scholarly journals The long-acting somatostatin analogue octreotide alleviates symptoms by reducing posttranslational conversion of prepro-glucagon to glucagon in a patient with malignant glucagonoma, but does not prevent tumor growth

1994 ◽  
Vol 72 (2) ◽  
pp. 127-133 ◽  
Author(s):  
F. Jockenhövel ◽  
S. Lederbogen ◽  
T. Olbricht ◽  
H. Schmidt-Gayk ◽  
E. P. Krenning ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Somatostatin Analogue ◽  
Long Acting ◽  
Prevent Tumor Growth ◽  
Analogue Octreotide

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

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

Effect of systemic glucagon administration on ACTH secretion in anaesthetized rats

1995 ◽  
Vol 145 (1) ◽  
pp. 51-58 ◽  
Author(s):  
R H Rao
Keyword(s):  
Direct Effect ◽  
Plasma Glucose ◽  
Glucose Infusion ◽  
Somatostatin Analogue ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Insulin Levels ◽  
Anaesthetized Rats ◽  
Long Acting ◽  
Analogue Octreotide

Abstract The effect of glucagon on ACTH secretion was studied in anaesthetized rats injected with either saline (0·1 ml i.m.) or glucagon (0·02 mg/kg i.m.). For the first 90 min after glucagon injection, plasma ACTH fell by 50% from the basal value of 23 ±4 pmol/l (mean ± s.e.m.) to 11 ±2 (P=0·011), after which an abrupt return to baseline occurred (120 min value: 26 ± 2 pmol/l). In saline injected rats, the baseline ACTH value was not significantly different from either the 90 min value or the 120 min value (27 ±3 vs 21 ± 4 and 24 ± 3 pmol/l respectively; P>0·10). Plasma glucose after glucagon peaked at 11·6 ± 1·1 mmol/l by 15 min but subsequently fell rapidly, attaining the baseline by 60 min. Insulin levels increased sharply after glucagon, from 381 ±78 pmol/l to 3172 ±668 pmol/l at 15 min, and plateaued at approximately 1000 pmol/l thereafter. No changes in glucose or insulin were seen in saline injected rats. The magnitude of suppression of ACTH after glucagon was not affected either by sustained hyperinsulinaemia (≃ 1400 pmol/l), induced with continuous glucose infusion to maintain plasma glucose>12 mmol/l, or by pretreatment with the long-acting somatostatin analogue octreotide (50 μg/kg s.c.). However, the return to baseline between 100 and 120 min was prevented both by hyperinsulinaemia induced with sustained hyperglycaemia, and by octreotide. It is postulated that glucagon may inhibit ACTH secretion either by a direct effect on the hypothalamus or indirectly through insulin, which is known to stimulate endogenous somatostatin release. Journal of Endocrinology (1995) 145, 51–58

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