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)

Unmodified synthetic somatostatin, given as a 200-microgram intravenous bolus, plus 200 microgram infused over 3 hours, had no effect on basal plasma insulin and pancreatic glucagon-like immunoreactivity (GLI) levels, both in controls and in patients with chronic pancreatitis. Somatostatin inhibited insulin-hypoglycaemia-induced pancreatic GLI release in controls and in patients with pancreatitis, and prolonged the insulin-induced fall in blood glucose in the patients. Arginine, presumably via insulin release, caused a fall in free fatty acids (FFA) in controls, which was inhibited by somatostatin. Somatostatin abolished the rebound rise in plasma FFA in patients with pancreatitis after insulin-hypoglycaemia. This effect may be related to inhibition of pancreatic GLI release or may be a direct action of somatostatin on lipolysis.
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PMID:The effects of somatostatin on hormonal and metabolic responses in chronic pancreatitis. 89 37

In man, 3 mug per kg per 90 min of linear somatostatin significantly inhibited basal as well as arginine induced insulin and glucagon release. One mug per kg per 90 min of somatostatin significantly inhibited basal insulin release but not basal glucagon release or arginine induced insulin and glucagon release. In the perfused rat pancreas, as little as one ng per ml of perfusate of somatostatin significantly inhibited argine induced insulin but not glucagon release, while 10 ng per ml of somatostatin by more than 50 per cent reduced the effect of arginine on insulin and glucagon release. Thus, linear somatostatin seemed to be a slightly more potent inhibitor of insulin than of glucagon release in man and in the perfused rat pancreas.
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PMID:Studies on the mechanism of somatostatin action on insulin release. III. Effect of somatostatin on arginine induced release of insulin and glucagon in man and perfused rat pancreas. 94 65

Effect of somatostatin on plasma gastrin levels was investigated in anesthetized dogs. Somatostatin was infused into the right gastroepiploic artery and plasma gastrin levels in the right gastroepiploic, superior pancreaticoduodenal and peripheral veins were measured by radioimmnuoassay. Somatostatin suppressed basal gastrin level promptly in the right gastroepiploic vein and impaired the normal gastrin secretion in response to intravenous infusion of arginine. The inhibitory effect of somatostatin on the plasma gastrin secretion was quite clearly demonstrated in the right gastroepiploic vein. It appears likely that the inhibition of gastrin secretion by somatostatin resulted in direct action on the gastrin secretory cell.
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PMID:Direct inhibitions of basal and arginine-induced plasma gastrin secretion by somatostatin in anesthetized dogs. 99 31

These studies were designed to elucidate the mechanism of inhibitory action of somatostatin (SRIF) on glucagon (IRG) and insulin (IRI) secretion. Studies were carried out in the unrecirculated isolated rat pancreas perfusion with arginine 19.2 mM and glucose 5.5 mM as stimulus primarily for IRG but also IRI secretion. The effects of excess Ca++ (15.2 mEq./L.) and excess K+ (12.8 mEq./L.) on IRG, IRI, and the SRIF-inhibited pancreas were studied. Ca++ excess in five perfusions strikingly stimulated IRG secretion (+92 per cent) but only stabilized IRI secretion compared with control perfusions. K+ excess (in seven perfusions) markedly inhibited IRG secretion (-39 per cent) while stimulating IRI secretion (+16 per cent). Restoration of normal concentrations of K+ resulted in a rebound of IRG to levels 120 per cent that of controls. SRIF, at concentrations from 0.1-20 ng./ml., produced inhibition of both IRG and IRI. In 11 perfusions, with SRIF at 10 ng./ml., IRG decreased more than IRI (-75.2 per cent IRG and -46.9 per cent IRI). In five perfusions, addition of Ca++ (15.2 mEq./L.) 10 minutes after SRIF was started resulted in a reversal of IRG inhibition to 69.4 per cent and IRI to 73.2 per cent of the arginine controls. The reversal by Ca++ of SRIF effect on IRG was greater at higher concentrations of Ca++, suggesting some form of competition. In four perfusions, excess K+ reversed SRIF-induced IRI inhibition to 79.6 per cent that of controls but had no effect on IRG inhibition. Studies in vitro with isolated islets revealed that SRIF (2 mug./ml.) inhibited 45Ca uptake of islets as did epinephrine (10(-5) M). It was concluded that SRIF-induced inhibition of hormone release appears related to an action on Ca++ uptake.
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PMID:Reversal of somatostatin inhibition of insulin and glucagon secretion. 99 24

Perfusion of growth hormone inhibitory factor (somatostatin) into rat pancreas inhibited secretion of glucagon and insulin into medium containing 5.5 mM glucose. A 15-min infusion of arginine (20 mM) greatly increased glucagon and insulin secretion. When perfused simultaneously with arginine, somatostatin (55 nM) abolished the increase in glucagon secretion. The acute phase of insulin secretion in response to arginine was attenuated by somatostatin, and subsequent secretion was decreased to control levels. Pretreatment for 5 min with somatostatin blocked even acute-phase insulin secretion in response to arginine. Somatostatin did not affect basal or glucose-stimulated secretion of insulin from rat pancreatic islets isolated by the collagenase technique. Arginine-stimulated secretion of insulin was enhanced by somatostatin in isolated islets. These results demonstrate a direct effect of somatostatin on the pancreas to inhibit secretion of glucagon and insulin. The failure of somatostatin to inhibit insulin secretion in pancreatic islets may be due to alterations in the beta cells produced by the isolation procedure. It is also possible that the effect of somatostatin on insulin secretion may be mediated indirectly.
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PMID:Inhibition of glucagon and insulin secretion by somatostatin in the rat pancreas perfused in situ. 108 35

In normal men, the administration of somatostatin almost completely abolished the glucose stimulated insulin-release seen during control studies (without somatostatin), and caused a further reduction in glucagon secretion beyond that induced by hyperglycemia. Following the infusion, there was a rapid and marked rebound for insulin but not glucagon secretion. These events were attended by a marked retardation of the glucose disappearance rate (K) which exhibited two clearly separable components; the initial slow component (mean K equals 0.64) coincided with the period of insulin suppression and was followed by a faster component (mean K equals 1.37) temporally related to the marked rebound increase in insulin release after discontinuation of the somatostatin infusion. Similarly, the addition of somatostatin infusion completely blocked the release of insulin and growth hormone and delayed the release of glucagon stimulated by arginine infusion. Following the somatostatin infusion there was a small rise in GH and a marked rebound for insulin and this was associated with a higher level of plasma glucose than that found following arginine infusion alone. These data establish that the administration of somatostatin can effectively block the release of insulin stimulated by arginine and glucose, can attenuate the release of glucagon induced by arginine and can enhance the glucose-mediated glucagon suppression. The attendance of a relative hyperglycemia during these events is probably the net result of an impediment in peripheral glucose disposition due to acute insulin lack and a decreased hepatic glucose output secondary to glucagon suppression.
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PMID:Inhibitory action of somatostatin on pancreatic alpha and beta cell function. 109 7

To determine whether somatostatin inhibits glucagon secretion directly at the pancreatic level and to study quantitatively the relative effects of somatostatin on glucagon and insulin secretion, the effects of various concentrations of somatostatin on glucagon and insulin release from the in vitro perfused rat pancreas in response to arginine (14.2 mM), isoproterenol (2 mg/ml) and theophylline (10 MM) were studied. Glucagon and insulin responses to arginine were progressively inhibited by somatostatin over a concentration range from 0.1-100 ng/ml. At all doses, somatostatin caused greater inhibition of glucagon secretion than of insulin secretion. Approximately 4 ng/ml somatostatin reduced glucagon responses 50%, whereas 90 ng/ml was required to produce comparable inhibition of insulin responses. Glucagon responses to isoproterenol, an activator of adenylate cyclase, and to theophylline, a phosphodiesterase inhibitor, were completely abolished by 100 ng/ml somatostatin. Isoproterenol did cause insulin release in this system, but insulin responses to theophylline were diminished by somatostatin. The present studies thus indicate that somatostatin is a potent inhibitor of both glucagon and insulin secretion and indicate that it acts directly on the pancreatic alpha and beta cells. Glucagon secretion is approximately 20 times more sensitive to the inhibitory effects of somatostatin than is insulin secretion. Furthermore, the present results suggest that somatostatin may act by modifying cAMP-dependent systems rather than by altering cAMP levels.
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PMID:Inhibition by somatostatin of glucagon and insulin release from the perfused rat pancreas in response to arginine, isoproterenol and theophylline: evidence for a preferential effect on glucagon secretion. 111 81

A dose-response study of the effect of somatostatin on plasma growth hormone (GH) and immunoreactive insulin (IRI) levels was performed in normal subjects and acromegalic patients. In normal subjects 150 mug of somatostatin completly suppressed GH and IRI responses to arginine, while with 75 and 37.5 mug only a partial suppression was usually observed. Basal levels of plasma IRI were significantly lowered within 15 min from the start of somatostatin injection at each of the three dose levels. In three acromegalics the doses of 150 and 75 mug of somatostatin were effective in lowering both GH and IRI levels; the dose of 37.5 mug was still effective in lowering plasma IRI levels, while GH levels were not significantly modified. A dose of somatostatin inhibiting GH secretion without affecting insulin secretion has not been found either in acromegalics and in normals. It was concluded that the effects of somatostatin on GH and IRI secretion cannot be easily dissociated.
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PMID:Dose-response study of the inhibiting effect of somatostatin on growth hormone and insulin secretion in normal subjects and acromegalic patients. 113 56

Filtration of basal plasma from normal, alloxan-diabetic, and depancreatized dogs on Bio Gel P-10 yielded four glucagon-immunoreactive fractions. One of them appeared in the true glycagon area with the glucagon-125I (3500 mol vt). Of the other three, one appeared in the void volume (greater than 20000 mol wt), another just before the insulin-125I (congruent to 9000 mol wt), and the last one close to the salt peak (less than 2000 mol wt). The increase of total plasma glucagon immunoreactivity observed in depancreatized and alloxan diabetic dogs was mainly due to an increase in the 3500 and 9000 molecular-weight fractions. Arginine infusion in depancreatized dogs caused an increase in the 3500 molecular-weight fraction. Somatostatin or insulin infusion in depancreatized and alloxan-diabetic dogs resulted in disappearance of the 3500 molecular-weight fraction.
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PMID:Heterogeneity of plasma glucagon immunoreactivity in normal, depancreatized, and alloxan-diabetic dogs. 115 74

The growth-hormone-release-inhibiting hormone somatostatin was infused in seven juvenile diabetic subjects during an arginine infusion test and in six juvenile diabetic subjects during an L-dopa stimulation test. The plasma growth hormone response to arginine and L-dopa was completely inhibited by somatostatin. The plasma pancreatic glucagon response to arginine was also inhibited by somatostatin. The plasma pancreatic glucagon level was not changed by L-dopa, but somatostatin induced a significant fall in this level. The plasma glucose increase after arginine and L-dopa administration was slightly inhibited by somatostatin. The arginine-induced fall in free fatty acids was prevented by somatostatin, and the L-dopa-induced rise in free fatty acids was enhanced by somatostatin. The growth hormone- and glucagon-surppressive effect of somatostatin may prove useful in controlling the metabolic state and in preventing the development of angiopathy in diabetic patients. A somatostatin preparation with prolonged activity is needed for lifelong administration, but the presently available compound may be of value as an adjunct in the standard treatment of diabetic ketoacidosis and coma.
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PMID:The effect of somatostatin on the rise of growth hormone and glucagon secretion induced by arginine and L-dopa in diabetic patients. 115 17


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