The Claim

In VPAC2 receptor-deficient mice under 12:12 light-dark conditions, the phase of Per1, Per2, and Bmal1 mRNA expression in the thyroid gland is advanced by approximately 5 hours compared to wild-type mice, indicating that VIP/VPAC2 signaling modulates the timing of circadian gene expression in this peripheral organ.

Source: The Circadian Clock Is Sustained in the Thyroid Gland of VIP Receptor 2 Deficient Mice

What the research says

Supports is higher

Support is ahead, but a single strong opposing study can change this.

Supports
10score
Challenges
0score

These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.

How it works
1 study reviewed
In plain English

Mice that are missing a certain brain signaling system have their daily body clock in the thyroid gland running about 5 hours earlier than normal mice — this suggests that the signaling system helps set the clock in that organ.

See the scientific wording

The phase of Per1, Per2, and Bmal1 mRNA expression in the thyroid gland is advanced by approximately 5 hours in VPAC2 receptor-deficient mice compared to wild-type mice under 12:12 light-dark conditions, indicating that VIP/VPAC2 signaling influences the timing of circadian gene expression in this peripheral organ.

What the research says

1 study
  1. Study: The Circadian Clock Is Sustained in the Thyroid Gland of VIP Receptor 2 Deficient Mice

    The study shows that mice missing a certain brain signaling pathway have their thyroid's daily gene rhythms shifted earlier by about 5 hours, which supports the idea that this pathway helps control the timing of the thyroid's internal clock.

Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies

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