Stimulation by a TRH precursor, TRH-Gly, of TSH and PRL secretion in rats: Effect of starvation

Mori, Masataka; Murakami, Masami; Iriuchijima, Tokuji; Miyashita, Kazuya; Satoh, Tetsurou; Monden, Tsuyoshi; Michimata, Toshio; Kobayashi, Isao; Kobayashi, Setsuo

doi:10.1016/0143-4179(90)90112-c

Cited by 9 publications

(1 citation statement)

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“…Since, in the median eminence, the content of TRH-Gly was negligible compared with the amount of proTRH160_169 and TRH, it seems unlikely that a-amidation of TRHGly is a rate-limiting step in hypothalamic TRH synthesis. Since TRH-Gly levels were also very low in hypophysial stalk blood (W J de Greef, unpublished data), it seems that TRH-Gly is probably not very important for pituitary function, since high amounts of TRH-Gly are required to alter TSH and prolactin release (Mori et al 1990). On the other hand, the presence of relatively high levels of proTRH]60_169 in hypophysial portal blood is probably of physiological importance since proTRH]60_169 modifies TSH release by potentiating the effect of TRH on the pituitary gland (Bulant et al 1990).…”

Section: Discussionmentioning

confidence: 95%

Starvation-induced changes in the hypothalamic content of prothyrotrophin-releasing hormone (proTRH) mRNA and the hypothalamic release of proTRH-derived peptides: role of the adrenal gland

Haasteren¹,

Linkels²,

Klootwijk³

et al. 1995

Journal of Endocrinology

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The purpose of this study was to investigate the mechanisms involved in the reduced thyroid function in starved, young female rats. Food deprivation for 3 days reduced the hypothalamic content of prothyrotrophin-releasing hormone (proTRH) mRNA, the amount of proTRH-derived peptides (TRH and proTRH160-169) in the paraventricular nucleus, the release of proTRH-derived peptides into hypophysial portal blood and the pituitary levels of TSH beta mRNA. Plasma TSH was either not affected or slightly reduced by starvation, but food deprivation induced marked increases in plasma corticosterone and decreases in plasma thyroid hormones. Refeeding after starvation normalized these parameters. Since the molar ratio of TRH and proTRH160-169 in hypophysial portal blood was not affected by food deprivation, it seems unlikely that proTRH processing is altered by starvation. The median eminence content of pGlu-His-Pro-Gly (TRH-Gly, a presumed immediate precursor of TRH), proTRH160-169 or TRH were not affected by food deprivation. Since median eminence TRH-Gly levels were very low compared with other proTRH-derived peptides it is unlikely that alpha-amidation is a rate-limiting step in hypothalamic TRH synthesis. Possible negative effects of the increased corticosterone levels during starvation on proTRH and TSH synthesis were studied in adrenalectomized rats which were treated with corticosterone in their drinking water (0.2 mg/ml). In this way, the starvation-induced increase in plasma corticosterone could be prevented. Although plasma levels of thyroid hormones remained reduced, food deprivation no longer had negative effects on hypothalamic proTRH mRNA, pituitary TSH beta mRNA and plasma TSH in starved adrenalectomized rats. Thus, high levels of corticosteroids seem to exert negative effects on the synthesis and release of proTRH and TSH. This conclusion is corroborated by the observation that TRH release into hypophysial portal blood became reduced after administration of the synthetic glucocorticosteroid dexamethasone. On the basis of these results, it is suggested that the reduced thyroid function during starvation is due to a reduced synthesis and release of TRH and TSH. Furthermore, the reduced TRH and TSH synthesis during food deprivation are probably caused by the starvation-induced enhanced adrenal secretion of corticosterone.

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Section: Discussionmentioning

confidence: 95%