ラット胎仔下垂体除去後およびTSHならびにGH投与後の甲状腺C細胞の電顕的研究

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  • Electron microscopic study on the fetal thyroid c cells following fetal hypophyseoprivia with or without TSH and GH therapies in the rat.
  • ラット胎仔下垂体除去後およびTSHならびにGH投与後の甲状腺C細胞の電顕的研究〔英文〕
  • ラットタイシカスイタイ ジョキョ ゴ オヨビ TSH ナラビニ GH トウヨ ゴ ノ コウジョウセン C サイボウ ノ デンケンテキ ケンキュウ 〔 エイブン 〕

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Thyroid C cells in fetal rats on days 21 and 22 of gestation had well-developed rough endoplasmic reticule (RER) and Golgi complexes and numerous secretory granules. The granules had vascular polarity in their location and some of them were attached to the cell membranes. Fetal hypophyseoprivia by subtotal decapitation (SD) caused fetal hypercalcemia, accompanied by a wide variation in electron density of the secretory granules, an increase in number of flattened RER and a further development of Golgi complexes. These changes in fine structure suggest a rise in calcitonin-producing activity of C cells, probably in response to hypercalcemia. Fetal thyroidectomy caused fetal hypocalcemia, probably owing to parathormone deficiency. TSH therapy of SD fetuses neither prevented the fetal hypercalcemia nor repaired the cytologic changes in C cells. GH therapy of SD fetuses partially prevented the hypercalcemia between day 20 and day 21 of gestation, but not between day 21 and day 22. Cytologic repair was not observed. Propylthiouracil injected into fetuses influenced neither the C cell's structure nor the plasma calcium levels. The observations suggest that the fetal hypercalcemia and the rise in secretory activity of C cells induced by fetal SD are not solely due to a deficiency of fetal pituitary TSH. The role of pituitary GH is questionable. Deficiencies of other brain factors should be considered as contributing to the observations.

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