Immunomodulation and inflammation: Role of GLP-1R and GIPR expressing cells within the gut.
Level 5 - mechanism / opinion, no new human data
Narrative review summarizing literature without systematic methodology or original data.
PubMed 38555054 · doi:10.1016/j.peptides.2024.171200
What was done
This narrative review synthesized preclinical and clinical literature regarding the immunomodulatory functions of GLP-1 and GIP signaling in the intestine. The authors evaluated GLP-1 receptor expression on natural and induced intraepithelial lymphocytes, GIP receptor signaling in hematopoiesis, and the roles of both incretin pathways in inflammation, gut microbiota, metabolism, and fasting-refeeding cycles.
What was found
No quantitative data were reported in the abstract. The authors describe that both endogenous signaling and pharmacological activation of GLP-1R impact local and systemic inflammation, gut microbiota, metabolism, and GLP-1 bioavailability. They note that the role of GIPR-expressing bone marrow-derived cells in gut immunology is not well understood and identify key literature gaps regarding sex differences and the effects of incretin-based pharmacotherapies on gut homeostasis.
Why it matters
With GLP-1R and dual GLP-1R/GIPR agonists widely used for diabetes and obesity, understanding their direct intestinal immunological mechanisms could clarify off-target effects and inform new strategies for inflammatory and metabolic disorders.
Limits
This is a narrative review with no systematic search methodology, quantitative synthesis, or risk-of-bias assessment. Primary data are largely preclinical, and critical aspects—including direct GIPR immune actions in the gut and sex-specific mechanisms—remain unmeasured and unaddressed.
Cited by
- supports GLP-1 binds directly to receptors on immune cells.