Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have measured somatostatin-like immunoreactivity SLI in cerebroventricular fluid of patients with Parkinson's disease (PD) and other extrapyramidal disorders with hyperkinesia. Patients with PD showed a significantly lower concentration of SLI when compared with levels in control patients with chronic stable multiple sclerosis or temporal lobe epilepsy. Less markedly decreased levels of SLI were also noted in patients with torsion dystonia. Of two patients with Huntington's disease one showed a high and one a medium concentration of SLI. According to the site of the stereotactic cannula, verified by ventriculopathy, SLI concentrations in CSF specimen obtained from the foramen Monro tended to be higher than in specimen from a supraforaminal level. Of 5 other patients with lateral and third ventricle being accessible during the passage of the stereotactic cannula, 4 showed higher SLI concentrations in the third ventricle compared to the lateral ventricle. High performance liquid chromatographic analysis combined with radioimmunoassay showed molecular heterogeneity of SLI in CSF. The ratio of SST-14 to SST-28 was higher in the third ventricle than in the lateral ventricle.
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PMID:Ventricular fluid neuropeptides in Parkinson's disease. I. Levels and distribution of somatostatin-like immunoreactivity. 197 61

The isolated stomach of rats was vascularly perfused to measure the secretion of gastrin, somatostatin (SLI) and bombesin-like immunoreactivity (BLI). The gastric lumen was perfused with saline pH 7 or pH 2, and electrical vagal stimulation was performed with 1 ms, 10 V and 2, 5 or 10 Hz, respectively. Atropine was added in concentrations of 10(-9) or 10(-7) M to evaluate the role of cholinergic mechanisms. In control experiments, vagal stimulation during luminal pH 2 elicited a significant increase of BLI secretion only at 10 Hz but not at 2 and 5 Hz. Somatostatin release was inhibited independent of the stimulation frequency employed. Gastrin secretion at 2 Hz was twice the secretion rates observed at 5 and 10 Hz, respectively. At luminal pH 7 BLI rose significantly at 5 and 10 Hz. SLI secretion was decreased by all frequencies. Gastrin secretion at 2 and 5 Hz was twice as high as during stimulation with 10 Hz. Atropine at doses of 10(-9), 10(-8), 10(-7) and 10(-6) M had no effect on basal secretion of BLI, SLI and gastrin. At luminal pH 2, atropine increased dose-dependently the BLI response at 2 and 5 but not at 10 Hz. The decrease of SLI during 2 and 5 Hz but not 10 Hz was abolished by atropine 10(-9) M. SLI was reversed to stimulation during atropine 10(-7) M at all frequencies. The rise of gastrin at 2 Hz was reduced by 50%. At luminal pH 7, atropine had comparable effects with a few differences: the BLI response at 10 Hz was augmented and the gastrin response to 2 and 5 Hz was reduced. In conclusion the present data demonstrate a frequency and pH-dependent stimulation of BLI and gastrin release. The stimulation of BLI is predominantly due to atropine-insensitive mechanisms while muscarinic cholinergic mechanisms exert an inhibitory effect on BLI release during lower stimulation frequencies (2 and 5 Hz) independent of the intragastric pH and also during higher frequencies at neutral pH. Both, atropine sensitive and insensitive mechanisms are activated frequency dependent. The atropine-sensitive cholinergic mechanisms but not the noncholinergic mechanisms involved in regulation of G-cell function are pH and frequency dependent. Somatostatin is regulated largely independent of stimulation frequency and pH by at least two pathways involving cholinergic mechanisms of different sensitivity to atropine. These data suggest a highly differentiated regulation of BLI, gastrin and SLI secretion and the interaction between these systems awaits further elucidation.
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PMID:Vagally induced release of gastrin, somatostatin and bombesin-like immunoreactivity from perfused rat stomach. Effect of stimulation frequency and cholinergic mechanisms. 197 85

Changes in the cholinergic, serotonergic, noradrenergic, dopaminergic, GABAergic and somatostatinergic neurons were investigated to determine their roles in Alzheimer's disease (AD). Markers for these systems were analyzed in postmortem brain samples from 20 patients with AD and 14 controls. In the CSF study, markers for the cholinergic neurons (choline esterase, ChE) and for the somatostatinergic neurons (somatostatin-like immunoreactivity, SLI) were assayed for 93 and 75 probable AD patients and 29 and 19 controls, respectively. Activity of choline acetyltransferase (CAT) was decreased by 50-85% in four cortical areas and hippocampus in patients with AD, but not in other areas of the brain, indicating a profound deficit in the function of cholinergic projections ascending from the nucleus basalis to the cerebral cortex and hippocampus in AD. Muscarinic receptor binding was reduced by 18% in the frontal cortex but not in other areas of the brain in AD. Serotonin (5HT) concentrations were reduced (by 21-37%) in hippocampal cortex, hippocampus and striatum; and 5HT metabolite levels were lowered (by 39-54%) in three cortical areas, thalamus and putamen in AD patients. Concentrations of noradrenaline (NA) were reduced (18-36%) in frontal and temporal cortex and putamen. These data imply that serotonergic and noradrenergic projections are also affected in AD but less than the cholinergic neurons. Dopamine (DA) concentrations in AD patients were reduced by 18-27% in temporal and hippocampal cortex and hippocampus, while HVA, the metabolite of DA, was unaltered. Glutamic acid decarboxylase activity was not altered in AD. SLI was decreased (28-42%) in frontal, temporal and parietal cortex, but not in thalamus and putamen in patients with AD. Frontal tangle scores correlated most strongly with cortical CAT activity reduction and less so with decreases of 5HT, NA and DA, indicating a closer correlation with the cholinergic changes and severity of AD than with other neurotransmitter deficiencies. ChE activity and SLI were reduced by 20% and 35%, respectively, in CSF of the whole group of AD patients as compared to the controls. Comparison of CSF findings between four subgroups of dementia severity indicated that the SLI was already reduced in the group of mildest AD (-31%), while ChE activity was not. Although ChE activity in CSF declined in relation to dementia severity, however, the maximal reduction was only modest (-30%). On the other hand, SLI in CSF showed only a slight further reduction (up to -41%) as the dementia become more severe.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurotransmitter changes in Alzheimer's disease: implications to diagnostics and therapy. 198 17

The level of cerebrospinal fluid somatostatin-like immunoreactivity (CSF SLI) was determined for 11 chronic schizophrenic patients with moderate cognitive impairment and for 8 controls. The CSF SLI was significantly reduced (37%) in schizophrenic patients, but this decrease did not correlate with the degree of cognitive decline measured by the Mini-Mental State Examination, with psychotic symptoms estimated by the Brief Psychiatric Rating Scale, or with the neuroleptic dose. Although a reducing effect of long-term neuroleptic treatment cannot be totally excluded, the present study suggests that the CSF SLI level is decreased in cognitively impaired schizophrenic patients, as in many other disorders with cognitive impairment.
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PMID:Decreased somatostatin-like immunoreactivity in the cerebrospinal fluid of chronic schizophrenic patients with cognitive impairment. 224 5

Cerebrospinal fluid somatostatin-like immunoreactivity (CSF SLI) was determined for 9 patients with chronic alcohol ingestion and dementia associated with alcoholism and for 8 age-equivalent controls. The CSF SLI was significantly reduced (32%) in the alcoholics with dementia as compared to the controls. This finding is in accordance with previous observations on the relationship between reduced CSF SLI and cognitive impairment in various neuropsychiatric disorders, and extends this finding to patients with dementia associated with alcoholism.
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PMID:Somatostatin-like immunoreactivity in the CSF of patients with dementia associated with alcoholism. 228 44

To determine if galanin is released during pancreatic neural activation, we measured galanin-like immunoreactivity (GLIR) in pancreatic venous and peripheral arterial plasma during 10 min of electrical stimulation of the mixed autonomic pancreatic nerves in halothane-anesthetized dogs, using a sensitive and specific radioimmunoassay. During mixed pancreatic nerve stimulation (MPNS), pancreatic venous GLIR increased by 174 +/- 20 fmol/ml, whereas arterial GLIR did not change. By use of the arteriovenous concentration difference and measurements of pancreatic venous blood flow, pancreatic spillover of GLIR was calculated and found to increase by 640 +/- 90 fmol/min during MPNS. This MPNS inhibited the output of immunoreactive insulin (IRI; delta = -53 +/- 9%) and somatostatin-like immunoreactivity (SLI, delta = -49 +/- 13%) and stimulated that of immunoreactive glucagon (IRG, delta = +600 +/- 200%). To determine if the amount of GLIR released during MPNS was sufficient to elicit these changes of pancreatic hormone secretion, we compared the effect of MPNS on IRI, SLI, and IRG output with the effect of synthetic galanin infused directly into the pancreatic artery at a rate that reproduced the MPNS-induced spillover of GLIR. Exogenous infusion of synthetic galanin (2.7 pmol/min) increased pancreatic venous levels of GLIR by 169 +/- 38 fmol/ml, did not change arterial GLIR levels, and thus increased calculated spillover (appearance) by 550 +/- 160 fmol/min, which was nearly identical to the increment produced by MPNS. This matched infusion of galanin inhibited IRI (delta = -58 +/- 3%) and SLI output (delta = -35 +/- 3%) and modestly stimulated IRG output (delta = +62 +/- 10%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Galanin release during pancreatic nerve stimulation is sufficient to influence islet function. 246 65

In streptozocin-induced diabetes in rats, there is a marked increase in the content and release of immunoreactive somatostatin (SLI) from the pancreas and upper gut. To elucidate whether these SLI changes are associated with alterations in somatostatin gene transcription, we measured somatostatin mRNA (SmRNA) accumulation in these and other SLI-producing tissues. Pancreas, stomach, jejunum, hypothalamus, and cerebral cortex were removed from control rats, 6-wk-diabetic rats, and diabetic rats treated with insulin for 6 wk. Total RNA was isolated by centrifugation through CsCl and fractionated on agarose gels. A sensitive radiodensitometric hybridization assay was used to determine SmRNA levels in absolute amounts by in vitro synthesized sense-strand RNA as a quantitative standard and antisense cRNA as a specific probe. SLI was determined by radioimmunoassay. SmRNA exhibited size heterogeneity between the different control and diabetic tissues. A 2- to 3-fold increase in total SmRNA was found in pancreas and stomach of the diabetic rats that suppressed toward normal with insulin treatment. These two tissues also exhibited significant 1.6- to 2.6-fold increases in SLI, respectively. The remaining tissues showed no diabetes-related changes in SLI or SmRNA. We conclude that in insulinopenic diabetes, tissue SLI and SmRNA accumulation undergo parallel changes; are increased in pancreas and upper gut, reflecting augmented somatostatin synthesis; are reciprocally related to insulin acting directly or indirectly on somatostatin-producing cells; and are unchanged in the lower gut and brain, suggesting tissue-specific regulation of somatostatin gene transcription in diabetes.
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PMID:Tissue-specific alterations in somatostatin mRNA accumulation in streptozocin-induced diabetes. 247 Jun 28

Neuropeptides have been proposed to play a role in regulation of the seizure threshold and interictal behavior in experimental models of epilepsy, but there are few studies concerning neuropeptides in human epilepsy. We compared the levels of two peptides, somatostatin (SLI) and beta-endorphin (BEP) in lumbar cerebrospinal fluid (CSF) of unmedicated (N = 18) and medicated (n = 24) epileptic patients with the levels of these peptides in control (n = 20). Peptide levels in the CSF of patients with panic disorder (8) were also evaluated. Patients with chronic medicated epilepsy had a SLl level 80% (p = 0.003, Mann-Whitney U-test) that of the controls, 76% (p = 0.011) that of unmedicated patients, and 84% (p = 0.028) that of the panic group. BEP in the CSF did not differ in unmedicated, medicated and control patients. On the other hand, patients with panic disorder had higher levels of BEP in CSF than did the controls (117%, p = 0.041). In panic patients SLl was at control level. The present study indicates that the peptidergic systems are affected differentially in epilepsy and in panic disorder. Furthermore, there seems to be selectivity in the affect on peptidergic systems during the period when the epilepsy becomes chronic.
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PMID:Somatostatin and beta-endorphin levels in cerebrospinal fluid of nonmedicated and medicated patients with epileptic seizures. 256 69

Cerebrospinal fluid somatostatin-like immunoreactivity (CSF SLI) was determined for 67 elderly patients who met the DSM-III criteria for delirium and for 19 age-matched controls. As a group, and also when subdivided according to the type of delirium, severity of cognitive decline or the type of central nervous system disease, the delirious patients showed significant reductions of SLI compared with the controls, together with a declining trend associated with increasing cognitive dysfunction. These findings are in accordance with previous observations that reduced CSF SLI is associated with diseases in which cognitive function is disturbed and they extend this finding to delirium.
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PMID:Cerebrospinal fluid somatostatin in delirium. 257 25

Ten obese and 10 control subjects were studied in basal conditions and after ingestion of a standard mixed test meal. Blood glucose, insulin, somatostatin (SLI) and vasoactive intestinal polypeptide (VIP) concentrations were determined before and 30, 60, 90, 120, 180 and 240 min after the start of the meal. Basal SLI levels in the obese (14.4 +/- 0.7 ng/l) were not significantly different from those in the controls (15.5 +/- 0.8 ng/l), whereas after the meal a blunted secretory response was recorded. Baseline plasma VIP levels were higher in the obese (29.7 +/- 1.5 ng/l) than in the control subjects (19.8 +/- 1.3 ng/l) and, similarly to the controls, were unaffected by meal ingestion. Data suggest that in the course of obesity an enhanced VIP secretion in association with a diminished SLI responsiveness to meals occurs.
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PMID:Plasma somatostatin and vasoactive intestinal polypeptide responses to an oral mixed test meal in obese patients. 257 74


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