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)

Glucagon is secreted not only by A2-cells of the pancreatic islets but also by A cells in the gastric fundus and duodenum. Several reports have demonstrated that the glucagon plasma concentration is increased in genetic diabetes as well as in many conditions associated with a decreased glucose tolerance such as hepatic cirrhosis, myocardial infarction, infectious diseases, burns, taumatic shock, glucagonomas, acute pancreatitis, acromegaly, pheochromacytoma and Cushing's syndrome. Hyperglucagonemia is particularly important in diabetic ketoacidosis and in non-ketotic hyperosmolar coma. The mechanisms responsible for the diabetic's hyperglucagonemia remain controversial. According to several authors, the increased glucagon secretion is, for its main part, secondary to a prolonged defect in insulin secretion and thus relatively insensitive to an acute insulin administration. According to others, the A cell abnormality is of primary origin, independant from insulin deficiency and its effects are cumulative with those of the insulin lack. Several reports dealing with induced or spontaneous experimental diabetes are in favor of the first or the second hypothesis. It appears likely that glucagon plays a role in the metabolic derangments of diabetes. Indeed, hepatic glucose production is closely related to the ratio of molar concentrations of insulin and glucagon. Finally, in insulin-dependant diabetics, somatostatin infusion reduces plasma glucagon concentration and blood glucose and prevents the development of ketosis after withdrawal of insulin therapy. These results illustrate the contribution of glucagon in the pathogenesis of hyperglycemia and ketosis. Several arguments have been accumulated in favor of the following concept: diabetes hyperglycemia results both from glucose under-utilization secondary to insulin lack and from hepatic glucose over-production due to glucagon excess. Although controversial, the role of glucagon in ketogenesis appears likely.
Diabete Metab 1975 Sep
PMID:[The role of glucagon in hyperglycemia. A review (author's transl)]. 79 28

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.
Diabete Metab 1976 Sep
PMID:[Somatostatin, a new hormone? (author's transl)]. 79 89

Using a specific radioimmunoassay technique for somatostatin (GHRIH), we have studied the ontogenesis of hypothalamic GHRIH in relation to pituitary and serum GH concentrations in immature rats. Hypothalamic GHRIH concentrations rose from minimal levels of 4.5 +/- 0.2 pg/microgram protein (mean +/- SEM) at 2 days to peak concentrations of 40.6 +/- 4.1 pg/microgram protein at 28 days followed by a progressive decline toward 50 days (7.0 +/- 0.8 pg/microgram protein). Pituitary GH concentration attained peak prepuberal values of 203.5 +/- 22.8 ng/microgram protein at 16 days with a further marked rise after puberty. Serum GH concentration was elevated to 2 days (53.3 +/- 5.7 ng/ml) and declined progressively to 5.9 +/- 1.5 ng/ml at 13 days. There was a highly significant inverse correlation between hypothalamic GHRIH and serum GH concentrations (r = 0.743, P less than 0.005). These data indicate that the hypothalamic regulatory mechanism for pituitary GH release develops during the neonatal period of the rat and suggest that GHRIH may play an important physiological role in this process.
Endocrinology 1977 Sep
PMID:The development of the hypothalamo-pituitary axis in the neonatal rat: hypothalamic somatostatin and pituitary and serum growth hormone concentrations. 89 65

The ontogenesis of immunoreactive somatostatin in the embryonic and fetal rat pancreas has been measured by radioimmunoassay following acid extraction. Somatostatin (GIF) is detectable at 14 days gestation at a concentration of 1.6 X 10(-3) ng/pancreas. At term the content is 3.8 ng/pancreas, by 2 days neonatally, 8.3 ng/pancreas, and in the adult rat, 71 ng/pancreas through the concentration (expressed per microgram DNA) is constant from 14-19 days of gestation and reaches a level characteristic of the fully differentiated pancreas by birth. The detection of GIF in cultured pancreatic explants in the absence of innervation indicates that synthesis can occur independent of neural influence.
Endocrinology 1977 Sep
PMID:The developmental pattern of somatostatin in the embryonic and fetal rat pancreas. 89 66

This neonate developed marked hyperglycemia four days after birth and required insulin therapy for eight weeks. During the acute phase of the disease, immunoreactive insulin was undetectable in portal venous serum. Neither tolbutamide nor theophylline administration significantly triggered insulin secretion. Somatostatin infusion inhibited growth hormone release but had no effect on plasma glucagon or blood glucose concentrations. At 2 1/2 months, two weeks after insulin withdrawal, the infant was still intolerant to an oral glucose load, insulin response was markedly delayed, and growth hormone secretion was paradoxical. At five months, the insulin, glucagon, and growth hormone responses to glucose and to somatostatin were normalized. Thus, in this patient, insulin secretion was transiently deficient. Peculiarities of glucagon and growth hormone secretion were also present but are more characteristic of this age group than of diabetes. The hyperglycemic state was managed by intraportal infusion of 0.1 to 0.2 IU regular insulin/kg/hour. This mode of insulin administration proved efficient, secure, and easy to manage.
J Pediatr 1977 Sep
PMID:Transient diabetes mellitus in a neonate. Evaluation of insulin, glucagon, and growth hormone secretion and management with a continuous low-dose insulin infusion. 89 7

To determine whether somatostatin, an inhibitor of glucagon and growth hormone secretion, might be useful as an adjunct to insulin the management of diabetic hyperglycaemia, seven insulin-requiring diabetic men were given somatostatin (100 microgram/h, IV) continuously for 3 days after their diabetes had been treated intensively by diet and insulin on a metabolic ward. During infusion of somatostatin and despite reduction in average insulin dose exceeding 50%, there was improvement in diabetic control as assessed by postprandial hyperglycaemia, 24-h glycosuria and the average daily serum glucose level and its fluctuation; when somatostatin was discontinued, but insulin doses held constant, diabetic control rapidly worsened. No adverse effects were observed. These results indicate that somatostatin plus insulin can be a more effective regimen than insulin alone in controlling diabetic hyperglycaemia. A longer acting and more selective somatostatin preparation may prove useful as an adjunct to insulin in the management of diabetes.
Diabetologia 1977 Sep
PMID:Clinical evaluation of somatostatin as a potential ajunct to insulin in the management of diabetes mellitus. 90 78

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.
Endocrinology 1976 Sep
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.
J Clin Endocrinol Metab 1976 Sep
PMID:Plasma thyrotropin, thyroxine, and triiodothyronine relationships in man. 95 41

The inhibitory effect of somatostatin on the secretion of glucagon permits the examination of the effect of glucagon on some metabolic parameters in the insulin-dependent diabetic patient. The results obtained in 5 insulin-dependent diabetics and in 4 pancreatectomized patients revealed an inhibitory effect of somatostatin on blood glucose in the juvenile-type diabetics, but failed to show this influence of somatostatin in the pancreatectomized patients. These observations indicate a participation of glucagon in the generation of hyperglycaemia in diabetes mellitus. However, the failure of somatostatin to influence the blood glucose level in pancreatectomized patients contrasts with the results obtained in dogs and emphasizes the difficulty and pit falls in the application of animal experiments with somatostatin to humans.
Wien Klin Wochenschr 1976 Sep 03
PMID:[ Somatostatin in insulin-dependent diabetics and in pancreatectomized patients (author's transl)]. 103 40

By immunofluorescence, somatostatin-, glucagon- and insulin-containing cells are localized in serial sections of the pigeon pancreas. The distribution of the somatostatin immunofluorescent-cells corresponds to that of the D-cells (A1-cells), which are particularly numerous in this animal species. This observation, coupled with the finding of D, A and B-cells at the ultrastructural level, indicates that the D-cell is responsible for the secretion of somatostatin.
Horm Metab Res 1975 Sep
PMID:Evidence for the D-cell of the pancreas secreting somatostatin. 110 9


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