HORMONE SECRETION BY CELLS DISSOCIATED FROM RAT ANTERIOR PITUITARIES

A new procedure has been developed for dissociating anterior pituitary tissue and producing a viable suspension of single cells. The procedure involves incubation of small tissue blocks in 1 mg/ml trypsin (15 min), followed by incubation in 8 µg/ml neuraminidase and 1 mM EDTA (15 min), followed by mechanical dispersion. Cell yields are ∼55%, based on recovered DNA. By electron microscopy five types of secretory cells (somatotrophs, mammotrophs, thyrotrophs, gonadotrophs, and corticotrophs) plus endothelial and follicular cells can be identified and are morphologically well preserved up to 20 h after dissociation. Throughout this period, the cells incorporate linearly [3H]leucine into protein for up to 4 h at a rate 90% greater than hemipituitaries, and they synthesize, transport intracellularly, and release the two major pituitary secretory products, growth hormone and prolactin. Immediately after dissociation the cells' ability to respond to secretogogues (high K+ and dibutyryl cyclic AMP) is impaired, but after a 6–12-h culture period, the cells apparently recover and discharge 24% and 52%, respectively, of their content of prelabeled growth hormone over a 3-h period in response to these two secretogogues. This represents a stimulation of 109% and 470% over that released by cells incubated in control medium. The results demonstrate that function and morphologic integrity are preserved in this cell system. Therefore it is suitable for the study of various aspects of pituitary secretion and its control.

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Molecular pathogenesis of pituitary tumours

Oxford Textbook of Endocrinology and Diabetes ◽

10.1093/med/9780199235292.003.2052 ◽

2011 ◽

pp. 112-121

Author(s):

Ines Donangelo ◽

Shlomo Melmed

Keyword(s):

Growth Hormone ◽

Pituitary Adenomas ◽

Single Cells ◽

Hormone Secretion ◽

Cell Types ◽

Pituitary Tumour ◽

Thyroid Stimulating Hormone ◽

Gene Products ◽

Pituitary Tumours ◽

Secretory Products

Pituitary adenomas are discovered in up to 25% of unselected autopsies, however, clinically apparent tumours are considerably less common. The pituitary gland is composed of differentiated cell types: somatotrophs, lactotrophs, corticotrophs, thyrotrophs, and gonadotrophs. Tumours may arise from any of these cell types and their secretory products depend on the cell of origin. The functional classification of pituitary tumorus is based on identification of cell gene products by immunostaining or mRNA detection, as well as measurement of circulating tumour and target organ hormone levels. Oversecretion of adrenocorticotropic hormone (ACTH) results in cortisol excess with Cushing’s disease. Growth hormone overproduction leads to acromegaly with typical acral overgrowth and metabolic abnormalities. Prolactin hypersecretion results in hypogonadism and galactorrhoea. Rarely, thyroid-stimulating hormone (TSH) hypersecretion leads to goitre and thyrotoxicosis, and gonadotropin excess results in gonadal dysfunction (1). Mixed tumours cosecreting growth hormone with prolactin, TSH, or ACTH may also arise from single cells. Clinically nonfunctional tumours are those that do not efficiently secrete their gene products, and most commonly they are derived from gonadotroph cells. Pituitary tumours are further defined radiographically as microadenomas (<1 cm in diameter) or macroadenomas (>1 cm in diameter). However, this classification does not reflect whether the pituitary tumour is amenable to total resection and limits assessment of invasive progression during serial imaging. Therefore, it is useful to apply the classification proposed by Hardy in 1973 and modified by Wilson in 1990 (Table 2.3.2.1), whereby pituitary tumours are classified into one of five grades and one of six stages, providing important preoperative information. Pituitary tumours cause morbidity by both abnormal hormone secretion as well as compression of regional structures. As a considerable proportion of patients do not achieve optimal therapeutic control of mass effects and/or hormone hypersecretion despite advances in therapeutic approaches, understanding pathogenesis and pituitary tumour growth patterns in individual patients will enable identification of subcellular treatment targets, ultimately decreasing tumour-related morbidity and mortality. Determinants of initiation and progression of pituitary adenomas are not fully understood. This chapter describes a spectrum of mechanisms implicated in pituitary tumorigenesis, including the role of pituitary plasticity, imbalances in cell cycle regulation, transcription factors, signalling pathways, and angiogenesis (Fig. 2.3.2.1). Molecular events related to tumorigenesis in human pituitary adenoma subtypes are summarized in Table 2.3.2.2. The causal role for selected genetic imbalances leading to development of pituitary tumours has been confirmed in several transgenic mouse models (Table 2.3.2.3).

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Response : Hypothalamic Stimulation of Growth Hormone Secretion

Science ◽

10.1126/science.163.3868.705-c ◽

1969 ◽

Vol 163 (3868) ◽

pp. 705-705

Author(s):

Lawrence A. Frohman ◽

Lee L. Bernardis ◽

Kenneth J. Kant

Keyword(s):

Growth Hormone ◽

Hormone Secretion ◽

Growth Hormone Secretion ◽

Hypothalamic Stimulation ◽

Stimulation Of

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Hypothalamic Stimulation of Growth Hormone Secretion

Science ◽

10.1126/science.162.3853.580 ◽

1968 ◽

Vol 162 (3853) ◽

pp. 580-582 ◽

Cited By ~ 66

Author(s):

L. A. Frohman ◽

L. L. Bernardis ◽

k. J. Kant

Keyword(s):

Growth Hormone ◽

Hormone Secretion ◽

Growth Hormone Secretion ◽

Hypothalamic Stimulation ◽

Stimulation Of

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Study on the Method of Stimulation of Human Growth Hormone Secretion with Special Consideration of Glucagon Stimulation

Pediatrics International ◽

10.1111/j.1442-200x.1972.tb02388.x ◽

1972 ◽

Vol 14 (1) ◽

pp. 23-23

Author(s):

Yukiko Morikawa ◽

S. Kusakawa

Keyword(s):

Growth Hormone ◽

Human Growth Hormone ◽

Hormone Secretion ◽

Growth Hormone Secretion ◽

Human Growth ◽

Special Consideration ◽

Stimulation Of

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Stimulation of growth hormone secretion by baclofen in man: Failure to confirm published findings

Human Psychopharmacology Clinical and Experimental ◽

10.1002/hup.470040209 ◽

1989 ◽

Vol 4 (2) ◽

pp. 135-138 ◽

Cited By ~ 3

Author(s):

Hameen Markar ◽

John Bennie ◽

Sheena Carroll ◽

Ann Chiswick ◽

Helen Wilson ◽

...

Keyword(s):

Growth Hormone ◽

Hormone Secretion ◽

Growth Hormone Secretion ◽

Stimulation Of

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Characterization of growth hormone-releasing hormone stimulation of the endocrine pancreas: Studies with α- and β-adrenergic and cholinergic antagonists

Acta Endocrinologica ◽

10.1530/acta.0.1140589 ◽

1987 ◽

Vol 114 (4) ◽

pp. 589-594 ◽

Cited By ~ 4

Author(s):

K. Hermansen ◽

A. M. Kappelgaard

Keyword(s):

Growth Hormone ◽

Hormone Receptors ◽

Islet Cells ◽

Hormone Secretion ◽

Cholinergic Receptor ◽

Cholinergic Antagonists ◽

Growth Hormone Releasing Hormone ◽

Releasing Hormone ◽

Islet Hormone ◽

Stimulation Of

Abstract. The 40 aminoacids residue of pancreatic growth hormone-releasing hormone stimulates the secretion of insulin, glucagon, an somatostatin from the pancreas. To determine whether this stimulation of islet hormone secretion is mediated via adrenergic or cholinergic receptor sites, we studied the effects of 30 nmol/l of the growth hormone-releasing hormone on the release of insulin, glucagon, and somatostatin in the presence of either α-adrenergic (phentolamine), β-adrenergic (propranolol) or cholinergic (atropine) blocking agents. The responses to the growth hormonereleasing hormone were not significantly modified by adrenergic or cholinergic blockers. The findings rule out an interaction with adrenergic and cholinergic receptors on islet cells. It is at present unknown whether the growth hormone-releasing hormone stimulates islet hormone secretion via an interaction with specific growth hormone-releasing hormone receptors or vasoactive intestinal peptide receptors.

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