Disappearance half-life times of exogenous and growth hormone-releasing factor-stimulated endogenous growth hormone in normal rats

1991 ◽  
Vol 128 (3) ◽  
pp. 369-374 ◽  
Author(s):  
I. M. Chapman ◽  
A. Helfgott ◽  
J. O. Willoughby
Keyword(s):  
Growth Hormone ◽  
Endogenous Growth ◽  
Half Life ◽  
Somatostatin Analogue ◽  
Blood Samples ◽  
Growth Hormone Releasing Factor ◽  
Hypothalamic Hormones ◽  
Significant Difference ◽  
Long Acting ◽  
Analogue Octreotide

ABSTRACT This study was performed to determine the disappearance half-life times of endogenous and exogenous rat GH in conscious normal rats and to compare these with the decay characteristics of GH at the end of spontaneous normal bursts. The endogenous half-life was determined in five rats by giving an i.v. injection of rat GH-releasing factor followed after 10 min by an i.v. injection of long-acting somatostatin analogue (octreotide) and taking blood samples for 85 min. The half-lives (mean ± s.e.m.) were 3·4±0·4 min and 13·2±1·1 min for the first and second exponential respectively as determined by bi-exponential analysis. The exogenous GH half-life was determined in ten rats by giving i.v. octreotide followed after 10 min by i.v. rat GH and sampling for 85 min. The half-lives of exogenous GH were 3·3±0·2 min and 17·5±1·4 min by bi-exponential analysis and there was no significant difference between the half-lives of endogenous and exogenous GH. The half-life of the decline of GH levels at the end of spontaneous bursts in nine rats was 14·4±0·9 min, not different from the half-life of endogenous GH, the secretion of which was terminated by octreotide. This suggests that the end of spontaneous GH bursts is marked by sudden cessation of GH release and may provide an indication of the rapidity of change in the levels of the underlying hypothalamic hormones which control GH release. Journal of Endocrinology (1991) 128, 369–374

PHARMACOKINETICS OF THE LONG-ACTING SOMATOSTATIN ANALOGUE OCTREOTIDE (SMS 201-995) IN ACROMEGALY

1990 ◽  
Vol 32 (5) ◽  
pp. 545-550 ◽  
Author(s):  
J. NICHOLLS ◽  
D. WYNICK ◽  
J. DOMIN ◽  
L. M. SANDLER ◽  
S. R. BLOOM
Keyword(s):  
Somatostatin Analogue ◽  
Long Acting ◽  
Analogue Octreotide

Aggravation of hypoglycemia in insulinoma patients by the long-acting somatostatin analogue octreotide (Sandostatin®)

1989 ◽  
Vol 121 (1) ◽  
pp. 34-40 ◽  
Author(s):  
C. D. A. Stehouwer ◽  
W. F. Lems ◽  
H. R. A. Fischer ◽  
W. H. L. Hackeng ◽  
M. A. B. Naafs
Keyword(s):  
Blood Glucose ◽  
Hormone Secretion ◽  
Somatostatin Analogues ◽  
Serum Glucose ◽  
Somatostatin Analogue ◽  
Transient Decrease ◽  
Glucoregulatory Hormones ◽  
Octreotide Therapy ◽  
Long Acting ◽  
Analogue Octreotide

Abstract. Recently somatostatin analogues were successfully used to control insulin-induced hypoglycemia in patients with insulinoma. We observed a transient decrease in glucose levels and symptomatic hypoglycemia after administration of the long-acting somatostatin analogue octreotide (Sandostatin®) in two insulinoma patients. We studied the acute effects of octreotide (administered before breakfast) on blood glucose and glucoregulatory hormones in these patients. In one patient, we studied the effects of glucagon replacement and changing the time of breakfast (relative to octreotide administration) on octreotide-associated changes in blood glucose and glucoregulatory hormones. Compared with control levels, octreotide therapy reduced insulin levels. During hypoglycemia glucagon and growth hormone levels were suppressed, but cortisol levels appropriately increased. The increase in catecholamine levels was normal in one patient, but markedly attenuated in the other. A transient decrease in serum glucose after octreotide was absent after glucagon replacement, but present when breakfast was taken before administration of octreotide. We conclude that in patients with insulinoma, octreotide therapy may be associated with clinically important hypoglycemia, during which counterregulatory hormone secretion may be attenuated.

Clinical use of the long acting somatostatin analogue octreotide in pediatrics

1994 ◽  
Vol 153 (5) ◽  
pp. 304-310 ◽  
Author(s):  
M. T. Tauber ◽  
A. G. Harris ◽  
P. Rochiccioli
Keyword(s):  
Somatostatin Analogue ◽  
Clinical Use ◽  
Long Acting ◽  
Analogue Octreotide

Reduction of pituitary size by the somatostatin analogue SMS 201-995 in a patient with an islet cell tumour secreting growth hormone releasing factor

1986 ◽  
Vol 113 (1) ◽  
pp. 23-28 ◽  
Author(s):  
Darrell M. Wilson ◽  
Andrew R. Hoffman
Keyword(s):  
Growth Hormone ◽  
Islet Cell ◽  
Substantial Reduction ◽  
Good Control ◽  
Cell Tumour ◽  
Somatostatin Analogue ◽  
Pancreatic Islet Cell ◽  
Growth Hormone Releasing Factor ◽  
Hormone Levels ◽  
Islet Cell Tumour

Abstract. Acromegaly is rarely caused by the ectopic secretion of growth hormone releasing factor (GRF) from peripheral neuroendocrine tumours. We evaluated the ability of a recently developed somatostatin analogue (SMS 201-995, Sandoz) to reduce hormone levels and pituitary size in a young woman with acromegaly and Zollinger-Ellison syndrome secondary to a metastatic pancreatic islet cell tumour secreting GRF and gastrin. Gastrin, GRF, and growth hormone (GH) levels declined dramatically following the initiation of therapy with the analogue by continuous iv infusion. Although intermittent sc therapy was not effective in suppressing hormone levels, continuous sc infusion of SMS 201-995 has provided good control of both GRF and GH levels for nine months. Moreover, treatment with SMS 201-995 was associated with a substantial reduction in pituitary enlargement and an improvement in her gastric symptoms. Continuous sc infusion of SMS 201-995 may be useful in treating enlarged pituitaries resistant to other modes of therapy.

Central effects of growth hormone-releasing hexapeptide (GHRP-6) on growth hormone release are inhibited by central somatostatin action

1995 ◽  
Vol 144 (3) ◽  
pp. 555-560 ◽  
Author(s):  
K M Fairhall ◽  
A Mynett ◽  
I C A F Robinson
Keyword(s):  
Growth Hormone ◽  
Somatostatin Analogue ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Central Action ◽  
Central Effects ◽  
Central Actions ◽  
Long Acting ◽  
Major Target

Abstract Growth hormone (GH) release is stimulated by a variety of synthetic secretagogues, of which growth hormone-releasing hexapeptide (GHRP-6) has been most thoroughly studied; it is thought to have actions at both pituitary and hypothalamic sites. To evaluate the central actions of this peptide, we have studied GH release in response to direct i.c.v. injections in anaesthetized guinea pigs. GHRP-6 (0·04–1 μg) stimulated GH release >10-fold 30–40 min after i.c.v. injection. The same GH response required >20-fold more GHRP-6 when given by i.v. injection. GH release could also be elicited by a non-peptide GHRP analogue (L-692,585, 1 μg i.c.v.), whereas a growth hormone-releasing factor (GRF) analogue (human GRF 27Nle(1–29)NH2, 2 μg, i.c.v.) was ineffective. A long acting somatostatin analogue (Sandostatin, SMS 201–995, 10 μg i.c.v.) (SMS) given 20 min before 200 ng GHRP-6 blocked GH release. This was unlikely to be due to a direct effect of SMS leaking out to the pituitary, since central SMS injections did not affect basal GH release, nor did they block GH release in response to i.v. GRF injections. We conclude that the hypothalamus is a major target for GHRP-6 in vivo. Since the GH release induced by central GHRP-6 injections can be inhibited by a central action of somatostatin, and other data indicate that GHRP-6 activates GRF neurones, we suggest that somatostatin may block this activation via receptors known to be located on or near the GRF cells themselves. Somatostatin may therefore be a functional antagonist of GHRP-6 acting centrally, as well as at the pituitary gland. Journal of Endocrinology (1995) 144, 555–560

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

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