Component

Hepatic triglyceride accumulation

Hepatic triglyceride accumulation. Species, exposure and limitations are retained in each linked claim.

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

Read recorded mechanisms Open recursive mind map

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 acts on it

  1. A168T mice had lower MTARC1 protein despite unchanged mRNA, but neither sex showed significant protection from steatosis, inflammation or fibrosis.

    Mouse Mtarc1 p.Ala168Thr → Hepatic triglyceride accumulation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/molybdenum-research/41428769.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ac3e4efcae2e5b23a255c61586bbff33d3114fe2c8e28befe2d9ad501f774bd", "start_char": 0, "end_char": 1816, "text_sha256": "5ac3e4efcae2e5b23a255c61586bbff33d3114fe2c8e28befe2d9ad501f774bd"}
    experimental_model
    Male/female mouse A168T knock-in in multiple MASH/fibrosis models
    exposure
    Mouse ortholog of human A165T; no global knockout
    limitations
    Partial variant effects are not identical to deleting the gene. No human molybdenum intervention.
    nutrient_topic
    Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
    organism
    Mus musculus
    plain_language
    Lower protein from this variant was not enough to reproduce knockout protection.
    primary_references
    [mo-p41428769] A mitochondrial amidoxime-reducing component 1 (mARC1) A168T amino acid substitution does not confer protection from MASH and fibrosis in multiple mouse models of chronic liver disease. (2026). https://pubmed.ncbi.nlm.nih.gov/41428769/ DOI: 10.1042/bcj20253411
    tissue_or_cell_type
    Liver disease and protein expression
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1587–1598

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male/female mouse A168T knock-in in multiple MASH/fibrosis models · source_derived_draft · unverified_draft

    ### mo-marc-a168t-null A168T mice had lower MTARC1 protein despite unchanged mRNA, but neither sex showed significant protection from steatosis, inflammation or fibrosis. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Lower protein from this variant was not enough to reproduce knockout protection. organism: Mus musculus tissue_or_cell_type: Liver disease and protein expression experimental_model: Male/female mouse A168T knock-in in multiple MASH/fibrosis models limitations: Partial variant effects are not identical to deleting the gene. No human molybdenum intervention. exposure: Mouse ortholog of human A165T; no global knockout evidence_span: {"source_cache": "artifacts/molybdenum-research/41428769.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "5ac3e4efcae2e5b23a255c61586bbff33d3114fe2c8e28befe2d9ad501f774bd", "start_char": 0, "end_char": 1816, "text_sha256": "5ac3e4efcae2e5b23a255c61586bbff33d3114fe2c8e28befe2d9ad501f774bd"} [mo-p41428769] A mitochondrial amidoxime-reducing component 1 (mARC1) A168T amino acid substitution does not confer protection from MASH and fibrosis in multiple mouse models of chronic liver disease. (2026). https://pubmed.ncbi.nlm.nih.gov/41428769/ DOI: 10.1042/bcj20253411
    Complete structured claim and evidence

  2. Whole-body Marc1 knockout did not protect against hepatic triglyceride accumulation, inflammation or fibrosis in this mouse study.

    Mouse mitochondrial amidoxime-reducing component 1 / Mtarc1 → Hepatic triglyceride accumulation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/molybdenum-research/38437227.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "152bcc386bca67c8cd4891d284098784ebbdbf9c507f713f96b996bb3c75bd1b", "start_char": 0, "end_char": 1333, "text_sha256": "152bcc386bca67c8cd4891d284098784ebbdbf9c507f713f96b996bb3c75bd1b"}
    experimental_model
    Multi-ancestry exome association, human protein studies and whole-body mouse Marc1 knockout
    exposure
    MARC1 variants and mouse global knockout
    limitations
    Human association and mouse intervention are separate. The knockout null result differs from later published mouse knockout protection.
    nutrient_topic
    Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
    organism
    Human genetics in about 540000 individuals; Mus musculus knockout
    plain_language
    Removing MTARC1 did not help in this experiment.
    primary_references
    [mo-p38437227] Divergent role of Mitochondrial Amidoxime Reducing Component 1 (MARC1) in human and mouse. (2024). https://pubmed.ncbi.nlm.nih.gov/38437227/ DOI: 10.1371/journal.pgen.1011179
    tissue_or_cell_type
    Liver phenotypes
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1509–1520

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Multi-ancestry exome association, human protein studies and whole-body mouse Marc1 knockout · source_derived_draft · unverified_draft

    ### mo-marc-ko-null Whole-body Marc1 knockout did not protect against hepatic triglyceride accumulation, inflammation or fibrosis in this mouse study. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing MTARC1 did not help in this experiment. organism: Human genetics in about 540000 individuals; Mus musculus knockout tissue_or_cell_type: Liver phenotypes experimental_model: Multi-ancestry exome association, human protein studies and whole-body mouse Marc1 knockout limitations: Human association and mouse intervention are separate. The knockout null result differs from later published mouse knockout protection. exposure: MARC1 variants and mouse global knockout evidence_span: {"source_cache": "artifacts/molybdenum-research/38437227.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "152bcc386bca67c8cd4891d284098784ebbdbf9c507f713f96b996bb3c75bd1b", "start_char": 0, "end_char": 1333, "text_sha256": "152bcc386bca67c8cd4891d284098784ebbdbf9c507f713f96b996bb3c75bd1b"} [mo-p38437227] Divergent role of Mitochondrial Amidoxime Reducing Component 1 (MARC1) in human and mouse. (2024). https://pubmed.ncbi.nlm.nih.gov/38437227/ DOI: 10.1371/journal.pgen.1011179
    Complete structured claim and evidence

  3. Global deletion and hepatocyte-specific knockdown of Mtarc1 reduced steatosis and fibrosis in multiple mouse models.

    Mouse mitochondrial amidoxime-reducing component 1 / Mtarc1 → Hepatic triglyceride accumulation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/molybdenum-research/39927988.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0ac1fb695999e1691580706469d581ce6bd90eeab03f7c26c1c79fbb4b4e169d", "start_char": 0, "end_char": 1938, "text_sha256": "0ac1fb695999e1691580706469d581ce6bd90eeab03f7c26c1c79fbb4b4e169d"}
    experimental_model
    Global deletion and hepatocyte-specific knockdown across mouse MASH/fibrosis models; cellular variants
    exposure
    Mtarc1 depletion under lipotoxic and diet/fibrosis challenges
    limitations
    Preclinical protein-targeting study. A165T retained mitochondrial localization in these experiments, unlike the endogenous HepG2 study; construct/model effects remain unresolved.
    nutrient_topic
    Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
    organism
    Mus musculus; human variant cell experiments
    plain_language
    Removing MTARC1 helped in these experiments.
    primary_references
    [mo-p39927988] Loss of mitochondrial amidoxime-reducing component 1 (mARC1) prevents disease progression by reducing fibrosis in multiple mouse models of chronic liver disease. (2025). https://pubmed.ncbi.nlm.nih.gov/39927988/ DOI: 10.1097/hc9.0000000000000637
    tissue_or_cell_type
    Liver and hepatocytes
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1535–1546

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Global deletion and hepatocyte-specific knockdown across mouse MASH/fibrosis models; cellular variants · source_derived_draft · unverified_draft

    ### mo-marc-ko-protection-2025 Global deletion and hepatocyte-specific knockdown of Mtarc1 reduced steatosis and fibrosis in multiple mouse models. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing MTARC1 helped in these experiments. organism: Mus musculus; human variant cell experiments tissue_or_cell_type: Liver and hepatocytes experimental_model: Global deletion and hepatocyte-specific knockdown across mouse MASH/fibrosis models; cellular variants limitations: Preclinical protein-targeting study. A165T retained mitochondrial localization in these experiments, unlike the endogenous HepG2 study; construct/model effects remain unresolved. exposure: Mtarc1 depletion under lipotoxic and diet/fibrosis challenges evidence_span: {"source_cache": "artifacts/molybdenum-research/39927988.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0ac1fb695999e1691580706469d581ce6bd90eeab03f7c26c1c79fbb4b4e169d", "start_char": 0, "end_char": 1938, "text_sha256": "0ac1fb695999e1691580706469d581ce6bd90eeab03f7c26c1c79fbb4b4e169d"} [mo-p39927988] Loss of mitochondrial amidoxime-reducing component 1 (mARC1) prevents disease progression by reducing fibrosis in multiple mouse models of chronic liver disease. (2025). https://pubmed.ncbi.nlm.nih.gov/39927988/ DOI: 10.1097/hc9.0000000000000637
    Complete structured claim and evidence

  4. Global and liver-specific Mtarc1 knockout protected against diet-induced triglyceride accumulation, inflammation and fibrosis.

    Mouse mitochondrial amidoxime-reducing component 1 / Mtarc1 → Hepatic triglyceride accumulation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/molybdenum-research/41641916.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "52b4d4d00867faaa1bb51ff6055f887a72c4c0d266bf7a1665b3780ce03aee64", "start_char": 0, "end_char": 1681, "text_sha256": "52b4d4d00867faaa1bb51ff6055f887a72c4c0d266bf7a1665b3780ce03aee64"}
    experimental_model
    Global/liver Mtarc1 knockout with Pnpla2, Lipa, Pemt and Cept1 interventions
    exposure
    Diet-induced liver disease with gene knockouts/knockdowns and multi-omics
    limitations
    Preclinical mechanism; no evidence that dietary molybdenum restriction selectively reproduces MTARC1 targeting.
    nutrient_topic
    Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
    organism
    Mus musculus; supporting cell studies
    plain_language
    This study also found protection after targeted MTARC1 loss.
    primary_references
    [mo-p41641916] MTARC1 Inactivation Remodels Lipid Droplets to Protect Against Metabolic Fatty Liver Disease. (2026). https://pubmed.ncbi.nlm.nih.gov/41641916/ DOI: 10.1111/liv.70539
    tissue_or_cell_type
    Hepatic lipid droplets
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1548–1559

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Global/liver Mtarc1 knockout with Pnpla2, Lipa, Pemt and Cept1 interventions · source_derived_draft · unverified_draft

    ### mo-marc-ko-protection-2026 Global and liver-specific Mtarc1 knockout protected against diet-induced triglyceride accumulation, inflammation and fibrosis. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: This study also found protection after targeted MTARC1 loss. organism: Mus musculus; supporting cell studies tissue_or_cell_type: Hepatic lipid droplets experimental_model: Global/liver Mtarc1 knockout with Pnpla2, Lipa, Pemt and Cept1 interventions limitations: Preclinical mechanism; no evidence that dietary molybdenum restriction selectively reproduces MTARC1 targeting. exposure: Diet-induced liver disease with gene knockouts/knockdowns and multi-omics evidence_span: {"source_cache": "artifacts/molybdenum-research/41641916.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "52b4d4d00867faaa1bb51ff6055f887a72c4c0d266bf7a1665b3780ce03aee64", "start_char": 0, "end_char": 1681, "text_sha256": "52b4d4d00867faaa1bb51ff6055f887a72c4c0d266bf7a1665b3780ce03aee64"} [mo-p41641916] MTARC1 Inactivation Remodels Lipid Droplets to Protect Against Metabolic Fatty Liver Disease. (2026). https://pubmed.ncbi.nlm.nih.gov/41641916/ DOI: 10.1111/liv.70539
    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