Component

N-Lactoyl-phenylalanine / Lac-Phe

Context-specific entity; species, compartment and exposure are stated on each claim.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

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 it acts on

  1. Lac-Phe rose after exercise in human cohorts of 36 and 8 participants; in the modality comparison, changes tracked lactate and were greatest after sprint exercise.

    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human metabolomics and endurance/sprint/resistance comparisons.
    limitations
    A biomarker rise is not evidence that taking phenylalanine reproduces exercise benefits.
    nutrient_topic
    L-Phenylalanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Phenylalanine
    plain_language
    Phenylalanine can join lactate in a metabolite that rises after exercise.
    primary_references
    An exercise-inducible metabolite that suppresses feeding and obesity. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35705806/ · DOI 10.1038/s41586-022-04828-5

    L-Phenylalanine: transport, protein synthesis, cofactor recycling and cross-nutrient mechanisms (2026-09-19) · lines 398–404

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human metabolomics and endurance/sprint/resistance comparisons. · source_derived_draft · unverified_draft

    ## l-phenylalanine-lacphe-exercise Phenylalanine can join lactate in a metabolite that rises after exercise. Lac-Phe rose after exercise in human cohorts of 36 and 8 participants; in the modality comparison, changes tracked lactate and were greatest after sprint exercise. Model: Human metabolomics and endurance/sprint/resistance comparisons. Limitations: A biomarker rise is not evidence that taking phenylalanine reproduces exercise benefits. Evidence access: Primary full text An exercise-inducible metabolite that suppresses feeding and obesity. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35705806/ · DOI 10.1038/s41586-022-04828-5
    Complete structured claim and evidence
  2. Injected Lac-Phe at 50 mg/kg reduced food intake in diet-induced obese mice; daily injection for ten days reduced intake, adiposity and weight.

    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Intraperitoneal pharmacological dosing in diet-induced obese mice.
    limitations
    Oral dosing did not reproduce the effect; lean mice did not respond even up to 150 mg/kg. Lactate and phenylalanine separately did not reproduce it.
    nutrient_topic
    L-Phenylalanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Phenylalanine
    plain_language
    The combined metabolite changed feeding in a specific mouse model.
    primary_references
    An exercise-inducible metabolite that suppresses feeding and obesity. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35705806/ · DOI 10.1038/s41586-022-04828-5

    L-Phenylalanine: transport, protein synthesis, cofactor recycling and cross-nutrient mechanisms (2026-09-19) · lines 406–412

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Intraperitoneal pharmacological dosing in diet-induced obese mice. · source_derived_draft · unverified_draft

    ## l-phenylalanine-lacphe-obese-mice The combined metabolite changed feeding in a specific mouse model. Injected Lac-Phe at 50 mg/kg reduced food intake in diet-induced obese mice; daily injection for ten days reduced intake, adiposity and weight. Model: Intraperitoneal pharmacological dosing in diet-induced obese mice. Limitations: Oral dosing did not reproduce the effect; lean mice did not respond even up to 150 mg/kg. Lactate and phenylalanine separately did not reproduce it. Evidence access: Primary full text An exercise-inducible metabolite that suppresses feeding and obesity. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35705806/ · DOI 10.1038/s41586-022-04828-5
    Complete structured claim and evidence

What acts on it

  1. Deleting CNDP2 in human RT4 bladder epithelial cells reduced Lac-Phe production; extracellular lactate stimulated production in the control cells.

    Experimental context and source evidence
    evidence_access
    Primary abstract and PMC full-text Figure 2 and CRISPR methods
    experimental_model
    Human RT4 cell knockout and 25 mM lactate treatment for 24 hours; Figure 2.
    limitations
    This is a shared-enzyme connection, not proof that carnosine changes appetite.
    nutrient_topic
    Carnosine collection; isomer, preparation, species, exposure and manipulation remain explicit. · L-Carnosine / beta-alanyl-L-histidine
    plain_language
    The peptide-processing enzyme also participates in another metabolic pathway.
    primary_references
    An exercise-inducible metabolite that suppresses feeding and obesity. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35705806/ · DOI 10.1038/s41586-022-04828-5

    Carnosine: synthesis, transport, carbonyl chemistry and nutrient interactions (2026-09-19) · lines 172–178

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human RT4 cell knockout and 25 mM lactate treatment for 24 hours; Figure 2. · source_derived_draft · unverified_draft

    ## carnosine-cndp2-lacphe The peptide-processing enzyme also participates in another metabolic pathway. Deleting CNDP2 in human RT4 bladder epithelial cells reduced Lac-Phe production; extracellular lactate stimulated production in the control cells. Model: Human RT4 cell knockout and 25 mM lactate treatment for 24 hours; Figure 2. Limitations: This is a shared-enzyme connection, not proof that carnosine changes appetite. Evidence access: Primary abstract and PMC full-text Figure 2 and CRISPR methods An exercise-inducible metabolite that suppresses feeding and obesity. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35705806/ · DOI 10.1038/s41586-022-04828-5
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Global Cndp2 knockout markedly reduced circulating Lac-Phe and attenuated the food-intake and weight response to chronic exercise on a high-fat diet.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse global Cndp2 knockout; repeated treadmill exercise with high-fat feeding.
    limitations
    Cndp2 has other substrates; the phenotype was conditional on exercise and diet and did not establish a human deficiency syndrome.
    nutrient_topic
    L-Phenylalanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Phenylalanine
    plain_language
    Removing a production enzyme weakened one part of the exercise response.
    primary_references
    An exercise-inducible metabolite that suppresses feeding and obesity. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35705806/ · DOI 10.1038/s41586-022-04828-5
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Phenylalanine: transport, protein synthesis, cofactor recycling and cross-nutrient mechanisms (2026-09-19) · lines 414–420

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse global Cndp2 knockout; repeated treadmill exercise with high-fat feeding. · source_derived_draft · unverified_draft

    ## l-phenylalanine-lacphe-genetic Removing a production enzyme weakened one part of the exercise response. Global Cndp2 knockout markedly reduced circulating Lac-Phe and attenuated the food-intake and weight response to chronic exercise on a high-fat diet. Model: Mouse global Cndp2 knockout; repeated treadmill exercise with high-fat feeding. Limitations: Cndp2 has other substrates; the phenotype was conditional on exercise and diet and did not establish a human deficiency syndrome. Evidence access: Primary full text An exercise-inducible metabolite that suppresses feeding and obesity. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35705806/ · DOI 10.1038/s41586-022-04828-5
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

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

    Evidence, AI assistance and curation standards