الفهرس 
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Abstract
Krulich et al. (1968) demonstrated that ovine hypothalamic extracts contain a factor Cs) capable of inhibiting the release of growth hormone.
Vale et al . (1971) demonstrated CHILI activity while searching for CHRH in ovine hypothalamic fractions.
Brazeau et al and Burgus et al. (1973) succeeded in isolation a peptide from ovine hypothalamic extracts which inhibit CLI re)ese.
They determined its primary structure and sequence, this peptide was named Somatostatin Css) or somatotrophin— Releasing Inhibiting factor (Slur) or growth hormone inhibiting hormone COHILI).
Subsequently somatostatin or peptide CS) with soma— tostatin—like—immunoreactivity has been detected in extrahypothalamic brain, sensory neurones, gastrointestinal endocrine cells, D cells of pancreatic islets, and thyroid parafollicular cells.
Almost every tissue that is acted upon by somatost— atm contains this peptide in specialized cells.
This substance has -been shown to inhibit growth hormone release in response to wide variety of stimuli Hn normal individuals and in patients with acromegaly. The therapeutic usefulness of somatostatin in treating acrom—
egalic patients is limited by its multiple effects on many secretory cells and its :short duration of action.
Recently, series of somatostatin analogues have been prepared in hopes of finding some which enhance one or more of the effects of somatostatin and reduce the other (Adrian et al 1981 & Kahn et al 1981).
Diabetic patients are also considered as possible candidates for treatment with somatostatin which is based on :(l) the plasma growth hormone is high in diabetics and clinical trial of controlling this effect by hypophyse— ctomy demonstrated a significant inhibition of retinopathy and a normalization of capillary fragility in longterm diabetics.
(2) In insulin dependent diabetics, somatostatin causes marked flattening of blood glucose curve after food intake (Lundbaek 1978).
Somatostatin can be used as supplement to traditional insulin treatment, in juvenile diabetics when two clinically acceptiable analogues become available, one that suppresses only growth hormone, another that suppresses glucogon, insulin suppressive effect would not be of importance, because no body would think of giving som— atostatin to juvenile diabetics without giving insulin.