T3/T4, TSH regulation

[Muggie]

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Hey guys,

What regulates TSH release? Free T3 or T4?....

I've been finding loads of conflicting answers to this question.

1) Goljan's RR Path states that an increase in T4/T3 ratio should produce a decrease in TSH (and vice versa), but...
2) UW question says free T3 is responsible for decreasing TSH release, by downregulating TSH Rc on thyrotrope cells of the anterior pituitary.
3) Still other books say that free T4 is most important in this regulation, but that it is converted to T3 in the ant. pituitary and that's what acts to decrease TSH.

I'm so confused... can someone make any sense of this?

Thanks

 

[Loanna]

Hi!From what I know, T4 is the main product of thyroid gland, but T3(the largest portion of which comes from conversion of T4 in periphery) is the most active form of the two.Now, since T3 is the major form, that is actually found circulating in periphery, and is the one that acts on the target-tissues, among which pituitary, it is T3 that exerts regulation on TSH.
In primary hypo-/hyper-thyroidism, T4 levels change,thus resulting in change in T3 levels,which in turn cause adverse change in TSH release from the pituitary.

 

[acpl]

Loanna is right on the ball.

 

[Muggie]

Thanks for clearing that up!

 

[osli]

Just ran across this very question in UW and missed it, and started searching for clarification. Information seems sketchy, and some very thorough sources like Guyton and Hall don't mention at all which is actually responsible. Part of my search turned up this thread so I thought I'd just resurrect it instead of starting a new one.

From my class lectures and notes, as well as what limited articles I can find online, I believe UW (as well as BRS phys and several other sources) is incorrect, or at least that it is a poorly defined question.

T3 is the molecule that binds to the receptor in the anterior pituitary and down regulates TRH receptors, but that molecule is not the same as the free T3 in peripheral circulation. It seems that the majority of research supports that the anterior pituitary does not permit entry of circulating free T3, and instead permits entry to circulating free T4 only. An internal iodinase converts this peripheral T4 into T3, which is the molecule that has regulatory activity.

Thus, it is free T4 that directly correlates to TSH regulation, even though T3 is a downstream molecule in the signaling pathway.

 

[docmd2010]

from what i understand, osli is correct.
this is exactly how we were taught in my physiology course.