Alemi · The Journal of clinical investigation 2013 · Animal and in vitro mechanistic study · n=?

The TGR5 receptor mediates bile acid-induced itch and analgesia.

Cited 380 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Mechanistic bench and animal research using mouse models and in vitro cell preparations

PubMed 23524965 · doi:10.1172/JCI64551 · record verified 2026-08-29

What was done

Researchers investigated the role of the G protein-coupled receptor TGR5 in mediating cholestatic pruritus and analgesia. Using mice (including wild-type, Tgr5 knockout [Tgr5-KO], and Tgr5-overexpressing transgenic [Tgr5-Tg] models), they assessed TGR5 localization in dorsal root ganglia (DRG), spinal cord peptidergic neurons, and dermal macrophages. They tested the effects of bile acids and a selective TGR5 agonist on DRG hyperexcitability and the release of gastrin-releasing peptide and leucine-enkephalin, alongside behavioral responses to intradermal, intraplantar, and intrathecal injections.

What was found

The abstract reports qualitative findings without numerical data: - TGR5 was identified in mouse DRG peptidergic neurons, spinal cord, and opioid-containing dermal macrophages. - Bile acids and a TGR5-selective agonist induced DRG neuronal hyperexcitability and stimulated the release of gastrin-releasing peptide and leucine-enkephalin. - Intradermal injection of bile acids or TGR5 agonist induced mouse scratching behavior via gastrin-releasing peptide- and opioid-dependent pathways; scratching was attenuated in Tgr5-KO mice and heightened in Tgr5-Tg mice (which exhibited spontaneous pruritus). - Intraplantar and intrathecal bile acid administration induced mechanical analgesia in mouse paws through an opioid-dependent mechanism, an effect completely absent in Tgr5-KO mice.

Why it matters

The study identifies TGR5 activation on sensory neurons as a direct mechanistic driver of both pruritus and analgesia caused by elevated bile acids. This provides a molecular explanation for symptoms such as pruritus and painless jaundice seen in cholestatic liver diseases, highlighting TGR5 as a potential therapeutic target.

Limits

This study was conducted exclusively in mouse models and isolated cell preparations, with no direct human clinical data reported in the abstract. Quantitative measurements, exact sample sizes (n), effect sizes, and statistical variance are not provided in the abstract.

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