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Primary topic: SLC25A13 gene cellular energy production

SLC25A13 Gene and Metabolism: What It Can Mean in a Pathway Report

SLC25A13 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 1 SNP and 1 curated claim.

What is the SLC25A13 gene?

Mitochondrial aspartate-glutamate carrier supporting the malate-aspartate NADH shuttle, urea-cycle aspartate supply, and hepatic metabolic balance.

How SLC25A13 affects metabolism

When SLC25A13-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 SLC25A13 is altered

Altered SLC25A13 signal should be treated as a DNA-based tendency, not a diagnosis. 1 claim currently passes the report-use gate. The useful question is whether symptoms, labs, and lifestyle context line up with the pathway signal.

Curated SNP evidence for SLC25A13

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

SLC25A13 currently has 1 curated SNPs, 1 claim-level scores, and 1 claims eligible for pathway scoring.

Open the sample report
rs80338720SLC25A13 c.852_855del / 851del41 claims · 2 study rows

transport activity · biallelic or compound-heterozygous SLC25A13 deficiency context

Citrin aspartate-glutamate carrier activity tendency

Strong

rs80338720 del / SLC25A13 c.852_855del / p.Met285fs is associated with lower citrin mitochondrial aspartate-glutamate carrier activity and malate-aspartate shuttle support in recessive or compound-heterozygous deficiency contexts.

SLC25A13 rs80338720 deletion is staged as a recessive citrin deficiency allele affecting mitochondrial aspartate-glutamate exchange.

Likely effectLower transport signal
Signal sizeLarge 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 SLC25A13 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

SLC25A13 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 SLC25A13 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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