The Claim
Dio1 heterozygous-null mice display elevated serum reverse triiodothyronine (rT3) levels and an increased rT3/T3 ratio, which correspond to the biochemical phenotype observed in humans carrying DIO1 p.Asn94Lys and p.Met201Ile variants.
What the research says
Supports is higher
Support is ahead, but a single strong opposing study can change this.
These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.
Mice with one nonfunctional copy of the Dio1 gene have higher levels of reverse T3 and a higher reverse T3 to T3 ratio in their blood, matching the biochemical pattern seen in humans with specific DIO1 gene variants.
See the scientific wording
Dio1 heterozygous-null mice exhibit elevated serum reverse triiodothyronine (rT3) and increased rT3/T3 ratio, mirroring the biochemical phenotype observed in humans with DIO1 p.Asn94Lys and p.Met201Ile variants, supporting the biological relevance of the human findings.
When one copy of the DIO1 gene is defective, the body produces half as much functional enzyme that breaks down thyroid hormones. This causes reverse T3 to build up in the blood because it isn't cleared properly, and less active T3 is made from its precursor, leading to a higher ratio of reverse T3 to T3.
What the research says
1 studyStudy: Human Type 1 Iodothyronine Deiodinase (DIO1) Mutations Cause Abnormal Thyroid Hormone Metabolism
Scientists found that mice with one broken copy of the Dio1 gene have the same weird thyroid hormone pattern as humans with specific gene mutations — high rT3 and high rT3/T3 ratio. This means the mice are a good model for understanding what happens in humans with these mutations.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.