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)

Seven adult male rats were observed for body weight and microregulation (feeding, drinking, and running patterns) after manipulation of insulin and glucagon levels. They received three injections per day for 3 days each week of 3 U of protamine zinc insulin, .25 mg of zinc glucagon, 50 microgram of protamine zinc somatostatin (SRIF), or protamine zinc vehicle. Diabetes was then induced with an iv injection of streptozotocin (65 mg/kg), and the injection schedule was repeated after the full diabetic syndrome emerged. In all rats whose insulin levels were increased relative to glucagon levels, body weight increased; in those whose glucagon levels were increased relative to insulin levels, body weight decreased. All injections except vehicle reduced meal sizes in both normal and diabetic rats, but only insulin increased the frequency of feeding. These effects could be predicted by the glucostatic theory of food intake regulation and are thus interpreted as supportive of this theory. These results also support the hypothesis that the relative concentration of insulin to glucagon is a regulator of body weight set point.
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PMID:Insulin and glucagon as determinants of body weight set point and microregulation in rats. 68 70

In a group of pancreatectomized subjects, immunoreactive glucagon (IRG) concentrations were normal after an overnight fast, increased after oral glucose, were not suppressed by somatostatin (SRIF) or insulin, and in two of four subjects they rose with an arginine infusion. Even though the SRIF infusion failed to lower IRG, there was a fall in plasma glucose concentration in both subjects. In two subjects, endogenous hyperglycemia occurred during insulin withdrawal without a rise in IRG, and, in one subject, mild diabetic ketoacidosis developed with only a minimal rise in IRG. These results support the presence of an extrapancreatic source of IRG in man. Secretion from these extrapancreatic alpha cells appears to be regulated differently than secretion from pancreatic alpha cells.
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PMID:Immunoreactive glucagon responses to oral glucose, insulin infusion and deprivation, and somatostatin in pancreatectomized man. 70 Feb 56

Extracts of discrete lobes of chicken pancreas were assayed for somatostatin (SRIF), insulin and glucagon immunoreactivity. The distribution of hormone concentration was correlated appropriately with the known distribution of A, B, and D-cells. Concentrations of all three hormones were highest in the splenic lobe. The glucagon content of the ventral and dorsal lobes was low. Evidence is presented that the SRIF-like material in the pancreatic extracts is very similar to synthetic cyclic SRIF; parallel immunoassay displacement curves and similar chromatographic elution profiles were obtained. The SRIF concentration in chicken pancreas is 21 times higher than that found in the rat. Chicken pancreas may provide a useful model for studies of somatostatin physiology.
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PMID:High concentration of somatostatin immunoreactivity in chicken pancreas. 77 28

The direct inhibitory action of somatostatin (cyclized SRIF) on the pancreatic endocrine function was investigated by a technique using pancreaticoduodenal arteriovenous system in vivo. Somatostatin was infused for 20 minutes at a speed of 2.5 mug/minute into the superior pancreaticoduodenal vein and femoral artery were measured before and every 5 minutes throughout the experiment for 30 minutes. The results were compared with those obtained from the control experiment which was carried out in the same time schedule under infusion of physiologic saline solution instead of somatostatin. Next, the effect of somatostatin on the glucose-induced insulin release from the pancreas was also evaluated. The following findings were obtained. (1) Somatostatin infused at a speed of 2.5 mug/minute into the superior pancreaticoduodenal artery caused a statistically significant inhibition of plasma levels of IRI and IRG and also pancreatic output of these hormones. With the sessation of somatostatin infusion an abrupt rise of the hormones were seen. This "rebound" phenomenon was more pronounced in insulin secretion than in glucagon. No significant changes in the plasma glucose levels in either the pancreaticoduodenal vein or the femoral artery throughout the experiment were found. (2)During infusion of somatostatin at a speed of 1.25 mug/minute, insulin response to glucose injected into the pancreaticoduodenal artery in a small dose, as well as having no effect on the plasma glucose level in systemic circulation, was also significantly inhibited. From these findings obtained by direct experiment using the pancreaticoduodenal arterio-venous system, it was confirmed that somatostatin exhibits a direct inhibitory action on pancreas endocrine in a very low concentration in vivo, and it was suggested that this action might be partly due to a reduction in pancreatic circulation.
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PMID:[Effect of somatostatin on pancreatic endocrine--experiment by somatostatin infusion into the pancreaticoduodenal artery in dogs--(author's transl)]. 78 54

Somatostatin, or SRIF (Somatotropin Release Inhibiting Factor), is a tetradecapeptide of hypothalamic origin, which inhibits the secretion of growth hormone. It has also been recognized in other parts of the central nervous system, in the islets of Langerhans, and the mucosa of the upper digestive tract. Parenteral administration of synthetic SRIF inhibits the release of growth hormone, basal and stimulated by muscular exercise, arginine, L-DOPA, insulin-induced hypoglycemia, and sleeping. It also inhibits insulin and glucagon secretion, basal and stimulated, and several other secretory processes in endocrine and exocrine glands. It may have a depressor effect on some neurons in the central nervous system. Considerable interest has been prompted in the field of diabetology by the demonstration of somatostatin-induced suppression of growth hormone and glucagon : both hormones are over-secreted in many diabetic patients, and both may be noxious for small blood vessels in the diabetic. The eventual therapeutic use of somatostatin in humans is restricted, for the moment, by the unavaibility of long-acting SRIF preparations and the possibility of some adverse effects mainly affecting hemostasis. Evaluation of the physiological role (s) for this newcomer, and of the eventual pathophysiology of endogenous somatostatin, represent an unexpected and exciting field of neuro-endocrinology.
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PMID:[Somatostatin, a new hormone? (author's transl)]. 79 89

In recent years a variety of peptide hormones have been isolated from the mammalian hypothalamus and pituitary. Several hypothalamic hormones, including thyroliberin (thyrotropin-releasing factory), luliberin (luteinizing hormone-releasing factor), and somatostatin (somatotropin release-inhibiting factor), have been characterized and synthesized. The subsequent development of radioimmunoassays for these hormones has made possible the study of their physiology. The measurement of prolactin in serum and the release of pituitary hormones after the administration of the hypothalamic hormones has proved to be useful in clinical diagnosis. The use of hypothalamic hormones in treating various clinical disorders and the isolation and characterization of new releasing and inhibiting hormones in the hypothalamus are actively being investigated.
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PMID:Recently discovered hypothalamic-pituitary hormones. 81 15

The effect of exogenously administered somatostatin (SRIF) on meal-stimulated secretions of the exocrine pancreas was studied in dogs with chronic pancreatic fistulas. Dogs were fed 600 gm. of raw meat, and pacreatic output of water, bicarbonate, and protein was measured. Bicarbonate and protein secretions rose markedly postfeeding in all control animals. Four hundred micrograms or 100 mug. of SRIF infused for one hour together with a meal completely prevented the postfeeding rise in pancreatic secretions. SRIF (100 mug./hr.) infused one hour after a meal suppressed pancreatic secretions to basal levels within 30 minutes. Pancreatic secretions rose promptly after discontinuation of SRIF in all dogs. These data indicate (1) SRIF completely prevents pancreatic bicarbonate and enzyme responses when given together with a meal; (2) it completely suppresses already initiated pancreatic responses when given one hour after a meal; (3) 100 mug. of SRIF is as effective as 400 mug. in suppressing the postprandial rise in pancreatic secretions. We conclude that SRIF severely interferes with pancreatic secretions during normal alimentation and that this observation should be considered if SRIF is to be used as a therapeutic agent.
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PMID:Effect of somatostatin on meal-stimulated pancreatic exocrine secretions in dogs. 83 May 67

Studies were conducted in newborn lambs to gain insight into the significance and mechanism(s) responsible for the rapid rise in plasma immunoreactive glucagon (IRG) which occurs in human and other newborn species immediately after delivery. Three sets of experiments were conducted: group A, control studies (n = 5) in which delivery into room air was followed 1 hr later by cutting of the umbilical cord and periodic blood sampling for a further hour; group B, studies (n = 5) in which somatostatin (SRIF), a known inhibitor of IRG and insulin (IRI) secretion, was infused int othe fetus for 10 min before, and for 1 hr after delivery and immediate cord cutting; group C, studies (n = 5) in which an identical dose regimen of SRIF was infused into fasting newborn lambs aged 24-72 hr. The doses of SRIF used were several fold higher than those proven to suppres pancreatic hormones secretion in other species. In the control studies, plasma IRG levels remained stable until the cord was cut, after which event levels rose 5-6-fold (59 +/- 15 pg/ml to 305 +/- 98 pg/ml, P less than 0.05). Simultaneously, plasma free fatty acid (FFA) concentrations rose significantly (280 +/- 80 to 780 +/- 100 muEq/liter, P less than 0.05) and IRI remained unchanged. Plasma glucose concentrations, however, in contrast to observations in other species, did not fall, and therefore, hypoglycemia was not the stimulus for the glucagon surge. SRIF infusion at birth (group B) did not prevent the rise in IRG. Again blood glucose values did not fall, but in contrast to the control studies plasma IRI levels rose and the rise in FFA did not occur. Later SRIF infusion (group C) resulted a prompt and sustained suppression of IRG and IRI and a significant fall in blood glucose. These results suggest that an adrenergic mechanism rather than curtailment of nutrients is the major stimulus to the neonatal surge in IRG.
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PMID:Possible mechanisms and significance of the neonatal surge in glucagon secretion: studies in newborn lambs. 87 5

Basal release of pre-labeled, stored tritiated rat growth hormone ([3H]rGH) from perfused rat pituitary explants is a constant fraction of pituitary [LH]rGH content. Synthetic somatostatin (SRIF) inhibits the release of pre-labeled, stored [3H]rGH in a dose-dependent fashion. Prolonged exposure to SRIF results in an immediate and continuous inhibition of [3H]rGH release. In the in vitro perifusion system, the maximal inhibition, which is achieved with 25 nM SRIF, results in a rate of [3H]rGH release which is 30 to 40 per cent of basal release. Pulses of SRIF produce inhibition of [3H]rGH release followed by rebound release after withdrawal of SRIF. When the time of exposure to SRIF is held constant, both the SRIF-induced inhibition and the rebound release of [3H]rGH are dose-dependent. A similar progressive response is seen when a constant SRIF concentration is pulsed for variable periods of time. There is no net inhibition of [3H]rGH release by pulses of SRIF.
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PMID:Influence of synthetic somatostatin upon growth hormone release from perifused rat pituitaries. 95 64

The physiologic relationships of plasma TSH, T4 and T3 levels measured every 20 min in seven healthy young men and one healthy young woman have been investigated. A nocturnal TSH surge was observed in all subjects on both nights of the 36-48 h baseline observation period. In males the maximum plasma TSH value occurred at 2300 h. The mean peak TSH level was 2.0 +/- 0.3 (se) muU/ml compared with a mean of 1.3 +/- 0.9 muU/ml for the entire baseline records of the 8 subjects. The effect of iv infusion of 32-1000 mug of somatostatin (SRIF) for 1 1/2-3 h was investigated in four of the male subjects during 2 or 4 consecutive nights following the control period. Temporal relationships between the hormonal fluctuations observed throughout the control period and during the nights of SRIF infusion were investigated using time series analysis and Student's t test. Rapid fluctuations of plasma T4 and T3 concentration were noted, even when corrected for changes in total protein concentration, with an average coefficient of variation of 10% for T3 and 12% for T4. No increment of plasma T4 or T3 followed the nocturnal TSH surge nor were the rapid fluctuations of the thyroid hormones altered by the TSH surge. SRIF infusion commencing at 2300 h suppressed the elevated TSH levels (P is less than 0.01) while similar infusions begun at 2100 h blocked the expected nocturnal TSH rise observed during control periods in male subjects. Plasma T4 and T3 levels were not significantly affected by the administration of SRIF. The relationship of the rapid plasma T4 and T3 variations to postural changes was investigated in four euthyroid male subjects. Serum levels of TSH, T4 and T3 and total protein were determined at 15 min intervals while postural changes were carefully monitored. The ratios of T4 and T3 to total protein were relatively stable (3-4% coefficient of variation) when the subjects were kept in a supine and motionless position. A 50 mug bolus infusion of T4 raised the basal T4 level by only 1-2 mug/dl. The data suggest that short-term fluctuation of plasma T4 and T3 result from changes in protein concentration due to hemodynamic responses to alteration of posture and physical activity and not to pulsatile secretion of T4 and T3.
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PMID:Plasma thyrotropin, thyroxine, and triiodothyronine relationships in man. 95 41


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