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)

We have studied the glucose response and catecholamine (CA) response to insulin in the conscious rat to evaluate the role of sensory fibers in these responses in animals pretreated with capsaicin as neonates. In contrast to previous results obtained in anesthetized rats (Z. Khalil, B.G. Livett, and P.D. Marley. J. Physiol. Lond. 370: 201-215, 1986; Z. Khalil, B.G. Livett, and P.D. Marley. J. Physiol. Lond. 391: 511-526, 1987.), in conscious rats, insulin (1 IU/kg iv) produced only a mild hypoglycemia, which quickly returned to resting levels and caused no significant changes in plasma epinephrine levels. Somatostatin and SMS-(201-995), a somatostatin analogue, both potentiated and prolonged the insulin-induced hypoglycemia, resulting in an increase in circulating CA levels that was suppressed by hexamethonium and atropine. In capsaicin-pretreated rats the blood glucose levels at 90 min after insulin were significantly lower than those in vehicle-pretreated rats both in the presence (1 IU/kg insulin, 48 +/- 6 vs. 92 +/- 6 mg/100 ml, P less than 0.01) and absence (10 IU/kg insulin, 38 +/- 4 vs. 51 +/- 2 mg/100 ml, P less than 0.01) of SMS-(201-995). The CA levels in capsaicin-pretreated rats at 90 min after insulin were higher than in vehicle-pretreated rats (epinephrine levels: 27 +/- 4 vs. 10 +/- 1 pmol/ml in 1 IU/kg insulin, P less than 0.01; 64 +/- 14 vs. 25 +/- 5 pmol/ml in 10 IU/kg insulin, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Capsaicin-sensitive nerves are required for glucostasis but not for catecholamine output during hypoglycemia in rats. 196 8

The glucose-dependent secretion of the neuropeptides, growth hormone-releasing factor (GRF) and somatostatin (SRIF), by hypothalamic fragments was studied in vitro using a superfusion system. After equilibration of mediobasal hypothalami in HEPES-buffered Krebs-Ringer solution containing 5.5 mM glucose, glucose levels in the superfusion medium were altered. Lowering the glucose concentration in the medium from 5.5 to 2.7 or 1.1 mM provoked a rapid increase in GRF and SRIF release in a concentration and Ca2+-dependent manner. At 1.1 mM glucose, neuropeptide secretion was elevated 3- to 4-fold. The increase of GRF and SRIF release induced by low glucose was transient since stimulated neuropeptide secretion declined to basal levels in the continued presence of low glucose. Furthermore, after reequilibration in 5.5 mM glucose, no second stimulation of neuropeptide release could be induced by reduced glucose. Intracellular glucopenia induced by addition of 2-deoxy-D-glucose (16.5 mM) to the superfusion medium containing 5.5 mM glucose, also evoked increases in GRF and SRIF release. The sensitivity of GRF and SRIF neurons to glucose was absent in the postnatal period until day 9 after birth and then gradually increased. The parallel increases of GRF and SRIF release in response to low glucose observed in the present in vitro study, together with the suppression of plasma GH levels occurring in hypoglycemia in the rat, suggest that, in this condition, the inhibition of GH release induced by elevated SRIF levels predominates whereas the increase of GRF release might serve to attenuate this effect of SRIF.
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PMID:Characterization of the glucose-dependent release of growth hormone-releasing factor and somatostatin from superfused rat hypothalami. 196 36

In 15 patients with insulinoma, six patients after successful removal of this tumour, two patients with previous pancreas resection because of hypoglycaemia elsewhere, and 10 control subjects, the diagnostic usefulness of euglycaemic clamp procedures (without exogenous insulin) was assessed in comparison with prolonged starvation. Only insulinoma patients developed sustained hypoglycaemia (less than or equal to 2.3 mmol l-1) within 2-44 h without caloric intake, because of inappropriately elevated immunoreactive insulin (IR-insulin) concentrations. IR-proinsulin values were elevated in most (7 out of 10), but not in all insulinoma patients. The steady-state glucose infusion rate necessary to maintain a stable plasma glucose concentration of 4.4-5.0 mmol l-1 was significantly (P less than or equal to 0.001) higher in insulinoma patients (2.5 +/- 0.6 mg kg-1 min-1) than in pancreas resected patients (0.6 +/- 0.2 mg kg-1 min-1), or in control subjects (0.5 +/- 0.1 mg kg-1 min-1). Due to a considerable degree of overlap, sensitivity (0.44) and specificity (0.95) were too low for such a procedure to qualify as a diagnostic test. There was no correlation of glucose infusion rates to IR-insulin values (r = 0.024, P = 0.461). One reason for this was the development of insulin resistance in some, but not in all insulinoma patients. When, in analogy to insulin/glucose ratios, a diagnostic index was derived by multiplying the steady state glucose infusion rate by the steady state IR-insulin concentration, the diagnostic accuracy was greatly increased (sensitivity and specificity 0.94, respectively), but still lower than that of 'amended' insulin/glucose ratios in fasting plasma or at the time of discontinuation of prolonged fasts (1.00). Somatostatin infusions inhibited insulin secretion (IR-C-peptide plasma concentrations) by 52-88% in subjects without insulinoma and in those insulinoma patients whose tumour cells ultrastructurally contained plenty of normal secretory granules, and to a lesser degree when only abnormal or virtually no secretory granules were present, i.e. in more de-differentiated tumours. In contrast to this significant (P = 0.036) association, malignancy, i.e. the presence of metastases, could not be predicted from whether or not insulin secretion was resistant to the inhibitory action of somatostatin. In conclusion, euglycaemic clamp experiments are less reliable for detecting or excluding a functioning insulinoma than the relation of glucose and insulin values during starvation. The inhibition of insulin secretion by somatostatin depends on the presence of normal beta-granules, and does not distinguish adenomas from carcinomas.
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PMID:Evaluation of a euglycaemic clamp procedure as a diagnostic test in insulinoma patients. 196 48

We determined islet amyloid polypeptide (IAPP) response in plasma to oral and intravenous glucose administration and intravenous insulin injection in nondiabetic subjects. Moreover, we studied the effect of somatostatin analogue SMS 201-995 on glucose-induced IAPP secretion in nondiabetic subjects. Plasma IAPP concentration was determined by radioimmunoassay. Oral administration of 75 g glucose (n = 8) significantly increased plasma IAPP levels from 4.5 +/- 0.7 to 14.0 +/- 1.7 pM (P less than 0.01) 60 min after administration. Intravenous administration of 10 g glucose (n = 7) also caused a significant increase in plasma IAPP from 5.0 +/- 0.4 to 11.6 +/- 0.9 pM (P less than 0.01) 5 min after injection. Plasma IAPP significantly decreased from 5.1 +/- 0.4 to 2.9 +/- 0.4 pM (P less than 0.01) 60 min after intravenous insulin injection (n = 8). Pretreatment with SMS 201-995 completely abolished IAPP and insulin secretion to intravenous glucose injection. A significant correlation was found between plasma IAPP and insulin levels in oral and intravenous glucose administration and between plasma IAPP and C-peptide levels during insulin-induced hypoglycemia. These results suggest that IAPP is cosecreted with insulin in response to a glucose load and secretion of IAPP is inhibited by hypoglycemia and somatostatin. IAPP may serve as a novel pancreatic hormone to control carbohydrate metabolism.
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PMID:Islet amyloid polypeptide response to glucose, insulin, and somatostatin analogue administration. 197 May 40

The aim of our study was to compare the effectiveness of bromocriptine vs. long acting somatostatin analogue (SMS 201-995) on growth hormone suppression in active acromegaly. A twenty year old female, student of law, was previously treated with Parlodel LA 50 mg i.m. injection and then with bromocriptine 30 mg orally for 2.5 years because of active acromegaly and very large intrasellar and suprasellar pituitary adenoma. She was partial bromocriptine responder with mean growth hormone levels prior the treatment 30 mU/L and after bromocriptine 13.7 mU/L and with gross tumor shrinkage. Since she failed to restore menstrual cycles, had clinical signs of the disease, she was taken off bromocriptine and treated with somatostatin analogue (SMS 201-995) 300 mcg s.c. daily and 400 mcg s.c. daily with mean growth hormone levels 10 mU/L. She was also treated with combined treatment (400 mcg s.c. SMS 201-995 plus 30 mg bromocriptine orally) and mean growth hormone levels were 11 mU/L. SMS 201-995 had a long lasting inhibitory effect on growth hormone secretion in acromegaly (p less than 0.01) but in comparison to daily growth hormone levels during bromocriptine treatment no difference was found (p greater than 0.01). Combined treatment with SMS 201-995 and bromocriptine did not achieve greater suppression of daily growth hormone levels than those achieved with SMS 201-995 alone (p greater than 0.1) or with bromocriptine alone (p greater than 0.05). No significant tumor shrinkage during chronic SMS treatment was seen. Severe clinical and biochemical signs of hypoglycaemia were registered on one occasion only during the first month of treatment with SMS 201-995.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison among the effectiveness of growth hormone suppression in active acromegaly of bromocriptine and long acting somatostatin analogue (SMS 201-995). 197 22

To elucidate the role of growth hormone (GH)-releasing hormone (GRH) and somatostatin (SRIH) in the regulation of the growth hormone (GH) secretory pattern, we collected portal blood from five unanesthetized ovariectomized ewes for repeated measurements of GRH and SRIH simultaneous with those of peripheral GH. Hormones were measured at 10-min intervals for 5.5 h and their interrelationships analyzed. Mean portal GRH was 20.4 +/- 6.7 (SD) pg/ml and the estimated overall secretion rate was 13 pg/min. GRH secretion was pulsatile with peaks of 25-40 pg/ml and a mean pulse interval of 71 min. Mean portal SRIH was 72 +/- 33 pg/ml and the estimated overall secretion rate was 32 pg/min. SRIH secretion was also pulsatile with peaks of 65-160 pg/ml and a mean pulse interval of 54 min. The GH pulse interval was 62 min. A significant association was present between GRH and GH secretory peaks though not between GRH and SRIH or SRIH and GH. Insulin hypoglycemia resulted in a rapid and brief stimulation of SRIH secretion followed by a decline in GH levels. No effect was observed on GRH secretion until 90 min, when a slight increase occurred. The results suggest (a) the presence of an independent neural rhythmicity of GRH and SRIH secretion with a primary role of GRH in determining pulsatile GRH secretion, and (b) that the inhibitory effects of insulin hypoglycemia on GH in this species are attributable to a combination of enhanced SRIH secretion and possibly other factors, though without significant inhibition of GRH.
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PMID:Measurement of growth hormone-releasing hormone and somatostatin in hypothalamic-portal plasma of unanesthetized sheep. Spontaneous secretion and response to insulin-induced hypoglycemia. 197 73

Growth hormone (GH) secretion in man is pulsatile and this pattern is regulated by both GH-releasing hormone (GHRH) and somatostatin. A large body of experimental evidence in both man and animals supports the model that bursts of GH secretion are mediated by a reduction of tonic hypothalamic somatostatin secretion. Our studies have been performed in normal subjects with frequent blood sampling for GH measurements (from 20-minute to 30-second intervals); the data have been analyzed by computer algorithms to objectively determine pulse characteristics and, in some studies, to estimate both pituitary secretion and clearance rates using deconvolution analysis. The studies include profiles of GH secretion in normal men and women in fed and fasted states; analysis of GH secretion during sleep; and administration of GHRH during different stages of sleep and after sleep deprivation. The variable GH response to exogenous GHRH and the attenuated response after 6 hours of GHRH infusion to GHRH, while not to hypoglycemia, as well as the pulsatile profile of GH secretion in response to continuous GHRH infusions (24 hours to 14 days), all support the thesis that it is hypothalamic somatostatin that determines the timing of bursts of GH secretion. This is further confirmed by the profile of GH secretion in a patient with ectopic GHRH secretion. Recently, we have initiated studies with the novel synthetic GH releasing hexapeptide, HisDTrpAlaTrpDPheLysNH2 (GHRP). Our studies show that it acts synergistically with GHRH. Several lines of evidence suggest that GHRP stimulates GH secretion independently of GHRH receptors and acts at both the hypothalamic and pituitary levels. It may act to functionally antagonize somatostatin.
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PMID:Physiological role of somatostatin on growth hormone regulation in humans. 197 18

The effect of cyclic somatostatin on early and late dumping syndrome was studied in 12 patients with gastric resection. Each patient underwent two glucose challenges with 75 grams of glucose administered orally. In the control study isotonic sodium chloride was given, while in the other study cyclic somatostatin in a dose of 250 micrograms bolus injection followed by infusion of 80 ng/kg/min for a period of 270 minutes. In the control study all patients showed subjective symptoms of the early dumping syndrome with significant increases in pulse rate, hematocrit, and vasoactive intestinal polypeptide. Ten patients showed asymptomatic hypoglycemia, as a sign of the late dumping syndrome associated with a significant increases of insulin, gastric inhibitory peptide and glucagon levels. During the administration of somatostatin these changes failed to develop. These results indicate that somatostatin alleviates the symptoms of early and late postprandial dumping syndrome.
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PMID:[The effect of somatostatin in dumping syndrome]. 197 48

Food intake results in a variety of responses, with the autonomic nervous system playing an important role in maintaining cardiovascular homeostasis. In patients with autonomic failure, who have severe sympathetic impairment, food substantially lowers blood pressure even in the supine position. This is related to a marked increase in splanchnic blood flow, without compensatory changes in the rest of the circulation. Of the food components, glucose causes similar effects to food, while an isosmotic, isocaloric load of the inert carbohydrate, xylose, causes only a small fall in blood pressure. Lipid causes a small, short-lived fall in blood pressure and protein causes minimal change. Insulin appears to contribute to the fall in blood pressure, as bolus injections of insulin (even before ensuing hypoglycaemia), or insulin infusions (with an euglycaemic clamp), when given intravenously lower blood pressure. Other vasodilatatory gut peptides released by food may also play a role. The somatostatin analogue, Octreotide (SMS 201-995), which inhibits the release of a range of peptides, prevents both glucose and food-induced hypotension. Studies of the mechanisms responsible for post-prandial hypotension in autonomic failure continue to provide insight into the relationship between food intake and the hormonal, peptidergic and neural responses which affect the cardiovascular system.
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PMID:Effect of food intake on cardiovascular control in patients with impaired autonomic function. 197 48

In order to enlighten the controversy on whether human and pork insulin result in different hormonal responses to insulin-induced hypoglycaemia, eight C-peptide negative, diabetic patients without measurable circulating insulin-binding antibodies were exposed to insulin-induced hypoglycaemia in random order with highly purified pork insulin (Actrapid) and semisynthetic human insulin (Actrapid Human). Hypoglycaemia was provoked by a constant rate IV infusion of insulin (0.034 U kg-1 h-1) for 3 h after which the blood glucose recovery was assessed for an additional period of 60 min. Both insulin preparations gave close to identical responses for glucose, glucagon, growth hormone, adrenaline, and somatostatin. The circulating noradrenaline levels were higher during the infusion of pork insulin which also yielded a more prominent response of pancreatic polypeptide and, after cessation of the insulin infusion, plasma cortisol was also higher following pork insulin. It is concluded that human and pork insulin induce close to identical responses of the important counter-regulatory hormones during hypoglycaemia in Type 1 diabetic patients.
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PMID:A comparative study on the hormonal responses to insulin-induced hypoglycaemia using semisynthetic human insulin and pork insulin in patients with type 1 diabetes mellitus. 197 63


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