Sodium ipodate increases triiodothyronine action in vivo
J H Hays1, C Eil, R C Smallridge
1Clinical Physiology Branch, Walter Reed Army Institute of Research, Washington, D.C.
Journal of Endocrinological Investigation
|July 1, 1992
Summary
Sodium ipodate (IPO) does not inhibit thyroid hormone (T3) effects in vivo by binding nuclear T3 receptors (NT3R). Instead, IPO may enhance T3
Area of Science:
- Endocrinology
- Molecular Pharmacology
- Thyroid Hormone Research
Background:
- Sodium ipodate (IPO) is known to bind nuclear T3 receptors (NT3R) in vitro.
- In vivo evidence for IPO-NT3R binding and its effect on T3 action has been conflicting.
- Thyroid hormone (T3) regulates mitochondrial alpha glycerophosphate dehydrogenase (alpha-GPDH) activity.
Purpose of the Study:
- To investigate in vivo evidence for IPO-NT3R binding.
- To determine if IPO binding to NT3R inhibits T3-induced increases in alpha-GPDH activity.
- To explore the interaction between IPO and T3 on alpha-GPDH activity in vivo.
Main Methods:
- Administered large doses of IPO to thyroidectomized (TDX) rats with low-dose T3 replacement.
- Measured serum T3, serum TSH, and alpha-GPDH activity in kidney, heart, and liver.
- Utilized vehicle-treated and IPO-treated groups across varying T3 concentrations.
Main Results:
- IPO administration decreased serum T3 and increased serum TSH in euthyroid rats.
- IPO did not significantly reduce alpha-GPDH activity in any T3-replaced TDX rat group.
- IPO significantly increased alpha-GPDH activity above T3-alone effects in multiple organs, suggesting enhanced T3 action.
Conclusions:
- IPO-NT3R binding is not the primary mechanism for IPO attenuating T3 effects in vivo.
- IPO may enhance T3 effects at the cellular level.
- IPO's enhancement of T3 action may not be reflected in standard serum TSH monitoring, which has clinical implications.
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