Vince
Super Moderator
Free T3 (triiodothyronine) lowers LDL cholesterol primarily by accelerating its clearance from the blood through the liver and enhancing the conversion of cholesterol into other substances for excretion.
As of 2025, research highlights several key biological pathways for this effect:
pmc.ncbi.nlm.nih.gov
As of 2025, research highlights several key biological pathways for this effect:
- Upregulation of LDL Receptors: Free T3 increases the expression of LDL receptor (LDLR) genes in the liver. These receptors act like "magnets" on the surface of liver cells, catching LDL particles from the bloodstream so they can be broken down.
- Activation of SREBP-2: T3 directly activates Sterol Regulatory Element-Binding Protein 2 (SREBP-2). This transcription factor is essential for switching on the production of more LDL receptors.
- Conversion to Bile Acids: T3 speeds up the conversion of cholesterol into bile acids. This process depletes the liver's stored cholesterol, forcing it to pull more LDL out of the blood to compensate.
- Non-LDLR Pathways: Some studies suggest T3 can also reduce LDL through independent pathways, such as by decreasing the liver's production of Apolipoprotein B (ApoB), the main protein component of LDL particles.
- Prevention of Oxidation: T3 helps inhibit the oxidation of LDL. Oxidized LDL is more likely to contribute to plaque buildup in arteries.
The role of free triiodothyronine in high-density lipoprotein cholesterol metabolism - PMC
The aim of this study was to analyze the correlation between free triiodothyronine (FT3), free thyroxine (FT4), thyroid-stimulating hormone (TSH), and serum high-density lipoprotein cholesterol (HDL-C), and to explore the significance of FT3 in ...