Failure to confirm a growth hormone-releasing activity of corticotropin-releasing hormone in acromegaly: Comparison with the effects of other hypothalamic hormones

1991 ◽  
Vol 125 (5) ◽  
pp. 487-490 ◽  
Author(s):  
Hajime Watanobe ◽  
Shinsuke Sasaki ◽  
Kazuo Takebe
Keyword(s):  
Growth Hormone ◽  
Vasoactive Intestinal Peptide ◽  
Corticotropin Releasing Hormone ◽  
Negative Data ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Hypothalamic Hormones ◽  
Active Acromegaly ◽  
Plasma Gh

Abstract. We re-examined whether CRH stimulates GH secretion in acromegaly. Human CRH (100 μg) was given as an iv bolus to 15 patients with active acromegaly, and plasma GH levels were measured before and at intervals up to 120 min after the injection. For comparison, we assessed in all the patients the effects of TRH (500 μg), GnRH (100 μg), vasoactive intestinal peptide (100 μg) and peptide histidine methionine (100 μg), which are known paradoxically to stimulate GH secretion in acromegaly. A paradoxical GH response (>50% above the basal) to TRH, GnRH, vasoactive intestinal peptide and peptide histidine methionine was observed in 12 (80%), 4 (27%), 5 (33%) and 2 (13%) patients, respectively. All the patients were responsive to at least one of these 4 peptides. However, none of the patients showed a positive GH response to hCRH. These results do not support a GH-releasing activity of CRH in acromegaly. Even if CRH has such an effect, it does not appear as potent as TRH, GnRH, vasoactive intestinal peptide and peptide histidine methionine. However, the possibility cannot be excluded that our negative data might have been due to the use of hCRH vs ovine CRH in earlier studies.

Hypothalamic hormones that release growth hormone stimulate hepatic 5′-monodeiodination activity in the chick embryo

1988 ◽  
Vol 118 (2) ◽  
pp. 233-236 ◽  
Author(s):  
E. R. Kühn ◽  
A. Vanderpooten ◽  
L. M. Huybrechts ◽  
E. Decuypere ◽  
V. Darras ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Plasma Concentration ◽  
Chick Embryo ◽  
Chick Embryos ◽  
Thyrotrophin Releasing Hormone ◽  
Growth Hormone Releasing Factor ◽  
Releasing Hormone ◽  
Pancreatic Growth ◽  
Hypothalamic Hormones ◽  
Plasma Gh

ABSTRACT Plasma GH, tri-iodothyronine (T3), thyroxine (T4) and liver 5′-monodeiodination (5′-D) activity were measured in 18-day-old chick embryos injected with thyrotrophin-releasing hormone (TRH) and human pancreatic growth hormone releasing factor (hpGRF). Injections of 0·1 and 1 μg TRH and 1·5 μg hpGRF increased the concentration of plasma GH while injection of 15 μg hpGRF had no effect. Concentrations of plasma T3 were raised after injection of TRH or hpGRF. Injections of TRH but not of hpGRF raised the concentration of plasma T4. The increases in concentration of plasma T3 after injection of TRH or hpGRF were parallelled by increases in liver 5′-D activity. An injection of 0·25 μg T4 significantly raised the concentration of T4 in plasma but had no effect on plasma T3 or liver 5′-D activity. It is concluded that the release of chicken GH by TRH or hpGRF is responsible for the observed increases in plasma concentration of T3 and liver 5′-D activity. J. Endocr. (1988) 118, 233–236

Growth hormone (GH) responses to the combined administration of GH-releasing hormone plus GH-releasing peptide 6 in adults with GH deficiency

1995 ◽  
Vol 132 (6) ◽  
pp. 712-715 ◽  
Author(s):  
A Leal-Cerro ◽  
E Garcia ◽  
R Astorga ◽  
FF Casanueva ◽  
C Dieguez
Keyword(s):  
Growth Hormone ◽  
Gh Deficiency ◽  
Hormone Deficiency ◽  
Santiago De Compostela ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Factor I ◽  
Gh Replacement ◽  
Combined Administration ◽  
Plasma Gh

Leal-Cerro A, Garcia E, Astorga R, Casanueva FF, Dieguez C. Growth hormone (GH) responses to the combined administration of GH-releasing hormone plus GH-releasing peptide 6 in adults with GH deficiency. Eur J Endocrinol 1995;132:712–5. ISSN 0804–4643 In recent years the health problems of adults with growth hormone deficiency (GHD) and the benefits of GH replacement therapy have received considerable attention. However, the reliability of conventional GH tests in the assessment of pituitary GH reserve in this group of patients is still controversial. In this study, we assessed GH secretion after the combined administration of GH-releasing hormone (GHRH) (1 μg/kg iv) and GH-releasing peptide 6 (GHRP-6, 1 μg/kg iv) in adult patients diagnosed with GHD by conventional GH testing, and correlate this response with insulin-like growth factor I levels. Twenty-one subjects (13 male, 8 female) with long-standing diagnosis of GHD aged 21–54 years were studied. In 13 subjects GH responses to GHRH plus GHRP-6 were markedly reduced (peak GH response <10 mU/I), whereas in the remaining eight the response was greater (range 11–100 mU/l), In conclusion, our data show that combined administration of GHRH plus GHRP-6 elicited a significant increase in plasma GH levels in about 40% of patients diagnosed with GHD by conventional GH testing. C Dieguez, PO Box 563, 15700 Santiago de Compostela, Spain

Activation of cholinergic tone by pyridostigmine reverses the inhibitory effect of corticotropin-releasing hormone on the growth hormone-releasing hormone-induced growth hormone secretion

1992 ◽  
Vol 126 (2) ◽  
pp. 113-116 ◽  
Author(s):  
SM Corsello ◽  
A Tofani ◽  
S Della Casa ◽  
R Sciuto ◽  
CA Rota ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Inhibitory Effect ◽  
Normal Male ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Cholinergic Tone ◽  
Ghrh Test

Previous studies have shown that corticotropin-releasing hormone (CRH) is capable of inhibiting growth hormone (GH) secretion in response to GH-releasing hormone (GHRH). In an attempt to clarify the mechanism of the CRH action, we have studied the effect of enhanced cholinergic tone induced by pyridostigmine on the CRH inhibition of the GH response to GHRH in a group of six normal men and six normal women. All subjects presented a normal GH response to 50 μg iv GHRH administration (mean peak±sem plasma GH levels 20±2.9 μg/l in men and 28.9±2.9 μg/l in women) with a further significant increase after pyridostigmine pretreatment (60mg orally given 60 min before GHRH) in men (GH peaks 43.1±6.9 μg/l, p<0.005) but not in women (GH peaks 39.2±3.0 μg/l). In the same subjects, peripherally injected CRH (100 μg) significantly inhibited the GH response to GHRH (GH peaks 8.1±0.6 μg/l in men, p<0.005 and 9.9±0.7 μg/l in women, p<0.005). Pyridostigmine (60 mg) given orally at the same time of CRH administration (60 min before GHRH) reversed the CRH inhibition of GHRH-induced GH secretion (GH peaks 35.3±8.2 μg/l in men and 35±3.3 μg/l in women) with a response not significantly different to that seen in the pyridostigmine plus GHRH test. Our data confirm that pyridostigmine is capable of potentiating the GHRH-induced GH release in normal male but not female subjects. In addition, our studies show that the potentiating action of pyridostigmine on the GHRH-induced GH secretion prevails on the inhibiting effect of CRH when the two drugs are given together 1 h before GHRH injection. Both CRH and pyridostigmine could exert their action by modifying, in opposite ways, somatostatin release from the hypothalamus.

Effects of hypothyroidism on the growth hormone axis in sheep

1994 ◽  
Vol 140 (3) ◽  
pp. 495-502 ◽  
Author(s):  
T P Fletcher ◽  
I J Clarke
Keyword(s):  
Growth Hormone ◽  
Pulse Amplitude ◽  
Pulse Frequency ◽  
Pulse Interval ◽  
Short Term ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Prolactin Response ◽  
Plasma Gh

Abstract This study examined the effect of thyroidectomy (TX) on the GH axis in sheep. The secretion of GH was monitored 10 and 77 days after TX or sham-TX when the effects on plasma GH and prolactin levels of the injection of 0·5 μg GH-releasing factor (GRF)/kg and 1 μg thyrotrophin-releasing hormone (TRH)/kg were also assessed. There were no significant differences in GH pulse amplitude, pulse frequency, inter-pulse interval and GH secreted/h between sham-TX and TX animals at 10 or 77 days after TX. There was no difference in the GH response to GRF injection in sham-TX sheep at any time but in TX sheep the GH response was significantly (P<0·05) attenuated 10 days after TX. After 77 days the GH response was similar to the response before TX. There was no measurable GH response to injection of TRH in sham-operated or TX sheep at any time. The prolactin response to TRH was not affected by TX or sham-TX. These results suggest that TX in sheep does not affect GH secretion but paradoxically the response to GRF is attenuated in hypothyroid sheep in the short term. TRH causes release of prolactin but not GH in sheep. Journal of Endocrinology (1994) 140, 495–502

DYNAMIC EVALUATION OF GROWTH HORMONE (GH) AND PROLACTIN (hPRL) SECRETION IN ACTIVE ACROMEGALY WITH HIGH AND LOW GH OUTPUT

1975 ◽  
Vol 78 (2) ◽  
pp. 251-257 ◽  
Author(s):  
G. Tolis ◽  
L. Kovacs ◽  
H. Friesen ◽  
J. B. Martin
Keyword(s):  
Growth Hormone ◽  
Fasting Serum ◽  
Thyrotrophin Releasing Hormone ◽  
Dynamic Evaluation ◽  
Releasing Hormone ◽  
Active Acromegaly ◽  
Plasma Gh ◽  
Serum Gh

ABSTRACT Ten patients with active acromegaly were studied. In 9 plasma GH levels failed to suppress after glucose (OGTT), in 8 an increase in serum GH occurred after thyrotrophin releasing hormone (TRH). After L-Dopa, 4 patients showed no change in serum GH, 3 exhibited a decrease and in 3 an increase in serum hGH occurred. With a combined insulin (ITT) and arginine (ATT) test, 2 patients exhibited an increase in hGH, and in 6 no change occurred. Fasting serum GH concentration was less than 11 ng/ml in 5 patients. Basal prolactin (hPRL) levels were normal in all patients including two with galactorrhea. L-Dopa suppressed and TRH stimulated hPRL secretion in all, but the responses which were seen were subnormal. Hydrocortisone infusion in two acromegalics did not affect the prolactin induced increase after TRH but blunted the GH increase after TRH.

Influence of endogenous cholinergic tone and α-adrenergic pathways on growth hormone responses to His-d-Trp-Ala-Trp-d-Phe-Lys-NH2 in the dog

1993 ◽  
Vol 138 (2) ◽  
pp. 211-218 ◽  
Author(s):  
J. Muruais ◽  
A. Peñalva ◽  
C. Dieguez ◽  
F. F. Casanueva
Keyword(s):  
Growth Hormone ◽  
Inhibitory Effect ◽  
Adrenergic Agonist ◽  
Stimulatory Action ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Combined Administration ◽  
Cholinergic Tone ◽  
Basal Plasma ◽  
Plasma Gh

ABSTRACT His-d-Trp-Ala-Trp-d-Phe-Lys-NH2 (GHRP-6) is a synthetic peptide unrelated to any known hypothalamic-releasing hormone including growth hormone-releasing hormone (GHRH). Interestingly, this peptide induces a dose-related increase in plasma GH levels in all species tested so far. The aim of this study was to investigate the action of GHRP-6 alone or in combination with GHRH on GH release in dogs. In addition, the activation or blockade of endogenous cholinergic tone and α-1 adrenoceptors on GHRP-6-stimulated GH secretion was assessed. In adult Beagle dogs (n = 10), GHRP-6 (90 μg i.v.) increased basal GH levels from 2·6 ± 1·5 to 14·4 ± 3·1 μg/l (mean ± s.e.m.) after 15 min. GHRH (50 μg i.v.) induced a GH peak of 9·7 ± 2·2 μg/l at 15 min. The combined administration of GHRP-6 and GHRH strikingly potentiated canine GH release with a peak of 54 ± 9·0 μg/l (P <0·01). Pretreatment with the cholinergic agonist pyridostigmine (30 mg per os) increased GHRP-6-stimulated GH secretion (37·9 ± 10·1 μg/l P <0·05), while the muscarinic blocker atropine (100 μg i.v.) completely abolished (GH peak lower than 2 μg/l) the stimulatory action of GHRP-6. On the other hand, administration of the α-2 adrenergic agonist clonidine (4 pg/kg i.v.) increased basal plasma GH levels without affecting GH responses to GHRP-6. Finally, while the α-1 adrenergic agonist methoxamine (5 mg i.v.) did not significantly increase GH responses to GHRP-6, administration of the α-1 adrenoceptor antagonist prazosin (20 mg i.v.) reduced GHRP-6-induced GH secretion (area under curve, 206 ± 39 vs 557 ± 172, P <0·05). In summary, the synergistic effect of the combined administration of maximal doses of GHRP-6 and GHRH suggests that these two peptides act through different mechanisms. The finding that cholinergic drugs were able to modulate the GH secretion elicited by GHRP-6 argues against the hypothesis that such a peptide acts by influencing hypothalamic somatostatin release and suggests that it acts directly at the pituitary level. Finally, the unexpected lack of effect of clonidine and the inhibitory effect of prazosin on GHRP-6-induced GH secretion suggests that the role of α-adrenergic pathways in GH secretion is more complex than previously thought. Journal of Endocrinology (1993) 138, 211–218

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