Pasquali D, Bellastella A, Field J B
Istituto di Endocrinologia, I Facoltà di Medicina e Chirurgia, Università di Napoli, Italy.
J Endocrinol Invest. 1991 Nov;14(10):825-30. doi: 10.1007/BF03347936.
The role of thyroid hormones in a short loop feedback in the thyroid is controversial. This process was studied in dog thyroid slices stimulated by TSH, carbachol and phorbol esters. Incubation of thyroid slices with T3 and T4 for 1 hour inhibited the subsequent stimulation of glucose oxidation induced by carbachol and phorbol esters but not by TSH. T3 also inhibited the stimulation of 32P incorporation into phospholipids stimulated by these two agonists. Glucose oxidation stimulated by TSH, carbachol and 12-0-tetradecanoyl-phorbol-13-acetate (TPA) was inhibited by rT3 and the inhibition was not reversed by methimazole, which did abolish the inhibition induced by iodide, MIT and DIT. TSH stimulation of cAMP was not blocked by T3 or T4 but was by rT3 and MIT- and DIT. The mechanism of such inhibition appears to be complex, possibly involving formation of iodide from rT3, MIT and DIT but also dependent on the intact iodothyronine. Moreover, our data suggest that T3 and T4 exert their inhibition on the thyroid through the phospholipids cascade and this mechanism is probably independent on the release of iodide from these iodocompounds.
甲状腺激素在甲状腺短反馈回路中的作用存在争议。在促甲状腺激素(TSH)、卡巴胆碱和佛波酯刺激的犬甲状腺切片中研究了这一过程。将甲状腺切片与T3和T4孵育1小时可抑制随后由卡巴胆碱和佛波酯而非TSH诱导的葡萄糖氧化刺激。T3还抑制了这两种激动剂刺激的32P掺入磷脂的过程。TSH、卡巴胆碱和12-0-十四烷酰佛波醇-13-乙酸酯(TPA)刺激的葡萄糖氧化受到反式T3(rT3)的抑制,且该抑制作用不能被甲巯咪唑逆转,而甲巯咪唑确实能消除碘化物、一碘甲腺原氨酸(MIT)和二碘甲腺原氨酸(DIT)诱导的抑制作用。TSH对环磷酸腺苷(cAMP)的刺激作用未被T3或T4阻断,但被rT3以及MIT和DIT阻断。这种抑制作用的机制似乎很复杂,可能涉及rT3、MIT和DIT形成碘化物,但也依赖于完整的碘甲状腺原氨酸。此外,我们的数据表明,T3和T4通过磷脂级联反应对甲状腺发挥抑制作用,且该机制可能独立于这些碘化合物释放碘。