Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was conducted to determine if glucagon release is involved in the hyperglycemic response to epinephrine and isoproterenol in the fasted and fed, unanesthetized rabbit. Epinephrine produced dose-related increases in plasma glucose and glucagon levels in fed and fasted rabbits whereas isoprotereol produced modest hyperglycemia without hyperglucagonemia. Infusion of somatostatin suppressed epinephrine-induced glucagon release and this was correlated with a 50% reduction in the hyperglycemic response. These data suggest that epinephrine-induced glucagon release is the primary reason for the difference in hyperglycemic activity between epinephrine and isoproterenol in the unanesthetized rabbit.
Horm Metab Res 1978 Sep
PMID:Catecholamine-induced changes in plasma glucose, glucagon and insulin in rabbits: effects of somatostatin. 36 31

Somatostatin is produced by gastrointestinal endocrine cells that have long, nonluminal, cytoplasmic processes. Such processes terminate on other cell types, including gastrin-producing and hydrochloric acid-producing cells, whose functions are profoundly affected by somatostatin. The findings suggest that somatostatin cells control the functions of other cells through local release of the peptide by way of cytoplasmic processes. Also, certain other types of gastrointestinal endocrine cells have similar cytoplasmic prolongations, which may have analogous local (paracrine) regulatory functions.
Science 1979 Sep 28
PMID:Somatostatin cell processes as pathways for paracrine secretion. 38 60

By using both immunofluorescence and peroxidase-anti-peroxidase procedures to detect cells producing the four islet hormones, supplemented by biochemical, biological, and radioimmunological assays of tissue extracts, it has been shown that insulin seems to be the most original hormone, apparently occurring already in invertebrates in cells of open type in the alimentary tract mucosa. Insulin cells also predominate in the first islet organ, namely that of the cyclostomes. The order of appearance in the endocrine pancreas during the subsequent evolution is: somatostatin; glucagon; and the pancreatic polypeptide. Even in lower vertebrates pancreatic polypeptide cells occur in those parts of the pancreas situated in close proximity to the gut.
J Histochem Cytochem 1979 Sep
PMID:Immunocytochemical studies of the evolution of islet hormones. 38 30

It has recently been suggested from experiments in dogs that somatostatin suppresses insulin release via a stimulation of the inhibitory alpha-adrenoceptors of the pancreatic B-cell. The effect of somatostatin on insulin secretion during alpha-adrenergic blockade with phentolamine was therefore studied in three different species; the rat, the cat and the mouse. It was found that somatostatin significantly depressed insulin release during alpha-adrenoceptor blockade in all three species. In the rat, infusion of somatostatin at a dose of 0.3 microgram/kg/min decreased basal plasma insulin concentration by 92%. In the presence of phentolamine, the same dose of somatostatin lowered plasma insulin by 85%. In the cat, a similar infusion of somatostatin lowered basal plasma insulin concentration by 87%, but its depressive effect during alpha-adrenergic blockade was comparatively less pronounced (68%) than in the rat. In the mouse, a single iv injection of somatostatin induced a short-lasting depression of plasma insulin concentration during alpha-adrenergic blockade. From these results it seems unlikely that somatostatin should inhibit insulin release simply by stimulation of alpha-adrenoceptors on the B-cell. It cannot be ruled out, however, that a more complex interaction exists between somatostatin and the sympatho-adrenal system with regard to the control of insulin secretion.
Acta Endocrinol (Copenh) 1979 Sep
PMID:Inhibitory effect of somatostatin on insulin secretion during alpha-adrenergic blockade in three different species. 38 85

Unspecific binding of immunoglobulins to gastrin G cells, glucagon A cells and somatostatin D cells of the gastric mucosa or pancreas, as well as to the calcitonin-somatostatin cells of rabbit thyroid has been found to occur through a non antigen-antibody mechanism mediated at least in part by the C1q fraction of complement. The phenomenon represents a major drawback in hormone immunohistochemistry, which can be prevented by incubating the specific anti-hormone sera with anti-C1q antibodies or with complement-fixing immunocomplexes.
Histochemistry 1979 Sep
PMID:Complement-mediated unspecific binding of immunoglobulins to some endocrine cells. 38 92

The effect of somatostatin on the thyrotropin (TSH), prolactin, growth hormone (GH) and insulin responses to the combined administration of thyrotropin releasing hormone (TRH) and arginine was studied in six healthy subjects, three hypothyroid patients and three acromegalic patients. Similar inhibition by somatostatin of the TSH and insulin responses was observed in the three groups. While the tetradecapeptide had no significant effect on the prolactin response in the healthy and acromegalic subjects, it caused an unexpected inhibition of the prolactin response in two of the hypothyroid subjects. Contrary to the findings in the healthy and hypothyroid subjects, somatostatin did not inhibit the GH response in the acromegalic patients. Normal inhibition by somatostatin of the insulin response, followed by a rebound in insulin secretion, was observed in all subjects. These preliminary data indicate increased sensitivity of the prolactin-secreting cells to somatostatin in hypothyroidism and suggest that decreased responsiveness of the somatotrophs to somatostatin could play a role in the pathogenesis of acromegaly.
Can Med Assoc J 1977 Sep 03
PMID:Effect of somatostatin on thyrotropin, prolactin, growth hormone and insulin responses to thyrotropin releasing hormone and arginine in healthy, hypothyroid and acromegalic subjects. 40 75

With a view toward the therapeutic use of somatostatin in the treatment of acute pancreatitis, a preliminary investigation was conducted with 6 healthy volunteers, in which the suppressive effect of somatostatin on endocrine and exocrine pancreatic function was observed. A 30-minute baseline measurement period was followed by the administration of cyclic somatostatin (100 microgram by i.v. injection plus a 90-minute infusion at a rate of 200 microgram/hr). After the first 45 minutes of this infusion secretion was submaximally stimulated by the infusion of secretin-cholecystokinin-pancreozymin (CCK-PZ) (75 U each), over two hours. No decrease was observed in basal bicarbonate or enzyme concentration under somatostatin administration alone. However, secretion did not show the usual steep rise after the commencement of stimulation. After the somatostatin infusion was stopped, i.e. under secretin-CCK-PZ alone, a significant increase occurred in the values of secretin-induced volume, bicarbonate concentration and total bicarbonate contents of the duodenal aspirate, as well as in CCK-PZ-induced enzyme secretion. The release of insulin, both basal and stimulated, was also significantly decreased by somatostatin.
Wien Klin Wochenschr 1977 Sep 16
PMID:[Suppressive effect of somatostatin on secretin-CCK-PZ-stimulated endocrine and exocrine pancreatic function in man (author's transl)]. 41 Jan 66

1) In electively immuno-induced carcinomas of the exocrine pancrease in Mice, where A (glucagon) and B (insulin) endocrine cells persist, cells with a pancreatic polypeptide immunoreactivity are also detected, even in late evolution stages. These cells, like D cells, containing somatostatin, are localized only in the pancreatic remains surrounding the anaplasic carcinomatous tissue: islets, adenomatous parenchyma, and ductular epithelium. Ultrastructure of these cells shows their active elaboration of numerous chracteristic secretion granules. (2) Immunocytoenzymatic detection of gastrin is negative in the exocrine and endocrine pancreatic tissues. However one of the anti-gastrin sera used gives a positive reaction, in some carinomatous cells only. Does this immunoreactivity characterize a polypeptide specific to the pancreatic carcinomatous cell?
C R Acad Hebd Seances Acad Sci D 1977 Sep 12
PMID:[Presence of "pancreatic polypeptide" cells, and gastrin immunoreactivity in immuno-induced exocrine pancreas carcinoma]. 41 May 28

Bombesin acts within the brain to produce a prompt and sustained hyperglycemia, hyperglucagonemia, and relative or absolute hypoinsulinemia. Bombesin does not decrease plasma glucose turnover. Acute adrenalectomy but not hypophysectomy prevents hyperglycemia and hyperglucagonemia after intracisternal administration of bombesin. Administration of bombesin into the lateral ventricle of awake, unrestrained animals results in elevation of plasma glucose, preceded by a significant increase in plasma epinephrine and no increase in plasma norepinephrine or dopamine. Systemic administration of somatostatin prevents bombesin-induced hyperglycemia and hyperglucagonemia. These data support the conclusion that bombesin acts within the brain to increase sympathetic outflow resulting in increased adrenalmedullary epinephrine secretion, followed by depression of plasma insulin and elevation of plasma glucagon and glucose.
Endocrinology 1979 Sep
PMID:Central nervous system action of bombesin: mechanism to induce hyperglycemia. 46 25

Somatostatin (SRIF) is present in nerve endings in the median eminence (ME) and posterior pituitary. Hypothalamic SRIF containing neuronal perikarya are predominantly located in the anterior hypothalamic area (AHA), a region implicated in the inhibitory control of GH secretion. The effect of AHA lesions on SRIF in the ME, posterior pituitary, pancreas, stomach, and small intestine was studied in the rat in order to elucidate the source of ME and posterior pituitary SRIF and to determine if depletion of hypothalamic SRIF affects peripheral organ concentrations of the peptide. Lesioned animals showed a highly significant (P less than 0.01) 83% and 82% reduction in ME and posterior pituitary SRIF and to determine if depletion of hypothalamic SRIF affects peripheral organ concentrations of the peptide. Lesioned animals showed a highly significant (P less than SRIF concentrations in the pancreas, stomach, and small intestine of the lesioned animals. Plasma and pancreatic insulin and pancreatic glucagon were likewise unchanged. These data suggest that the hypothalamic SRIF pathway begins in the AHA, from where axons of somatostatinergic neurosecretory neurons project to both ME and posterior pituitary. AHA lesions have no effect on gut and pancreatic SRIF or pancreatic insulin and glucagon.
Endocrinology 1979 Sep
PMID:Effect of anterior hypothalamic lesions on neurohypophysial and peripheral tissue concentrations of somatostatin in the rat. 46 31


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