How thyroid hormones turn off their own production
Fundamentally distinct roles of thyroid hormone receptor isoforms in a thyrotroph cell line are due to differential DNA binding.
Not medical advice. For informational purposes only. Always consult a healthcare professional. Terms
Surprising Findings
THRA depletion alone had no effect on T3-mediated suppression at any concentration.
Scientists previously assumed both receptors played similar roles in feedback; this shows THRA is inactive under normal conditions, which contradicts prior assumptions.
Practical Takeaways
If you have unexplained high TSH despite normal thyroid hormone levels, ask your doctor about potential receptor-level issues — not just thyroid function.
Not medical advice. For informational purposes only. Always consult a healthcare professional. Terms
Surprising Findings
THRA depletion alone had no effect on T3-mediated suppression at any concentration.
Scientists previously assumed both receptors played similar roles in feedback; this shows THRA is inactive under normal conditions, which contradicts prior assumptions.
Practical Takeaways
If you have unexplained high TSH despite normal thyroid hormone levels, ask your doctor about potential receptor-level issues — not just thyroid function.
Publication
Journal
Molecular endocrinology
Year
2012
Authors
M. Chiamolera, A. Sidhaye, Shunichi Matsumoto, Qiyi He, K. Hashimoto, T. Ortiga-Carvalho, F. Wondisford
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Claims (4)
When thyroid hormone levels in the blood are high, the pituitary gland reduces production of thyroid-stimulating hormone. When thyroid-stimulating hormone levels are low, the thyroid gland produces thyroid hormones without normal regulatory control.
When the THRB protein is removed from a specific type of pituitary cell in the lab, more THRA protein binds to the DNA region that controls the Tshb gene.
In a laboratory cell line derived from pituitary tissue, removing the thyroid hormone receptor beta prevents T3 from suppressing the production of Tshb mRNA, while removing receptor alpha does not, indicating that receptor beta is required for T3 to reduce Tshb mRNA levels under physiological conditions.
In a laboratory cell line derived from pituitary tissue, removing both versions of the thyroid hormone receptor prevents the hormone T3 from suppressing the production of Tshb mRNA, even when T3 is present at very high levels.