Thyrotropin-Releasing Hormone Stimulation and Somatostatin Inhibition of Growth Hormone Secretion from Perfused Rat Adenohypophyses*

Carlson, Harold E.; Mariz, Ida K.; Daughaday, William H.

doi:10.1210/endo-94-6-1709

Cited by 104 publications

(34 citation statements)

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“…Ishibashi and Yamaji demonstrated that an unexpected increase in GH secretion was induced by the direct action of TRH on the pituitary locus by using perfused pituitary adenoma (Ishibashi and Yamaji, 1978). Furthermore, TRH resulted in a release of GH secretion from perfused rat hemipituitaries (Carlson et al, 1974). It was also reported by Fagilia et al (1973) that GH response to TRH may be due either to an alteration of the cellular membrane of pituitary locus and/or to an extra-pituitary portion, probably situated at the hypothalamic locus in patients with acromegaly.…”

Section: Discussionmentioning

confidence: 53%

Growth hormone response to thyrotropin-relesing hormone in cancer patients.

et al. 1980

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Plasma GH responses to TRH were investigated in 50 cancer patients.Out of 50 cancer patients, 33 were found to be responders.At 15, 30 and 60 min after TRH injection, the mean values GH for cancer patients was significantly higher than the corresponding value for normal controls and the base-line level following saline injection in cancer patients (p<0.001).Our results suggests that a possible alteration of hypothalamic-pituitary function regulating GH secretion may occur in patients with cancer.

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Section: Discussionmentioning

confidence: 53%

Growth hormone response to thyrotropin-relesing hormone in cancer patients.

et al. 1980

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“…Although serum growth hormone (GH) generally shows no appreciable rise following administration of TRH to normal humans (Anderson et al, 1971), such responses have been described in pathological human states (Irie and Tsushima, 1972;Hasegawa et al, 1975;Maeda et al, 1975 a and b), in vivo in bovines (Convey, 1973) and rats (Kato et al, 1975), and in vitro using various animal preparations (Carlson et al, 1974;Machlin and Jacobs, 1973).…”

Section: Synopsismentioning

confidence: 99%

Increase of serum GH concentration following TRH injection in patients with primary hypothyroidism.

Hamada¹,

Uoi²,

Nishizawà³

et al. 1976

Endocrinol Japon

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SynopsisThe effect of TRH administration on serum GH was studied in 6 normal subjects, 13 patients with primary hypothyroidism and 6 thyrotoxic subjects. Although no appreciable changes of serum GH were noted in the normal subjects, TRH administration provoked an increase of serum GH in 6 out of 13 patients with primary hypothyroidism.Serum GH levels in response to TRH administration were decreased in patients who were euthyroid following treatment with a preparation of desiccated thyroid.In patients with hyperthyroidism, no significant response of serum GH was observed at 30 or 60 min after TRH administration.Some of the patients with hyperthyroidism showed a slight increase in serum GH at 120 min after TRH injection.These results suggest that hypothalamo-pituitary function regulating GH secretion is altered in patients with primary hypothyroidism.

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“…Alternatively, the islet TRH may arise from a small subpopulation of streptozotocin-sensitive cells that are distinct from the majority of beta cells, or from nerve endings, closely associated with beta cells, that undergo parallel atrophy after streptozotocin treatment. The recent demonstration of the hypothalamic peptide somatostatin in the islets of Langerhans (21-23) and its relatively increased content in streptozotocin-diabetic rats (24) are also of interest, especially in view of the generally antagonistic effects of TRH and somatostatin on the secretory control of a number of peptide hormones (25)(26)(27)(28)(29)(30)(31)(32)(33)(34). Thus, while TRH stimulates the secretion of growth hormone (25,27), prolactin (29,32), and thyrotropin (28,31), somatostatin inhibits the basal and/or stimulated secretion of these same hormones (25)(26)(27)(28)(29)(30).…”

mentioning

confidence: 99%

High concentration of thyrotropin-releasing hormone in pancreatic islets.

Martino¹,

Lernmark

Seo³

et al. 1978

Proc. Natl. Acad. Sci. U.S.A.

115

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The concentration of thyrotropin-releasing hormone (TRH, thyroliberin) in rat islets of Langerhans is 30-fold higher than in whole rat pancreas, indicating that the islets are the main source of pancreatic TRH. The TRH extracted from islets is indistinguishable from synthetic TRH in its immunological and biological properties and in its inactivation by human serum. The physiologic function of islet TRH is unknown. However, because TRH is antagonistic to somatostatin in other systems, and somatostatin also is concentrated in islets in high concentrations, it is possible that islet TRH may serve a similar antagonistic function in the regulation of islet cell secretory activity. A rather ubiquitous distribution of thyrotropin-releasing hormone (TRH, thyroliberin) has been demonstrated through the use of a sensitive and specific radioimmunoassay. Significant amounts of TRH have been found in extra hypothalamic areas of the human brain (1-3) as well as in the central nervous system of several mammalian and submammalian species (4-6). The presence of TRH has also been reported in human placenta (7), rat retina (8), and frog skin (9). For this reason, it has been postulated that TRH may not only play a role in the regulation of pituitary thyrotropin and prolactin secretion but may also act as a neurotransmitter or modulator of synaptic function (5, 10). Recently Morley et al. (11) reported that TRH is present throughout the rat gastrointestinal tract as well as in the pancreas. This report confirms the latter finding and localizes TRH to the islets of Langerhans.MATERIALS AND METHODS Preparation of Animals. All rats were males weighing 200-250 g. Strains used were CD (Charles River Breeding Laboratories, Waltham, MA), Lewis (Microbiological Associates, Bethesda, MD), and Sprague-Dawley (Laboratory Supply, Indianapolis, IN). Purina rat chow was continuously available except during 48-hr fast. The animals were housed in screen-floor cages and were given tap water ad lib. Hypothyroid rats were prepared by surgical thyroidectomy, followed by intraperitoneal injection of 80 uCi of 13'I per rat and maintained on low-iodine diet (Teklad Mills, Madison, WI). They were used two months after the induction of hypothyroidism. Thyroid hormone-replaced rats were hypothyroid rats treated with 15 ,gg of triiodothyronine intraperitoneally 24 hr before the tissues were obtained. Rats of the Lewis and Sprague-Dawley strains were made diabetic by a single intravenous injection of streptozotocin (65 mg/kg of body weight) and used 7 and 10 days later.Isolation of Whole Pancreas and Islets. Rats were killed by decapitation and the pancreases were immediately excised.Fat and lymph nodes were trimmed away, and the residual tissue was weighed and frozen on dry ice. For isolation of pancreatic islets, rats were injected intraperitoneally with 0.25 ml of 4% pilocarpine-HCl 2 hr prior to decapitation. A group of rats was similarly pretreated prior to the isolation of the whole pancreas to check whether pilocarpine had any effect on the c...

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Thyrotropin-Releasing Hormone Stimulation and Somatostatin Inhibition of Growth Hormone Secretion from Perfused Rat Adenohypophyses*

Cited by 104 publications

References 0 publications

Growth hormone response to thyrotropin-relesing hormone in cancer patients.

Growth hormone response to thyrotropin-relesing hormone in cancer patients.

Increase of serum GH concentration following TRH injection in patients with primary hypothyroidism.

High concentration of thyrotropin-releasing hormone in pancreatic islets.

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