In morbidly obese adults who undergo bilio-pancreatic bypass surgery, thyroid-stimulating hormone levels do not change even when free triiodothyronine levels and body weight change significantly, and...
Mechanism
Synthesis from 1 study
After surgery that stops fat digestion, the body makes less active thyroid hormone but doesn't lower the signal to make more. Instead, the brain starts using how much protein is being broken down to decide how much signal to send — more protein breakdown keeps the signal steady.
Most probable mechanism
After surgery that blocks fat digestion, the body makes less active thyroid hormone because it lacks the fats needed to convert it. Even though thyroid hormone levels drop, the brain keeps the signal to make more thyroid hormone steady. Instead of responding to thyroid hormone levels, the brain starts responding to how much protein the body is breaking down for energy — more protein breakdown keeps the signal the same.
Bilio-pancreatic bypass diverts bile and pancreatic enzymes away from the duodenum, impairing fat emulsification and digestion.
Reduced dietary fat absorption limits fatty acids and cholesterol availability, decreasing deiodinase type 1 activity in liver and kidney.
Decreased deiodinase activity reduces conversion of thyroxine (T4) to triiodothyronine (T3), lowering circulating free T3 levels.
Persistent low free T3 does not suppress thyroid-stimulating hormone secretion from the pituitary gland.
Increased postabsorptive protein oxidation generates metabolic signals that maintain thyroid-stimulating hormone secretion independently of free T3 or free T4 levels.
Evidence from Studies
Supporting (1)
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