People taking synthetic thyroid hormone (levothyroxine) for thyroid conditions show lower levels of a specific enzyme activity that converts T4 to T3 in the body, compared to people whose thyroid glands overproduce hormones due to Graves' disease or a toxic nodule.

Blocking a specific enzyme called D2 stops the hormone leptin from changing thyroid hormone levels in the body. This shows that the D2 enzyme is absolutely necessary for leptin to do its job in regulating thyroid function.

In patients who have had their entire thyroid removed due to thyroid cancer, the amount of type 2 deiodinase enzyme present in remaining thyroid tissue is lower when thyroid-stimulating hormone (TSH) levels are high (above 4.2 mU/L) than when TSH levels are low (below 2.0 mU/L), even when thyroid hormone levels in the blood are normal.

In patients who have had their thyroid removed and are taking levothyroxine, those with high TSH levels despite high FT4 levels show reduced activity of an enzyme that converts T4 to T3, lower T3 relative to T4, and increased sensitivity to thyroid hormones in the brain, suggesting a biological mechanism may limit the effectiveness of hormone replacement therapy.

Giving leptin directly to the brain causes fat tissue to produce more of an enzyme that converts inactive thyroid hormone into the active form, raising active thyroid levels in the body. This shows that fat tissue isn't just passive storage but actively helps control your thyroid hormone levels based on signals from your brain.

In people with thyrotoxicosis caused by taking thyroid hormone medication, the rise in active thyroid hormone (FT3) is smaller and less proportional to the increase in precursor hormone (FT4) than in people whose thyroid gland overproduces hormones, because of lower enzyme activity and lack of natural signaling from the thyroid.