After bariatric surgery, morbidly obese adults maintain normal levels of free thyroxine and thyroid-stimulating hormone over three to three and a half years, even though their free triiodothyronine...
Mechanism
Synthesis from 1 study
After surgery that stops fat digestion, the body makes less of its active thyroid hormone because it can't convert the stored form properly. At the same time, burning more protein for energy tells the brain to keep the thyroid control signal steady, so the main hormone and the brain's signal stay...
Most probable mechanism
After surgery that blocks fat digestion, the body can't make enough active thyroid hormone from its stored form, so levels of the active hormone drop. At the same time, the body starts burning more protein for energy, which signals the brain to keep the thyroid control signal steady even though the active hormone is low. This keeps the main thyroid hormone and the brain's signal normal, even as the active hormone falls.
Bilio-pancreatic bypass diverts bile and pancreatic enzymes away from the duodenum, preventing fat emulsification and absorption.
Reduced dietary fat absorption limits fatty acids and cholesterol availability, decreasing deiodinase type 1 activity in the liver and kidney.
Lower deiodinase type 1 activity reduces conversion of thyroxine (T4) to triiodothyronine (T3), causing sustained reduction in circulating free triiodothyronine (FT3).
Shift in substrate utilization toward protein oxidation increases amino acid catabolism, generating metabolic signals that modulate hypothalamic-pituitary-thyroid axis feedback.
Pituitary thyrotrophs adjust TSH secretion based on protein oxidation rates, maintaining TSH within normal range despite low FT3 and stable FT4.
Evidence from Studies
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