Relative Potencies of Human, Rat, Bovine/Caprine, Porcine and Ovine Hypothalamic Growth Hormone-Releasing Factors to Release Growth Hormone by the Rat Anterior Pituitary in vitro

1986 ◽  
Vol 42 (4) ◽  
pp. 273-276 ◽  
Author(s):  
Andrew Baird ◽  
William B. Wehrenberg ◽  
Nicholas Ling
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Releasing Factors ◽  
Relative Potencies

scholarly journals Biosynthesis of growth hormone in the rat anterior pituitary gland. Stimulation of biosynthesis in vitro by insulin

1973 ◽  
Vol 134 (4) ◽  
pp. 1103-1113 ◽  
Author(s):  
A. Betteridge ◽  
M. Wallis
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Rna Synthesis ◽  
Glucose Utilization ◽  
Actinomycin D ◽  
Hormone Synthesis ◽  
Pituitary Glands ◽  
Hormone Biosynthesis ◽  
Stimulation Of

The effect of insulin on the incorporation of radioactive leucine into growth hormone was investigated by using rat anterior pituitary glands incubated in vitro. A 50% stimulation over control values was observed at insulin concentrations above 2μm (280munits/ml). The effect was specific for growth hormone biosynthesis, over the range 1–5μm-insulin (140–700munits/ml). Lower more physiological concentrations had no significant effect in this system. Above 10μm (1.4 units/ml) total protein synthesis was also increased. The stimulation of growth hormone synthesis could be partially blocked by the addition of actinomycin D, suggesting that RNA synthesis was involved. Insulin was found to stimulate the rate of glucose utilization in a similar way to growth hormone synthesis. 2-Deoxyglucose and phloridzin, which both prevented insulin from stimulating glucose utilization, also prevented the effect of insulin on growth hormone synthesis. If glucose was replaced by fructose in the medium, the effect of insulin on growth hormone synthesis was decreased. We conclude that the rate of utilization of glucose may be an important step in mediating the effect of insulin on growth hormone synthesis.

Characterization of the somatostatin-like immunoreactivity extracted from an adrenal medullary tumour

1982 ◽  
Vol 2 (3) ◽  
pp. 147-154 ◽  
Author(s):  
R. Corder ◽  
J. E. C. Sykes ◽  
P. J. Lowry
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Gel Filtration ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Identical Composition ◽  
Salt Fractionation ◽  
Somatostatin 14

Significant amounts of somatostatin-like immunor reactivity (SLI) were detected in the extract of a human catecholamine-secreting adrenal medullary tumour. After salt fractionation and reconstitution the major portion of SLI was purified by gel filtration and two HPLC steps; in all three systems it eluted in the position of somatostatin-14. The purified somatostatin-like peptide inhibited, in a dose-related manner, growth hormone release from stimulated perfused rat anterior pituitary ceils in vitro. Amino acid analysis showed the purified peptide to have an identical composition to somatostatin found in other species.

POSSIBLE INTERACTION OF LUTEINIZING HORMONE-RELEASING FACTOR WITH OTHER HYPOTHALAMIC RELEASING FACTORS AT THE LEVEL OF THE ADENOHYPOPHYSIS

1969 ◽  
Vol 44 (3) ◽  
pp. 405-410 ◽  
Author(s):  
D. B. CRIGHTON ◽  
H. P. G. SCHNEIDER ◽  
S. M. McCANN
Keyword(s):  
Growth Hormone ◽  
Luteinizing Hormone ◽  
Gel Filtration ◽  
The Other ◽  
Male Rats ◽  
Corticotrophin Releasing Factor ◽  
Lh Release ◽  
Releasing Factors ◽  
Factor C

SUMMARY Anterior pituitary halves from adult male rats were incubated in vitro for 6 hr. in tissue culture Medium 199. Luteinizing hormone (LH) released from these glands under the influence of purified preparations of growth hormone-releasing factor (GH-RF), growth hormone-inhibiting factor (GH-IF), corticotrophin-releasing factor (C-RF) and follicle-stimulating hormone-releasing factor (FSH-RF) was determined by the ovarian ascorbic acid depletion (OAAD) assay. The effects of these factors, both alone and together with purified luteinizing hormone-releasing factor (LH-RF), were examined and compared with the response to purified LH-RF alone. While LH-RF consistently produced significant increases in LH release, none of the other factors did so, although FSH-RF showed some indication of LH-releasing activity, probably due to incomplete separation from LH-RF on the Sephadex gel filtration column used for purification. The LH released in response to LH-RF was not affected by the presence of any of the other factors. An apparent slight augmenting effect of FSH-RF could be accounted for by its contamination with LH-RF. The results are discussed in relation to the physiological mechanisms concerned in modifying LH release from the adenohypophysis.

GRF increases release of growth hormone and arachidonate from anterior pituitary cells

1985 ◽  
Vol 248 (4) ◽  
pp. E438-E442
Author(s):  
A. M. Judd ◽  
K. Koike ◽  
R. M. MacLeod
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Concentration Dependent Manner ◽  
Anterior Pituitary Cells ◽  
Arachidonate Release

Arachidonate and its metabolites increase growth hormone release in vitro. A study was designed to determine whether arachidonate release from anterior pituitary cells is modified by growth hormone-releasing factor (GRF) or somatostatin (SRIF). Cultured pituitary cells were incubated with [3H]arachidonate to esterify the long-chain fatty acid into cellular lipids. The cells were extensively washed with medium containing no [3H]arachidonate and then incubated with GRF and/or SRIF for 30 min. The incubation medium was then extracted with ethyl acetate, and following thin-layer chromatographic separation, the radioactivity in the [3H]arachidonate band was measured. GRF in a concentration-dependent manner (1-30 nM) stimulated growth hormone and arachidonate release, whereas SRIF (100 nM) blocked the GRF-induced increase of growth hormone and arachidonate release. The effects of GRF on growth hormone and arachidonate were evident at time intervals as brief as 5 min. These findings support the hypothesis that arachidonate may play a role in the GRF-induced growth hormone release.

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