Multiple subcutaneous injections of somatostatin induce tachyphylaxis of the suppression of plasma insulin, but not glucagon, in the rat

Märki, F; Bucher, U; Richter, J.

doi:10.1016/0167-0115(82)90144-6

Cited by 16 publications

(5 citation statements)

References 7 publications

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“…The long-acting somatostatin analogue is particularly useful in patients with pancreatic microadenomatosis because it may obviate the need for near-total pancreatectomy for a benign condition and spares the patient the numerous complications that can be associated with this operation. It had been reported that repeated injections of a somatostatin analogue in rats rapidly induces tachyphylaxis of the suppression of insulin release (Marki et al, 1982) but this was not experienced in our patient after therapy for 6 months.…”

Section: Discussioncontrasting

confidence: 58%

Prevention of Hypoglycaemia in a Patient With Pancreatic Microadenomatosis by a Long‐acting Somatostatin Analogue SMS 201‐995

Kung

Wang

et al. 1987

Clinical Endocrinology

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Acute suppression of insulin secretion from pancreatic insulinomas by long-acting somatostatin analogue SMS 201-995 has been documented. We report the chronic use of the drug in a patient with persistent hypoglycaemia due to benign pancreatic microadenomatosis with satisfactory control of plasma glucose level and reduction of insulin production. There was no tachyphylaxis or untoward side-effect noted during the 6-month treatment period.

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Section: Discussioncontrasting

confidence: 58%

Prevention of Hypoglycaemia in a Patient With Pancreatic Microadenomatosis by a Long‐acting Somatostatin Analogue SMS 201‐995

Kung

Wang

et al. 1987

Clinical Endocrinology

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“…Comparable results were obtained in acromegalics treated with BIM for 1 year [35]. The transient effect of somatostatin analogues on glucose tolerance could be accounted for by a receptor desensitization, as has been shown for some subtypes of somatostatin receptor [36,37,38]. Several subtypes or somatostatin receptors have been described [36,39,40,41].…”

Section: Discussionmentioning

confidence: 80%

Effects of the new somatostatin analogue (BIM 23014) on blood glucose homeostasis in normal men

Kuhn

Basin

Mollard

et al. 1992

Eur J Clin Investigation

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Changes in blood glucose homeostasis induced by the new somatostatin analogue BIM 23014 (BIM) were studied. Eight normal men (study 1) received either vehicle or 1000, 2000 and 3000 micrograms BIM as a 24 h s.c. infusion. Blood glucose, plasma insulin, C-peptide, glucagon and growth hormone (GH) were measured before treatment and then hourly for 24 h. In five normal men (study 2) an oral glucose tolerance test (OGTT) was performed during vehicle infusion and then on days 1 and 7 of a continuous s.c. infusion of 2000 micrograms BIM daily for 7 days. The same biological parameters as in study 1 were measured before OGTT and then twice-hourly for 5 h. Dose-dependent and transient glucose intolerance was observed in the first half of study 1. Except for glucagon, BIM significantly (P < 0.01) reduced plasma insulin, C-peptide and GH levels. In study 2 BIM infusion induced glucose intolerance and a drop in plasma insulin and C-peptide on day 1 which disappeared on day 7 of infusion. Higher on day 7 than on day 1, plasma GH secretion was significantly (P < 0.01) reduced throughout BIM infusion. In contrast plasma glucagon levels were not modified at any time. Side-effects were abdominal cramps and diarrhoea which were observed in most subjects when increasing BIM daily dose. In conclusion, BIM infusion induced transient changes in glucose homeostasis and insulin secretion in normal men. By contrast, plasma GH levels remained reduced throughout the treatment. BIM appears to be a useful tool to selectively inhibit GH secretion.

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“…It was shown previously that repeated adminis¬ tration of high doses of SMS 201-995 induces desensitization or tachyphylaxis of its inhibitory effect on normal GH secretion in the rat (Lamberts et al 1986) and of its inhibitory effect on the growth of transplantable PRL-secreting pituitary tumours (Lamberts et al 1986). Prolonged soma¬ tostatin pretreatment in vitro also desensitizes its inhibitory effect on ACTH release by cultured mouse anterior pituitary tumour cells (Reisine & Axelrod 1986), whereas multiple sc injections of another somatostatin analogue were reported to induce in rats very rapidly tachyphylaxis of its suppressive effect on insulin, but not on glucagon se-cretion (Marki et al 1982). It is currently unknown why this desensitization phenomenon or tachyphylaxis to SMS 201-995 therapy in man seems to be confined to endocrine pancreatic tumours (Lamberts 1986).…”

Section: Discussionmentioning

confidence: 99%

Development of resistance to a long-acting somatostatin analogue during treatment of two patients with metastatic endocrine pancreatic tumours

Lamberts

Pieters²,

Metselaar³

et al. 1988

Acta Endocrinologica

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Abstract. Two patients with metastatic endocrine pancreatic tumours initially responded well to therapy with the long-acting somatostatin analogue SMS 201-995. In the first patient with an insulinoma both the number of hypoglycemic attacks and the increased insulin levels decreased initially, but returned to pretreatment intensity and concentrations within 9 days after the start of therapy with 200–300 μg SMS 201-995 daily. After a short interruption, no effect was observed of re-institution of therapy at a dose of 400 μg SMS 201-995 daily. In the other patient with a metastatic vipoma both diarrhea, hypokalemia and plasma VIP levels reacted initially well to SMS 201-995 treatment with 300 μg per day, but resistance to therapy developed after 2 weeks. An increase in the dose of the analogue to maximally 600 μg/day was followed by a transient improvement, but finally both the volume of diarrhea and the levels of vasoactive intestinal polypeptide were higher than those before the start of therapy. Conclusions: Development of resistance to SMS 201-995 both with regard to the clinical effect and to the inhibitory effect on tumour hormone secretion can be expected in some patients with metastatic endocrine pancreatic tumours. On the basis of our clinical observations down-regulation of somatostatin receptors is suggested to be one of the mechanisms of this development.

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Multiple subcutaneous injections of somatostatin induce tachyphylaxis of the suppression of plasma insulin, but not glucagon, in the rat

Cited by 16 publications

References 7 publications

Prevention of Hypoglycaemia in a Patient With Pancreatic Microadenomatosis by a Long‐acting Somatostatin Analogue SMS 201‐995

Prevention of Hypoglycaemia in a Patient With Pancreatic Microadenomatosis by a Long‐acting Somatostatin Analogue SMS 201‐995

Effects of the new somatostatin analogue (BIM 23014) on blood glucose homeostasis in normal men

Development of resistance to a long-acting somatostatin analogue during treatment of two patients with metastatic endocrine pancreatic tumours

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