Transgenic Mice Overexpressing the Growth-Hormone-Releasing Hormone Gene Have High Concentrations of Tachykinins in the Anterior Pituitary Gland

1999 ◽  
Vol 70 (2) ◽  
pp. 107-116 ◽  
Author(s):  
Luciano Debeljuk ◽  
James C. Wright ◽  
Carol Phelps ◽  
Andrzej Bartke
Keyword(s):  
Growth Hormone ◽  
Transgenic Mice ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Anterior Pituitary Gland ◽  
Growth Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
High Concentrations

THYROTROPHIN RELEASING HORMONE-INDUCED GROWTH HORMONE AND PROLACTIN RELEASE: PHYSIOLOGICAL STUDIES IN INTACT RATS AND IN HYPOPHYSECTOMIZED RATS BEARING AN ECTOPIC PITUITARY GLAND

1977 ◽  
Vol 72 (3) ◽  
pp. 301-311 ◽  
Author(s):  
A. E. PANERAI ◽  
IRIT GIL-AD ◽  
DANIELA COCCHI ◽  
V. LOCATELLI ◽  
G. L. ROSSI ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Time Lapse ◽  
Anterior Pituitary Gland ◽  
Plasma Prolactin ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Clear Cut ◽  
Urethane Anaesthesia ◽  
Releasing Effect

SUMMARY To determine how the sensitivity of the ectopic anterior pituitary gland to the GH-releasing effect of thyrotrophin releasing hormone (TRH) might be affected by the time lapse from transplantation, TRH (0·15 and 0·6 μg) was injected i.v. into hypophysectomized (hypox)-transplanted rats under urethane anaesthesia 1,3, 8,15, 30 and 60 days after transplantation, and plasma samples were taken 5 and 10 min later. Baseline GH values gradually decreased with time from about 16·0 ng/ml (1 day) to about 3·0 ng/ml (30 and 60 days). The TRH-induced GH release was absent 1 day after transplantation, present only with the higher TRH dose 3 and 8 days after transplantation, and clearly elicitable, also with the lower TRH dose (0·15 μg), from 15 up to 60 days. Determination of plasma prolactin concentrations showed a decline from about 85·0 ng/ml (1 day) to about 32·0 ng/ml (8 days); subsequently (15–60 days) prolactin values stabilized. Plasma prolactin levels increased 15 and 60 days after transplantation only when a dose of 0·6 μg TRH was given. In intact weight-matched rats, TRH induced a GH response only at the dose of 1·2 μg while a short-lived but clear-cut prolactin response could be obtained even with the 0·3 μg dose. The present results indicate that: (1) disconnexion between the central nervous system and the anterior pituitary gland greatly enhances GH responsiveness while blunting prolactin responsiveness to TRH; (2) the sensitivity of the anterior pituitary gland to the GH-releasing effect of TRH increases with time from transplantation; (3) TRH is a more effective prolactin-than GH-releaser on the pituitary gland in situ.

Posttranscriptional regulation of rat growth hormone gene expression: increased message stability and nuclear polyadenylation accompany thyroid hormone depletion

1992 ◽  
Vol 12 (6) ◽  
pp. 2624-2632
Author(s):  
D Murphy ◽  
K Pardy ◽  
V Seah ◽  
D Carter
Keyword(s):  
Growth Hormone ◽  
Thyroid Hormone ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Posttranscriptional Regulation ◽  
Anterior Pituitary Gland ◽  
Growth Hormone Gene ◽  
Gh Gene ◽  
Rat Growth ◽  
Pituitary Glands

In thyroid hormone-depleted rats, the rate of transcription of the growth hormone (GH) gene in the anterior pituitary gland is lower than the rate in euthyroid controls, and there is a corresponding reduction in the abundance of the GH mRNA. Concomitantly, the poly(A) tail of the GH mRNA increases in length. Examination of nuclear RNA from anterior pituitary glands of control and thyroid hormone-depleted rats revealed no difference in the length of pre-mRNAs containing the first and last introns of the GH gene. However, mature nuclear GH RNA is differentially polyadenylated in euthyroid and hypothyroid animals. We suggest that the extent of polyadenylation of the GH transcript is regulated in the cell nucleus concomitant with or subsequent to the splicing of the pre-mRNA. Experiments with anterior pituitary gland explant cultures demonstrated that the GH mRNA from thyroid hormone-depleted rats is more stable than its euthyroid counterpart and that the poly(A) tail may contribute to the differential stability of free GH ribonucleoproteins.

Acromegaly, diabetes insipidus, and visual loss caused by metastatic growth hormone—releasing hormone-producing malignant pancreatic endocrine tumor in the pituitary gland

1995 ◽  
Vol 83 (4) ◽  
pp. 719-723 ◽  
Author(s):  
Shigeru Genka ◽  
Hitoshi Soeda ◽  
Manabu Takahashi ◽  
Hideki Katakami ◽  
Naoko Sanno ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Pituitary Gland ◽  
Diabetes Insipidus ◽  
Metastatic Cancer ◽  
Growth Hormone Releasing Hormone ◽  
Serum Growth Hormone ◽  
Content Type ◽  
Releasing Hormone ◽  
Metastatic Growth ◽  
Fine Print

✓ The case of a 52-year-old woman with acromegaly, diabetes insipidus, and visual impairment caused by a metastatic growth hormone—releasing hormone (GRH)—produced pancreatic tumor is reported. Serum growth hormone (GH) and somatomedin C levels were elevated to 14 ng/ml (normal < 5 ng/ml), and 3.20 U/ml (normal < 1.88 U/ml), respectively. Paradoxical increases were observed in GH levels after glucose tolerance and thyrotropin—releasing hormone-stimulation tests. Biopsy of a pituitary tumor observed on computerized tomography scans and magnetic resonance studies revealed a metastatic cancer. When circulating GRH levels were measured, a marked increase in plasma GRH (1145 pg/ml; normal < 4—1 pg/ml) was observed. The patient died of cachexia due to metastases. Postmortem examination revealed that a primary tumor, a malignant endocrine lesion, was present in the pancreas, with metastatic tumors in the pituitary, lung, liver, and adrenal glands. Synthesis and production of GRH by the tumor was demonstrated by Northern blotting and immunohistochemical analysis. The pituitary gland showed hyperplastic, but not adenomatous changes. The authors stress the importance of both exploration for an ectopic source of GRH and the search for a GH-producing pituitary adenoma when unusual signs and symptoms are seen in patients with acromegaly.

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