Mouse primary intestinal I-cell CCK secretion: molecular mechanisms & dependencies

How nutrients influence it

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Human evidence only

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

L-phenylalanine stimulated CaSR-dependent calcium signaling and CCK release in primary mouse duodenal I cells; CCK responses were greater at 2.5 than at 1.26 mM extracellular calcium.
L-Phenylalanine → Mouse primary intestinal I-cell CCK secretion source_derived_draftungraded
Experimental context and source evidence
evidence_access
Primary abstract
experimental_model
Primary mouse I cells; stereoselective L- versus D-phenylalanine responses.
limitations
Cell assay responses do not establish that calcium supplements enhance satiety in humans.
nutrient_topic
L-Phenylalanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Phenylalanine
plain_language
Gut amino-acid sensing can depend on both the amino acid and calcium.
primary_references
The extracellular calcium-sensing receptor is required for cholecystokinin secretion in response to L-phenylalanine in acutely isolated intestinal I cells. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21252045/ · DOI 10.1152/ajpgi.00342.2010
L-Phenylalanine: transport, protein synthesis, cofactor recycling and cross-nutrient mechanisms (2026-09-19) · lines 278–284
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary mouse I cells; stereoselective L- versus D-phenylalanine responses. · source_derived_draft · unverified_draft
## l-phenylalanine-casr-cck Gut amino-acid sensing can depend on both the amino acid and calcium. L-phenylalanine stimulated CaSR-dependent calcium signaling and CCK release in primary mouse duodenal I cells; CCK responses were greater at 2.5 than at 1.26 mM extracellular calcium. Model: Primary mouse I cells; stereoselective L- versus D-phenylalanine responses. Limitations: Cell assay responses do not establish that calcium supplements enhance satiety in humans. Evidence access: Primary abstract The extracellular calcium-sensing receptor is required for cholecystokinin secretion in response to L-phenylalanine in acutely isolated intestinal I cells. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21252045/ · DOI 10.1152/ajpgi.00342.2010
Complete structured claim and evidence
CaSR knockout abolished the phenylalanine-evoked calcium response in primary mouse I cells and prevented the normal stimulatory CCK response; responses to KCl and tryptone were preserved.
Mouse calcium-sensing receptor / Casr → Mouse primary intestinal I-cell CCK secretion source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_access
Primary abstract
experimental_model
CaSR-null compared with wild-type primary mouse intestinal I cells.
limitations
This is receptor failure, not phenylalanine or calcium dietary deficiency.
nutrient_topic
L-Phenylalanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Phenylalanine
plain_language
Removing one sensor disables that route without disabling every secretion trigger.
primary_references
The extracellular calcium-sensing receptor is required for cholecystokinin secretion in response to L-phenylalanine in acutely isolated intestinal I cells. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21252045/ · DOI 10.1152/ajpgi.00342.2010
trigger_kind
machinery_impairment Imported condition classification; unverified.
L-Phenylalanine: transport, protein synthesis, cofactor recycling and cross-nutrient mechanisms (2026-09-19) · lines 286–292
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · CaSR-null compared with wild-type primary mouse intestinal I cells. · source_derived_draft · unverified_draft
## l-phenylalanine-casr-loss Removing one sensor disables that route without disabling every secretion trigger. CaSR knockout abolished the phenylalanine-evoked calcium response in primary mouse I cells and prevented the normal stimulatory CCK response; responses to KCl and tryptone were preserved. Model: CaSR-null compared with wild-type primary mouse intestinal I cells. Limitations: This is receptor failure, not phenylalanine or calcium dietary deficiency. Evidence access: Primary abstract The extracellular calcium-sensing receptor is required for cholecystokinin secretion in response to L-phenylalanine in acutely isolated intestinal I cells. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21252045/ · DOI 10.1152/ajpgi.00342.2010
Complete structured claim and evidence

The events it takes part in

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Situations it appears in

Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.

In the sources

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Open hypotheses

Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.

This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

Mouse primary intestinal I-cell CCK secretion