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)

Previous studies have demonstrated that the dentate granule and the CA3 pyramidal cells of the rat hippocampal formation are neuronal populations vulnerable to the toxic effects of ethanol. It also has been shown that the resulting alterations do not end after withdrawal from ethanol. As the neurons in the dentate hilus are heavily interconnected with the dentate granule cells, the authors decided to examine the fate of the hilar neurons after chronic alcohol consumption and withdrawal, inasmuch as the hilar somatostatin-immunoreactive (SS-I) neurons were found to be sensitive to cerebral ischemia and to seizures. The following groups of adult rats were studied: (1) alcohol-fed for 6 and 12 months; (2) alcohol-fed for 6 months and then switched to water for a further 6 months; (3) pair-fed controls; and (4) controls fed ad libitum. The authors determined the numerical density of hilar neurons and the number of its SS-I subpopulation. These were found to be significantly reduced in both the alcohol-fed and withdrawal groups when compared with the respective age-matched controls. The consequent loss of the integrative action of the hilar neurons, including the SS-Is, could explain some of the alcohol-related functional deficits as well as their persistence after withdrawal.
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PMID:Effects of chronic alcohol consumption and withdrawal on the somatostatin-immunoreactive neurons of the rat hippocampal dentate hilus. 136 47

To determine whether a synthetic somatostatin analogue, octreotide, and a cholecystokinin receptor antagonist, L-364,718, may be beneficial in acute pancreatitis, 33 dogs were assigned to four groups. Each dog underwent laparotomy with injection of autologous bile into the dorsal pancreatic duct. Thirty minutes after the induction of pancreatitis, Group 1 received a subcutaneous injection of octreotide (200 micrograms/kg), Group 2 received an equal volume of the octreotide carrier, Group 3 received an hourly intravenous bolus of L-364,718 (60 micrograms/kg), and Group 4 received an equal volume of the L-364,718 carrier. Hemodynamic profiles, arterial blood gases, plasma glucose, and serum amylase were obtained before laparotomy, at bile injection, and at hourly intervals. The pancreas was removed after 8 hours for gross evaluation, measurement of water content, and histologic examination. A significant decrease in cardiac index and a significant increase in serum amylase and pancreatic edema occurred in all four groups 8 hours after the induction of pancreatitis (P less than 0.05), but there was no statistical difference between any group. Likewise, there was no difference in gross or histologic changes in the pancreas of any group. The somatostatin analogue, octreotide, and the cholecystokinin receptor antagonist, L-364,718, did not ameliorate the effects of severe, bile-induced pancreatitis in dogs.
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PMID:Effect of somatostatin analogue and cholecystokinin receptor antagonist on bile-induced acute canine pancreatitis. 137 11

Lithuania's environment is heavily polluted as a result of domestic and transboundary contamination. The main ecological problems are related to atmospheric pollution; water contamination; soil, water, and forest acidification; nitrogen-compounds overload of soil, water, and food; and contamination with agricultural chemicals and heavy metals. The increased environmental distress is a menace to public health in Lithuania. Experimental studies need to be designed and used to ascertain the effects of environmental distress on the gastrointestinal tract epithelial barrier. Our electronmicroscopic and immunohistochemical study of human gastrointestinal endocrine cells revealed changes in the amount of secretory material and intracytoplasmic vacuolization after exposure to the environmental chemicals such as hexavalent chromium and the herbicide Saprol. The most affected were the EC (serotonin, motilin, substance P), D (somatostatin), A (glucagon), B (insulin), and mast (histamine, serotonin, heparin) cells. These results provide ultrastructural evidence of digestive tract epithelial barrier reaction as an expression of environmental distress signals of the organism.
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PMID:Environmental monitoring in Lithuania. Environmental distress signals: gastrointestinal epithelial barrier after exposure to chemical agents. 146 10

The effects of 1-methyl-4-phenylpyridinium (MPP+) were studied in rat striatum. Using freeze-clamp, microwave, and water-suppressed proton chemical shift magnetic resonance imaging techniques, MPP+ resulted in marked increases in lactate and a depletion of ATP for up to 48 h after the injections. MPP+ produced dose-dependent depletions of dopamine, serotonin, gamma-aminobutyric acid, and substance P that were partially blocked at 1 week by prior decortication or completely blocked by MK-801 at 24 h. The lesions showed relative sparing of somatostatin-neuropeptide Y neurons, consistent with N-methyl-D-aspartate (NMDA) excitotoxicity. MPP+ produces impairment of oxidative phosphorylation in vivo, which may result in membrane depolarization with persistent activation of NMDA receptors and excitotoxic neuronal degeneration. An impairment of energy metabolism may therefore underlie slow excitotoxic neuronal death in neurodegenerative diseases.
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PMID:1-Methyl-4-phenylpyridinium produces excitotoxic lesions in rat striatum as a result of impairment of oxidative metabolism. 156 Feb 46

The effect of thyroid hormone deficiency and growth hormone (GH) treatment on hypothalamic GH-releasing hormone (GHRH)/somatostatin (SS) concentrations, GHRH/SS mRNA levels, and plasma GH and somatomedin-C (IGF-I) concentrations were studied in 28- and 35-day-old rats made hypothyroid by giving dams propylthiouracil in the drinking water since the day of parturition. Hypothyroid rats, at both 28 and 35 days of life, had decreased hypothalamic GHRH content and increased GHRH mRNA levels, unaltered SS content and SS mRNA levels, and reduced plasma GH and IGF-I concentrations. Treatment of hypothyroid rats with GH for 14 days completely restored hypothalamic GHRH content and reversed the increase in GHRH mRNA, but did not alter plasma IGF-I concentrations. These data indicate that, in hypothyroid rats, the changes in hypothalamic GHRH content and gene expression are due to the GH deficiency ensuing from the hypothyroid state. Failure of the GH treatment to increase plasma IGF-I indicates that the feedback regulation on GHRH neurons is operated by circulating GH and/or perhaps tissue but not plasma IGF-I concentrations. Presence of low plasma IGF-I concentrations would be directly related to thyroid hormone deficiency.
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PMID:Hypothalamic-pituitary somatotropic function in prepubertal hypothyroid rats: effect of growth hormone replacement therapy. 167 66

Somatostatin is an ubiqutary neuropeptide and hormone which has been reported to exert hemodynamic effects and to bind to receptors on the red cell membrane. We investigated its effects on red cell deformability by three filtration methods: (a) filtration of red cells resuspended at hematocrit 8% in Tris-Albumin-Glucose buffer under atmospheric pressure; (b) filtration of red cells resuspended at hematocrit on native plasma at 8% hematocrit under a negative pressure of 5 cm of water; (c) filtrability of whole blood under a negative pressure of 20 cm of water. Aprotinin (Antagosan*) was added to the different suspensions in order to avoid rapid destruction of somatostatin. Increased quantities of somatostatin (from 1 pg/ml to 1 microgram/ml) were obtained by adding natural somatostatin (Modustatin*) to the media, before they were incubated at 37 C for 30 minutes. In 11 samples from healthy subjects, somatostatin was shown to increase red cell flow rate in technique (c) (+ 118%, p less than 0.05) and to reduce red cell rigidity index in technique (b) (- 71%, p less than 0.025) whereas a nonsignificant similar tendency (- 56%) was observed with technique (a). Similar results (p less than 0.05) are observed when adding somatostatin to blood of diabetics. These in vitro data suggest that somatostatin, like other previously studied hormones, may modify red cell deformability.
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PMID:In vitro effects of somatostatin on red cell filterability measured by three methods. 167 5

The effect of intracerebroventricular (i.c.v.) infusion (50 micrograms/h over 3 h) of somatostatin (SOM) on Na and water intake of sheep was determined. In Na-deplete sheep, infusion of SOM-(28) but not SOM-(14) decreased (P less than 0.05) Na intake, while both SOM-(28) and SOM-(14) increased water intake. I.c.v. infusion of SOM-(28) did not significantly affect Na or water intake of Na-replete sheep. I.c.v. infusion of SOM-(28) decreased (P less than 0.01) Na intake but did not alter the high water intakes of water-deprived sheep or sheep infused i.c.v. with angiotensin II. The results are compatible with an inhibitory action of somatostatin on stimulated brain mechanisms subserving Na appetite but not on stimulated brain mechanisms subserving thirst. Somatostatin may antagonize the inhibition of thirst in Na-deplete sheep. The results suggest that somatostatin may have a regulatory role in ingestive behavior concerned with body fluid and Na homeostasis. The difference between SOM-(14) and SOM-(28) in decreasing the Na intake of Na-deplete sheep may be due to a difference in potency or mechanism of action.
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PMID:Central administration of somatostatin suppresses the stimulated sodium intake of sheep. 167 28

To determine the effects of chronic hyperinsulinemia on glucagon release, rats were made hyperinsulinemic for 14 days by supplementation of drinking water with sucrose (10%; sucrose-fed) to increase endogenous release or by implantation of osmotic minipumps (subcutaneous, s.c.; or intraperitoneal, i.p.) to deliver exogenous insulin (6 U/day). Both s.c. and i.p. rats also had sucrose in the drinking water to prevent hypoglycemia. Plasma insulin levels were significantly elevated in sucrose-fed, s.c., and i.p. rats. However, glucose levels were significantly elevated in sucrose-fed rats only. Surprisingly, plasma glucagon concentrations were elevated in i.p. and s.c. rats and were not suppressed in sucrose-fed rats. Inverse relationships were found between the plasma levels of insulin and glucose (n = 65; r = -0.42, p less than 0.0001) and between glucose and glucagon (n = 73; r = -0.46, p less than 0.0001). However, unexpectedly, a positive correlation between insulin and glucagon (n = 65; r = 0.47, p less than 0.0001) was established. As suppression of plasma glucagon levels below basal was not observed in any of the hyperinsulinemic or hyperglycemic rats, we wished to establish further whether pancreatic glucagon release could be suppressed below basal levels in the rat by another means. Thus, high doses of somatostatin (50-100 micrograms.kg-1.min-1) were infused for 45 min into normal rats without or with a concomitant hyperinsulinemic, hyperglycemic glucose clamp. Somatostatin fully suppressed insulin, but although plasma glucagon levels were decreased by somatostatin infusion relative to saline-infused animals, there was still no suppression below basal levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Failure of chronic hyperinsulinemia to suppress pancreatic glucagon in vivo in the rat. 167 40

The distribution and level of labeling for the messenger RNA encoding preprosomatostatin was studied in the striatum and entopeduncular nucleus of rats with and without a selective destruction of the dopaminergic nigrostriatal pathway. 6-Hydroxydopamine was injected unilaterally in the substantia nigra and the animals were killed 2 or 3 weeks after the lesion. Preprosomatostatin messenger RNA was visualized with a 35S-labeled RNA or DNA probe in frontal cryostat-cut sections by in situ hybridization histochemistry. The number of labeled cells as well as the intensity of labeling overlying each cell were measured on radioautograms developed before saturation of the emulsion. In rats with a 6-hydroxydopamine lesion, the number of labeled cells and the intensity of labeling over each cell were decreased in the striatum ipsilateral to the lesion compared to the contralateral side and to both striata of control rats. In the same sections, the number of cells in the cerebral cortex was lower in the ipsilateral side of the lesion but the difference was only significant in the frontoparietal cortex. In contrast, a massive increase (+300%) in the number of labeled cells and in the intensity of labeling per cell was observed in the entopeduncular nucleus and the adjacent lateral hypothalamus on the side ipsilateral to the lesion when compared to the contralateral side and to control rats. The results suggest that dopamine exerts opposite effects on somatostatin gene expression in neurons of the striatum and the entopeduncular nucleus/lateral hypothalamus, effects which are likely to be of importance for the control of basal ganglia output activity. In addition, the dramatic changes observed in the somatostatinergic neurons of the lateral hypothalamus, an area involved in the control of food and water intake, may be related to some aspects of the symptomatology of Parkinson's disease.
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PMID:Lesions of the dopaminergic nigrostriatal pathway alter preprosomatostatin messenger RNA levels in the striatum, the entopeduncular nucleus and the lateral hypothalamus of the rat. 167 45

A total of 112 3-week old Wistar rats were separated into eight groups: control groups I-IV (n = 62) and propranolol-treated groups V-VIII (n = 50). Propranolol hydrochloride (100 mg/kg) was present in the rats' drinking water until 26 weeks of age and growth rates of all groups were monitored daily until 53 days of age and thereafter every third day throughout the study. Chronic oral propranolol administration produced growth retardation (P less than 0.05) in both sexes that was reversible when treatment was discontinued. Organ weights were generally smaller in propranolol-treated rats; on the other hand, the ratio of most organ weights per 100 g of body weight was greater in propranolol-treated rats (especially females). The radio-immunological determination of plasma growth hormone showed increased concentrations of growth hormone in propranolol-treated rats (P less than 0.05), whereas hypothalamic somatostatin content was not significantly changed. The results showed that the retarded growth rate following chronic oral propranolol administration to growing rats was independent of changes in plasma growth hormone and hypothalamic somatostatin concentrations, and that retardation was entirely reversible when the beta-adrenoceptor antagonist was discontinued.
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PMID:Mechanism of growth retardation following chronic administration of beta-adrenoceptor antagonists to developing rats. 168 Jul 61


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