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Primary topic: SLC25A20 gene cellular energy production

SLC25A20 Gene and Metabolism: What It Can Mean in a Pathway Report

SLC25A20 is tracked because it connects to fatty-acid oxidation, mitochondrial transport, organic-acid handling, or high-demand energy metabolism. The current evidence index links this gene to Mitochondrial energy with 4 SNPs and 4 curated claims.

What is the SLC25A20 gene?

Carnitine-acylcarnitine translocase moving long-chain acylcarnitines across the mitochondrial inner membrane for fatty-acid oxidation.

How SLC25A20 affects metabolism

When SLC25A20-related function is shifted, the practical effect is interpreted through fatty-acid oxidation, mitochondrial transport, organic-acid handling, or high-demand energy metabolism. This does not mean the pathway is active or impaired right now; it means the gene can help prioritize what to check next.

What happens when SLC25A20 is altered

Altered SLC25A20 signal should be treated as a DNA-based tendency, not a diagnosis. 4 claims currently pass the report-use gate. The useful question is whether symptoms, labs, and lifestyle context line up with the pathway signal.

Curated SNP evidence for SLC25A20

These SNPs come from the approved study-level evidence model. Each claim is scored from curated study rows, then gated before it can influence pathway scoring.

Evidence-backed report connection

SLC25A20 currently has 4 curated SNPs, 4 claim-level scores, and 4 claims eligible for pathway scoring.

Open the sample report
rs1330578621SLC25A20 c.823C>T / Arg275Ter1 claims · 2 study rows

transport activity · AA or compound-heterozygous SLC25A20 deficiency context

Carnitine-acylcarnitine translocase activity tendency

Strong

rs1330578621 A (forward-genomic; SLC25A20 c.823C>T / p.Arg275Ter transcript context) is associated with lower mitochondrial carnitine-acylcarnitine translocase activity tendency and impaired long-chain acylcarnitine transport in recessive or compound-heterozygous CACT deficiency contexts.

SLC25A20 rs1330578621 A is staged as the forward-genomic recessive CACT deficiency nonsense allele affecting mitochondrial long-chain fatty-acid oxidation support.

Likely effectLower transport signal
Signal sizeModerate signal
Evidence supportStrong support
Report useIncluded in pathway scoring
Show study evidence
rs28934589SLC25A20 c.713A>G / Gln238Arg1 claims · 2 study rows

transport activity · CC or compound-heterozygous SLC25A20 deficiency context

Carnitine-acylcarnitine translocase activity tendency

Strong

rs28934589 C / SLC25A20 c.713A>G p.Gln238Arg is associated with lower mitochondrial carnitine-acylcarnitine translocase activity tendency in recessive or compound-heterozygous deficiency contexts.

SLC25A20 rs28934589 C is staged as a recessive CACT deficiency allele affecting mitochondrial long-chain fatty-acid oxidation support.

Likely effectLower transport signal
Signal sizeModerate signal
Evidence supportStrong support
Report useIncluded in pathway scoring
Show study evidence
rs541208710SLC25A20 c.199-10T>G1 claims · 2 study rows

transport activity · CC or compound-heterozygous SLC25A20 deficiency context

Carnitine-acylcarnitine translocase activity tendency

Strong

rs541208710 C (forward-genomic; SLC25A20 c.199-10T>G transcript context) is associated with lower mitochondrial carnitine-acylcarnitine translocase activity tendency in recessive or compound-heterozygous deficiency contexts.

SLC25A20 rs541208710 C is staged as the forward-genomic recessive CACT deficiency splice-region allele affecting mitochondrial long-chain fatty-acid oxidation support.

Likely effectLower transport signal
Signal sizeModerate signal
Evidence supportStrong support
Report useIncluded in pathway scoring
Show study evidence
rs756998699SLC25A20 c.10C>T / Gln4Ter1 claims · 2 study rows

transport activity · AA or compound-heterozygous SLC25A20 deficiency context

Carnitine-acylcarnitine translocase activity tendency

Strong

rs756998699 A / SLC25A20 c.10C>T / p.Gln4Ter is associated with lower mitochondrial carnitine-acylcarnitine translocase activity tendency and impaired long-chain acylcarnitine transport in recessive or compound-heterozygous CACT deficiency contexts.

SLC25A20 rs756998699 A is staged as a recessive CACT deficiency nonsense allele affecting mitochondrial long-chain fatty-acid oxidation support.

Likely effectLower transport signal
Signal sizeModerate signal
Evidence supportStrong support
Report useIncluded in pathway scoring
Show study evidence

Common symptoms people report

  • low energy under fasting, illness, or exercise
  • slow recovery after exertion
  • fatigue that feels out of proportion to workload

Biomarkers to validate

CBC, ferritin, and thyroid context

Rules out common non-DNA explanations for low energy.

Glucose and HbA1c

Checks whether fuel handling is adding pressure.

Organic acids or acylcarnitines when available

Adds more specific mitochondrial and fatty-acid oxidation context.

Where DNA analysis helps

DNA helps decide whether SLC25A20 deserves attention inside the broader Mitochondrial energy pathway. It is most useful when combined with biomarkers instead of used as a standalone answer.

Example interpretation

SLC25A20 may add context to fatty-acid oxidation, mitochondrial transport, organic-acid handling, or high-demand energy metabolism, especially when its SNP evidence lines up with other genes in the same pathway.

Suggested validation: CBC, ferritin, and thyroid context.

What to do next

  • Review the Mitochondrial energy pathway result before interpreting SLC25A20 on its own.
  • Use relevant biomarkers to confirm whether this DNA tendency is visible in current biology.
  • Treat supplement or nutrition decisions as follow-up steps only after the pattern fits symptoms or labs.

Upload your DNA file and receive a structured metabolic pathway analysis with prioritized insights and suggested validation markers.

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