusion

This study provides transcriptomic insights into loperamide-induced gastric dysmotility. The findings suggest coordinated downregulation of genes associated with neuronal/synaptic signaling together with enrichment of inflammatory response-related transcriptional pathways in the gastric antrum, providing a molecular framework for this widely used experimental model.

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Cite

BibTeXRIS
BibTeX
@article{lee2026transcriptomic,
  title = {{Transcriptomic insights into loperamide-induced gastric dysmotility: RNA-seq analysis of a mouse model.}},
  author = {Chunggeon Lee and Seung-Ju Hwang and Young-Su Yang and Bokyung Kim and Dong-Seon Kim and Daeui Park and Chang-Woo Song and Chang-Gue Son},
  journal = {Frontiers in physiology},
  year = {2026},
  month = oct,
  doi = {10.3389/fphys.2026.1924065},
  url = {https://europepmc.org/article/MED/42908841},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Transcriptomic insights into loperamide-induced gastric dysmotility: RNA-seq analysis of a mouse model.
AU  - Chunggeon Lee
AU  - Seung-Ju Hwang
AU  - Young-Su Yang
AU  - Bokyung Kim
AU  - Dong-Seon Kim
AU  - Daeui Park
AU  - Chang-Woo Song
AU  - Chang-Gue Son
PY  - 2026
DA  - 2026/10/07
JO  - Frontiers in physiology
DO  - 10.3389/fphys.2026.1924065
UR  - https://europepmc.org/article/MED/42908841
AB  - Background  Loperamide, a μ-opioid receptor agonist that slows gastrointestinal transit, is widely used as an antidiarrheal agent and an experimental model of gastric dysmotility and functional dyspepsia (FD). However, transcriptomic alterations associated with loperamide-induced delayed gastric emptying remain poorly characterized. This study aimed to investigate gastric gene-expression profiles associated with loperamide-induced gastric dysmotility using RNA sequencing.Methods  Male BALB/c mice were intraperitoneally injected with loperamide after 20 h of fasting. Delayed gastric emptying was assessed in one cohort, while gastric antrum tissues from a separate cohort were collected for RNA sequencing. Differentially expressed genes (DEGs) were identified using fold change ≥1.5 and false discovery rate (FDR) <0.01. Gene set enrichment analysis (GSEA) and pathway-network analysis were conducted to characterize biological pathways associated with loperamide treatment.Results  Loperamide significantly delayed gastric emptying, as demonstrated by increased gastric retention of phenol red. Transcriptomic analysis identified 1,356 DEGs, including 553 upregulated and 803 downregulated genes. GSEA revealed enrichment of inflammatory response-related pathways among upregulated genes, whereas synaptic transmission- and calcium signaling-related pathways were predominantly downregulated. Representative genes involved in cholinergic signaling (Chrm2 and Chrna9), glutamatergic signaling (Grm7), and calcium-channel function (Cacna1a) showed reduced expression, while Il33 was increased.Conclusion  This study provides transcriptomic insights into loperamide-induced gastric dysmotility. The findings suggest coordinated downregulation of genes associated with neuronal/synaptic signaling together with enrichment of inflammatory response-related transcriptional pathways in the gastric antrum, providing a molecular framework for this widely used experimental model.
SN  - 1664-042X
ER  -