ArticleInternational journal of molecular sciences2025
Bitter Taste Receptor TAS2R43 Co-Regulates Mechanisms of Gastric Acid Secretion and Zinc Homeostasis.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Chemo-Diversity Landscape Using Physico-Biochemical, Elemental, and Metabolic Profiling in Different Stages and Accessions ofMolecules (Basel, Switzerland) · 2026Article
- A Digestive Herbal Mixture Preparation Stimulates Proton Secretion in Human Parietal Cells through Phenolic Compounds Targeting Bitter Taste Receptors.Molecular nutrition & food research · 2026Article
- Chemosensory response to Pt-based chemotherapeutics via bitter taste receptors in vitro reveals a new mechanism for bitter taste disorders.Scientific reports · 2026Article
- Bitter Taste Receptors TAS2R8 and TAS2R10 Reduce Proton Secretion and Differentially Modulate Cadmium Uptake in Immortalized Human Gastric Cells.International journal of molecular sciences · 2025Article
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Authors and funding
13 authors.
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Abstract
The essential micronutrient zinc is known to inhibit gastric acid secretion (GAS), where its homeostasis is strictly regulated. We hypothesized that the gastric bitter taste receptors, TAS2Rs, regulate the following: (i) zinc-modulated proton secretory activity (PSA) as a key mechanism of GAS and (ii) zinc homeostasis in immortalized parietal cells. To confirm this hypothesis, human gastric tumor cells (HGT-1) were exposed to 100-1000 µM of zinc salts for 30 min in order to quantitate their TAS2R-dependent PSA and intracellular zinc concentration using a fluorescence-based pH sensor and ICP-MS, respectively. Thereby, we identified TAS2R43 as a key player in parietal cell PSA and zinc homeostasis, with both conclusions being verified by a CRISPR-Cas9 knockout approach. Moreover, by regulating the zinc importer protein ZIP14, TAS2R43 proved to perform a protective role against excessive zinc accumulation in immortalized parietal cells.
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