Effects of Thyroidectomy on Thyrotropin-Releasing Hormone (TRH) and Somatotropin Release-lnhibiting Factor (SRIF) Patterns in Intrahypophysial Microdialysates in Rats.

Mizobuchi, Miki; Ishikawa, Masatoshi; Okauchi, Yasuhiro; Bando, Hiroshi; Saito, Shiro

doi:10.1507/endocrj.43.679

Cited by 5 publications

(4 citation statements)

References 38 publications

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“…In contrast to observations in other mammals, in dogs both basal and integrated GH levels were significantly higher in hypothyroidism than in euthyroidism. In some mammals, such as sheep and steers, primary hypothyroidism does not seem to affect GH secretion (Elsasser et al 1992, Fletcher & Clarke 1994, whereas in rats (Varela et al 1991, Santini et al 1993, Mizobuchi et al 1996, Tam et al 1996, Osorio et al 1998) and pigs (Morovat & Dauncey 1998) primary hypothyroidism is associated with low circulating GH levels.…”

Section: Discussionmentioning

confidence: 99%

“…The GH secretory profile has been found to shift from a low-frequency, high-amplitude pattern in euthyroid rats to a high-frequency, low-amplitude pattern in rats with mild hypothyroidism induced by methimazole (Bruhn et al 1992). Severe hypothyroidism in rats is associated with markedly reduced circulating GH levels (Varela et al 1991, Santini et al 1993, Mizobuchi et al 1996, Tam et al 1996, Osorio et al 1998, abolished GH bursts (Takeuchi et al 1978, Katakami et al 1986, blunted GH response to GHRH (Williams et al 1985, Tam et al 1996 and decreased pituitary content of mRNA encoding for GH (Martinoli & Pelletier 1989, Lloyd et al 1990, Tam et al 1996. In addition, hypothyroidism in rats causes a reduction in pituitary GH content (Szabo et al 1985, Katakami et al 1986, Wood et al 1987, Lloyd et al 1990, Varela et al 1991, pituitary GHRH receptor mRNA (Tam et al 1996, Korytko & Cuttler 1997, hypothalamic SS content (Tam et al 1996) and hypothalamic SS mRNA (Tam et al 1996).…”

Section: Introductionmentioning

confidence: 99%

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Primary hypothyroidism in dogs is associated with elevated GH release

Diaz-Espineira²,

Mol³

et al. 2001

Journal of Endocrinology

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The pulsatile secretion patterns of GH were investigated in seven beagle bitches by collecting blood samples every 10 min for 6 h during euthyroidism and 1·5 years after induction of primary hypothyroidism. Hypothyroidism was induced by surgical removal of the thyroid gland and subsequent destruction of any remnant thyroid tissue by oral administration of sodium [131 I]iodide. Some of the physical changes observed in the dogs with primary hypothyroidism mimicked those of acromegaly. During both euthyroidism and hypothyroidism GH was secreted in a pulsatile fashion. The mean ( ...) basal plasma GH concentration was significantly higher (P=0·003) in the hypothyroid state (4·1 1·6 µg/l) than in the euthyroid state (1·2 0·4 µg/l). Likewise, the mean area under the curve (AUC) for GH above the zero-level during hypothyroidism (27·0 10·0 µg/l 6 h) was significantly higher (P=0·004) than that during euthyroidism (11·7 2·0 µg/l 6 h). The mean AUC for GH above the baseline was significantly lower (P=0·008) during hypothyroidism (2·4 0·8 µg/l 6 h) than during euthyroidism (4·5 1·8 µg/l 6 h), whereas there was no significant difference in GH pulse frequency. The mean plasma IGF-I level was significantly higher (P<0·01) in the hypothyroid state (169 45 µg/l) than in the euthyroid (97 15 µg/l). The results of this study demonstrate that primary hypothyroidism in dogs is associated with elevated basal GH secretion and less GH secreted in pulses. This elevated GH secretion has endocrine significance as illustrated by elevated plasma IGF-I levels and some physical changes mimicking acromegaly. It is discussed that the increased GH release in hypothyroid dogs may be the result of the absence of a response element for thyroid hormone within the canine pituitary GH gene and alterations in supra-pituitary regulation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Primary hypothyroidism in dogs is associated with elevated GH release

Diaz-Espineira²,

Mol³

et al. 2001

Journal of Endocrinology

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“…Although results are frequently variable, hypothyroid states are usually associated with re¬ duced hypothalamic somatostatin levels (32,34-36). A more recent study, using microdialysis in freely moving animals, measured the release of hypothalamic somatostatin in rats and found a reduction in somatostatin release in the hy¬ pothyroid state (37). Additionally, studies using in vitro cerebrocortical cell cultures have shown that thyroid hormone stimulates somatostatin gene expression and peptide release at low doses, inhibits at higher doses and is influenced by the hormonal milieu prior to culture (38).…”

Section: Discussionmentioning

confidence: 99%

The Effect of Thyroid Hormone and a Long-Acting Somatostatin Analogue on TtT-97 Murine Thyrotropic Tumors

Woodmansee¹,

Gordon²,

Dowding³

et al. 2000

Thyroid

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Thyroid hormone inhibits thyrotropin (TSH) production and thyrotrope growth. Somatostatin has been implicated as a synergistic factor in the inhibition of thyrotrope function. We have previously shown that pharmacological doses of thyroid hormone (levothyroxine [LT4]) inhibit growth of murine TtT-97 thyrotropic tumors in association with upregulation of somatostatin receptor type 5 (sst5) mRNA and somatostatin receptor binding. In the current study, we examined the effect of physiological thyroid hormone replacement alone or in combination with the long-acting somatostatin analogue, Sandostatin LAR, on thyrotropic tumor growth, thyrotropin growth factor-beta (TSH-beta), and sst5 mRNA expression, as well as somatostatin receptor binding sites. Physiological LT4 replacement therapy resulted in tumor shrinkage in association with increased sst5 mRNA levels, reduced TSH-beta mRNA levels and enhanced somatostatin receptor binding. Sandostatin LAR alone had no effect on any parameter measured. However, Sandostatin LAR combined with LT4 synergistically inhibited TSH-beta mRNA production and reduced final tumor weights to a greater degree. In this paradigm, Sandostatin LAR required a euthyroid status to alter thyrotrope parameters. These data suggest an important interaction between the somatostatinergic system and thyroid hormone in the regulation of thyrotrope cell structure and function.

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“…Thus, a primary effect of thyroid hormones on somatostatin biosynthesis and release appears unlikely to account for their actions on GH and TSH secretion. This is further suggested by the minimal effect of thyroidectomy on somatostatin levels in rat hypophysial portal blood (150) or in intrahypophysial microdialysates (285).…”

Section: By Other Hormonesmentioning

confidence: 94%