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)

Somatostatin is a known inhibitor of hormone secretion and of nutrient transport. Because somatostatin-like immunoreactivity has been detected in amniotic fluid and the placenta has both hormone secretory and nutrient transport functions, we investigated the possible existence of somatostatin receptors on placenta cell membranes. Binding of 125I-Tyr1- and 125I-Tyr11-somatostatin (5-21%) to solubilized placenta cell membranes was observed. Binding was time-, temperature-, and pH-dependent and occurred maximally with incubation at concentrations of 25 micrograms of membrane protein. Displacement of binding of 125I-Tyr1 and Tyr11 somatostatin by cold cyclic and linear somatostatin and somatostatin analogs Ala-5, Ala-8, and Ala-11 was observed. Scatchard analysis of data revealed high capacity of (Ro 0.44 mol/micrograms X 10(-12) but low affinity (Kd 1.8 M X 10(-7) binding sites similar to that reported in other tissues. Binding was not reversible under our experimental conditions. The significance of this low affinity binding of somatostatin to placenta cell membranes remains to be determined.
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PMID:Characterization of somatostatin specific binding in plasma cell membranes of human placenta. 614 16

Because hypothalamic and extrahypothalamic levels of thyrotropin-releasing hormone immunoreactivity (TRH-IR) undergo profound changes during the prenatal and early postnatal period in rats, similar effects with advanced aging were anticipated. For this reason we measured hypothalamic and reproductive tissue levels of TRH-IR, hypothalamic levels of somatostatin (SRIF), and beta-endorphin (EP), serum levels of prolactin (Prl), growth hormone (GH), thyrotropin (TSH), and thyroxine (T4) in young, sexually mature and 24-28 month-old male Long-Evans and Sprague-Dawley rats. Hypothalamic and prostatic levels of TRH-IR were consistently reduced as were the levels of T4 in old rats compared to young controls. Aging did not change the ratio of TRH to the major TRH-like peptide in prostates, as determined by high pressure liquid chromatography (HPLC) or the levels of hypothalamic SRIF and EP. All of the hypothalamic TRH-IR in both old and young male rats consisted of TRH by HPLC. Falling hypothalamic TRH levels and TRH secretory capacity may play a role in the blunted TSH response to cold stress in old rats.
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PMID:Thyrotropin-releasing hormone levels decrease in hypothalamus of aging rats. 615 Nov 24

Neurotensin (NT) and bombesin, which are heterogeneously distributed in both brain and gastrointestinal tissue of several mammalian species, inhibit the formation of stress-induced gastric ulcers in rats. Many other endogeneous neuropeptides have also been reported to be present in brain and gastrointestinal tissue. The present study was conducted to evaluate the effect of some of these peptides on the development of cold-restraint stress (CRS)-induced gastric ulcers in rats. In addition, the effect of thyrotropin-releasing hormone (TRH), which antagonizes many of the CNS effects of NT, was investigated to determine whether this tripeptide antagonizes the cytoprotective effect of NT in this CRS model. All peptides were initially administered intracisternally (ic) in doses equimolar to 30 micrograms NT. As previously reported, NT (30 micrograms, ic) completely prevented the development of gastric ulcers in rats exposed to three hours of CRS. Bombesin, beta-endorphin, substance P, and somatostatin also exhibited cytoprotective activity. Several other peptides studied in the CRS model exerted no significant effects on the development of gastric ulcers; these included cholecystokinin octapeptide, gastrin, leu-enkephalin, met-enkephalin, and bradykinin. Two peptides, vasoactive intestinal polypeptide and TRH, significantly increased the severity of gastric ulcerations. The cytoprotective effect of NT was dose dependent. In contrast, lower doses of beta-endorphin, substance P, and somatostatin were cytoprotective whereas higher doses were not. Finally, concomitant ic injections of TRH antagonized the cytoprotective effects of NT and bombesin, but not that of beta-endorphin. The present results suggest that certain brain peptides may participate in modulating the gastric mucosal barrier, thereby increasing or decreasing its vulnerability to stress-induced lesions.
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PMID:The effect of centrally administered neuropeptides on the development of stress-induced gastric ulcers in rats. 630 95

A number of human diseases with intestinal adaptation have been investigated, including acute infective diarrhoea, intestinal resection, jejuno-ileal bypass, coeliac disease, tropical sprue, chronic pancreatitis and cystic fibrosis. In all, the newly isolated hormone enteroglucagon appeared to be elevated in proportion to the degree of adaptation. In rats after gut resection and cold adaptation, enteroglucagon was also elevated and the degree of elevation correlated closely with the crypt cell production rate (CCPR). Chronic administration of somatostatin suppressed both enteroglucagon and CCPR, while bombesin stimulated both. A crude preparation of enteroglucagon was found to directly stimulate DNA synthesis in enterocyte cultures. It is thus concluded that, at present, the most likely candidate for the humoral component of intestinal adaptation is the hormonal peptide enteroglucagon.
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PMID:The hormonal pattern of intestinal adaptation. A major role for enteroglucagon. 695 45

The glucose metabolic clearance (CMG) was measured by using tritiated glucose in dogs either resting at neutral ambient temperature (TaN = + 25 degrees C) or shivering in the cold (TaC = 21 degrees C). Between two control periods, insulin and/or glucagon deficiencies were provoked by jugular somatostatin infusion without or with portal insulin (glucagon deficiency) or glucagon infusion (insulin deficiency). It was observed that: (1) In absence of hormonal deficiency, CMG was about twice as high at TaC as at TaN; (2) A simultaneous insulin and glucagon deficiency decreased CMG only at TaC; (3) Both at TaN and TaC, the CMG was either decreased or increased by insulin or glucagon deficiency respectively; (4) The magnitude (16-30%) of the hormonal-induced variations were small by comparison with the increase induced by the lowering of the ambient temperature.
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PMID:[Glucose metabolic clearance during acute cold exposure. Effects of insulin and glucagon (author's transl)]. 704 57

Intravenous infusion of D-[3-3H]glucose at a constant rate was used to measure glucose production (rate of appearance, Ra) and utilization (rate of disappearance, Rd) in normal overnight-fasted dogs exposed to either neutral (TaN = +25 degrees C) or cold (TaC = -21 degrees C) ambient temperature. At TaC the metabolic rate was 4.1 times greater than at TaN and the dogs remained normothermic under both conditions. During control periods, cold exposure provoked a 2.2 times increase in hepatic Ra while plasma glucagon remained unaffected. Between two control periods somatostatin (1 microgram.kg-1.min-1 iv) and insulin (0.5 mU.kg-1.min-1 intraportal) were infused in such a manner that plasma insulin remained fairly constant at basal levels while glucagon dropped by 51% (TaN) and 66% (TaC), these percentages being not significantly different. This selective glucagon deficiency resulted in a 24% (TaN) and 30% (TaC) reduction in plasma glucose concentration, due to a 23% (TaN) and 25% (TaC) reduction in glucose production. There was a significant (r = 0.82, P less than 0.01) correlation between the control Ra and the reduction induced by the glucagon deficiency. At TaN and TaC, two significant parallel relationships were found between hepatic Ra and plasma glucagon concentration suggesting that glucagon has a modulatory effect on more fundamental mechanisms triggered by the cold-increased metabolic needs.
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PMID:Effects of endogenous glucagon on glucose kinetics in shivering dogs. 705 58

Primary hypothyroidism and partial primary adrenocortical deficiency (isolated glucocorticoid deficiency) were diagnosed in an 8-year-old spayed female boxer dog, presented because of progressive symmetrical truncal alopecia, lethargy, and intolerance to cold. The diagnosis was based upon the combination of low, non-TSH-responsive concentrations of plasma thyroxine and low urinary excretion of corticoids together with high plasma concentrations of ACTH. Normal suppressibility of ACTH concentrations by a low dose of dexamethasone indicated an intact feedback system. Plasma growth hormone levels were elevated, most probably because somatostatin release was depressed by the glucocorticoid deficiency. The dog improved during oral replacement therapy with thyroxine until death ensued after 9 months as a result of intercurrent disease. Autopsy revealed thyroid atrophy and lymphocytic adrenalitis with complete destruction of the zona fasciculata and zona reticularis of the adrenal cortex. The combination of primary hypothyroidism and primary adrenocortical deficiency in this dog is identical to the entity known as type II polyglandular autoimmunity or Schmidt's syndrome in humans. The adrenocortical insufficiency remained confined to glucocorticoid deficiency during the observation period; on no occasion did electrolyte concentrations in the plasma reach values suggestive of mineralocorticoid deficiency.
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PMID:Polyglandular deficiency syndrome in a boxer dog: thyroid hormone and glucocorticoid deficiency. 757 Dec 81

The effects of cold water swim stress (CWSS) on the nociceptive responses to i.t. administered substance P (SP) and somatostatin (SST) were examined. Male ICR mice, weighing about 30 g, were forced to swim in water at 20 degrees C for 3 min. In unstressed mice, i.t. injection of SP (0.1 nmol) and SST (1 nmol), respectively, produced nociceptive-related behaviors. Although CWSS had no effect on the intensity of the SP-induced nociceptive responses, CWSS significantly reduced the intensity of the SST-induced nociceptive responses. The effect of CWSS on the SST-induced nociceptive responses was blocked by naloxone (5 mg/kg, s.c.) and naltrindole (1 mg/kg, s.c.), a selective delta-opioid receptor antagonist, but not by beta-funaltrexamine (20 mg/kg, s.c.), a selective mu-opioid receptor antagonist. These results indicate that CWSS may selectively reduce the SST-induced nociceptive responses primarily through delta-opioid receptors.
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PMID:Cold water swim stress inhibits the nociceptive responses to intrathecally administered somatostatin, but not substance P. 768 27

This work was undertaken to investigate whether the inhibitory tone exerted by GABA on somatostatin (SRIH) release operates in the control of thyrotropin (TSH) secretion in both basal and cold-stimulated conditions. In a first group of animals (G1) undergoing both carotid and third ventricle push-pull cannulation, i.vt. injection of picrotoxin (10(-5) M) induces a significant decrease in plasma TSH level under basal conditions (0.09 +/- 0.02 versus 0.27 +/- 0.4 ng/100 microliters; P < 0.03, n = 5). In a median eminence (ME) push-pull cannulated group of rats (G2), picrotoxin, peripherally administered, blocks cold-induced inhibition of SRIH release (35.0 +/- 1.8 versus 7.4 +/- 3.3 pg/15 min; P < 0.005; n = 5). In a third group of intact rats (G3), peripheral administration of picrotoxin (2 mg/kg i.p.) blunts the cold-induced TSH release (0.17 +/- 0.03 versus 0.46 +/- 0.04 ng/100 microliters; P < 0.001; n = 5). Our results strongly suggest that a decrease in SRIH release is involved in the GABAergic control of basal and cold-induced TSH secretion.
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PMID:The inhibitory effect of picrotoxin on basal and cold-induced thyrotropin secretion involves somatostatin mediation. 774 6

The effects of cold-restraint stress on immunoreactive thyrotropin-releasing hormone (ir-TRH) and immunoreactive somatostatin (ir-SOM) concentrations in the rat stomach were investigated. Rats immobilized with a spring-loaded metallic plate were placed in a room maintained at 4 degrees C for 1-3 h and then decapitated serially for investigation. Gastric ir-TRH and ir-SOM concentrations were measured by individual radioimmunoassays. Cold-restraint stress induced gastric mucosal lesions as well as a decrease of the ir-TRH concentration in the glandular stomach, an increase of the ir-TRH concentration in the gastric juice, and a decrease in gastric pH. In contrast, this stress caused an increase of ir-SOM in the glandular stomach and a decrease of ir-SOM in the gastric juice. However, cold or restraint stress alone did not induce gastric mucosal lesions or changes in gastric ir-TRH and ir-SOM concentrations or the gastric pH. To clarify the endocrine influence of peripheral TRH, pretreatment with thyroid hormone was performed to inhibit elevation of the serum TRH level during cold-restraint stress. Despite this pretreatment, cold-restraint stress still induced ulcer formation, along with changes in gastric ir-TRH and ir-SOM concentrations and gastric pH. These findings suggest that changes in gastric ir-TRH and ir-SOM concentrations may be closely related to ulcer formation due to cold-restraint, and that TRH may act in a paracrine manner in the stomach.
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PMID:Effect of cold-restraint stress on immunoreactive thyrotropin-releasing hormone and immunoreactive somatostatin in the rat stomach. 777 42


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