Somatostatin receptors: From signaling to clinical practice

Publisher Summary This chapter focuses on the investigations conducted over the past few years on the interaction between the hypothalamic hormone(s) and gonadal steroids in the regulation of cyclic gonadotropin output by the adenohypophysis in humans. It describes hypothalamus as a neuroendocrine regulator. It also reviews the observations on the biological actions of hypothalamic somatostatin in humans. The description of the hypothalamic-hypophysial portal system and the subsequent presentation of a number of anatomical and physiological observations led to the proposal that the hypothalamus is critically involved in the control of anterior pituitary function. The chapter presents the three elements of the hypothalamic-hypophysial portal system: (1) the CNS-hypothalamus complex that may be regarded as a signal generator, (2) the pituitary as a signal transmitter, and (3) the cyclic ovarian steroid output as a signal modulator. It reviews the regulation of the hypothalamic-hypophysial- gonadal system in humans within this general context.

The operating characteristics of the hypothalamic-pituitary system during the menstrual cycle and observations of biological action of somatostatin.

We treated a two-month-old infant with servere intractable hypoglycemia and nesidioblastosis with continuous glucose infusions (0.75 g per kilogram per hour) via a central venous catheter. Preprandial glucose levels on this regimen were 37+/-2 mg per deciliter (+/-S.E.M.). Basal serum insulin levels were within normal fasting levels for this age group but inappropriately elevated for the blood glucose levels. The beta cells were exquisitely sensitive to infusions of synthetic cyclic somatostatin, with a dose-dependent rise in blood glucose and concomitant suppression of serum insulin levels. There was only minimal suppression of plasma glucagon levels. Single subcutaneous injections of 50 microng of protamine zinc somatostatin raised preprandial blood glucose levels to 83+/-3 mg per deciliter for four to five days although preprandial hormone levels were unchanged. These findings indicate that hypoglycemia of infancy is a hyperinsulin state with abnormal basal regulation of insulin secretion.

Hypoglycemia of infancy and nesidioblastosis. Studies with somatostatin.

Somatostatin-like immunoreactivity (SLI) was measured by RIA in the plasma of normal and severely alloxan diabetic dogs in the fasting state and after the administration of nutrients. The iv infusion of glucose for 6 h was associated with a small but significant decline in plasma SLI (162 ± 10 to 146 ± 9 pg/ml; P < 0.01). In nine alloxan diabetic dogs, the baseline SLI levels averaged 212 ± 16 pg/ml, significantly higher than normal (P < 0.005), and there was little or no change during glucose infusion. Intragastric glucose elicited only a small transient rise in SLI in normal dogs, while in the diabetic dogs, a significant change in SLI was not observed. Intragastric administration of casein hydrolysate to nine normal dogs was associated with a rise in plasma SLI from < 0.02). After a liver meal, SLI rose in normal dogs from 134 ± 7 to 190 ± 15 pg/ml within 30 min (P < 0.001) and in the diabetic dogs, it rose from 240 ± 20 to a 30-min level of 244 ± 33 pg/ml (P < 0.005). In normal dogs, a fat-protein mea...

The response of plasma somatostatin-like immunoreactivity to nutrients in normal and alloxan diabetic dogs.

Somatostatin inhibition of insulin release from freshly isolated and organ cultured rat islets of Langerhans in vitro.

This study demonstrates that synthetic somatostatin (SRIF) induces a suppressive effect on circulating insulin and glucose levels in normal human subjects.

Acute suppression of insulin and glucose levels by synthetic somatostatin in normal human subjects.

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Acute suppression of insulin and glucose levels by synthetic somatostatin in normal human subjects.