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)

Reduced brain and cerebrospinal fluid (CSF) levels of somatostatin, corticotropin-releasing hormone (CRH) and corticotropin (ACTH) have been reported among neuropsychiatric patients with cognitive dysfunction. Alcoholism is a disorder in which associated neuropsychiatric disorders occur. Therefore, we compared CSF levels of somatostatin, CRH and ACTH in alcoholics (n = 100) and normal controls (n = 30). There were no significant differences between the groups in concentrations of the 3 peptides. Moreover, there were no significant correlations between concentrations of the peptides in CSF and computed tomographic measures of the size of brain ventricles. There were, however, significant correlations between CSF concentrations of CRH and ACTH and between CSF concentrations of CRH and somatostatin in both the alcoholic and control groups.
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PMID:Cerebrospinal fluid levels of somatostatin, corticotropin-releasing hormone and corticotropin in alcoholism. 197 69

Neuropeptide Y is found in brain tissue. In dogs it has been shown to enhance activation of the hypothalamic-pituitary-adrenal axis by corticotropin-releasing hormone. It is localized in certain catecholamine neurons and to some extent colocalized with somatostatin. Disturbances of the central noradrenergic system may underlie some forms of alcoholism. Therefore, we compared male alcoholics and normal controls on cerebrospinal fluid (CSF) levels of neuropeptide Y. There was no significant difference between the two groups for neuropeptide Y. There was also no significant difference for CSF levels of growth hormone releasing hormone. However, there were significant positive correlations between CSF levels of neuropeptide Y and CSF levels of corticotropin-releasing hormone, somatostatin, and growth hormone releasing hormone.
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PMID:CSF neuropeptide Y in alcoholics and normal controls. 197 53

1. Acute ethanol administration resulted in an increase in the total number of specific somatostatin receptors in rat frontoparietal cortex and hippocampus, and a decrease in the level of somatostatin-like immunoreactivity in the hippocampus but not in the frontoparietal cortex. 2. Chronic administration of ethanol caused a decrease in the number of somatostatin receptors in the frontoparietal cortex but not in the hippocampus, although the level of somatostatin-like immunoreactivity was unchanged in both brain areas. 3. A week after suppressing ethanol the value for specific binding of tracer to somatostatin receptors in the frontoparietal cortex was not significantly different from that of the control rats, although the actual number of receptors was slightly lower. 4. These results suggest a possible role for somatostatin in the nervous system during alcoholism and the post-withdrawal reaction.
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PMID:Effects of acute and chronic ethanol administration and its withdrawal on the level and binding of somatostatin in rat brain. 197 22

1. Cysteamine is formed by degradation of coenzyme A (CoA) and causes somatostatin (SS), prolactin and noradrenaline depletion in the brain and peripheral tissues. 2. Cysteamine influences several behavioral processes, like active and passive avoidance behavior, open-field activity, kindled seizures, pain perception and SS-induced barrel rotation. 3. Cysteamine has several established (cystinosis, radioprotection, acetaminophen poisoning) and theoretical (Huntington's disease, prolactin-secreting adenomas) indications in clinical practice. 4. Pantethine is a naturally occurring compound which is metabolized to cysteamine. 5. Pantethine depletes SS, prolactin and noradrenaline with lower efficacy compared to that of cysteamine. 6. Pantethine is well tolerated by patients and has been suggested to treatment of atherosclerosis. The other possible clinical indications (alcoholism, Parkinson's disease, instead of cysteamine) are discussed.
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PMID:Preclinical and clinical studies with cysteamine and pantethine related to the central nervous system. 227 50

Although abdominal complaints are frequent in both acute and chronic alcoholism, little is known of the effect of ingestion of ethanol with a meal on the function of the upper digestive tract. We have studied the effects of oral ethanol (1 g/kg body wt) taken with food on the gastric emptying rate of a solid-liquid meal as measured by a dual radioisotope technique in six normal subjects; and the gastric response (emptying and secretion), biliopancreatic secretions, and duodenal nutrient absorption after an homogenized meal, as evaluated by a gastroduodenal intubation-marker perfusion technique on seven healthy volunteers. In the latter experiments, radioimmunoassays of gastrin, secretin, cholecystokinin, pancreatic polypeptide, motilin, somatostatin, gastric inhibitory polypeptide, and vasoactive intestinal polypeptide were performed serially. As compared with the control experiment, alcohol induced the following effects: marked delay of gastric emptying of solids, smaller slowing effect on gastric emptying of the liquid phase of the solid-liquid meal and of the homogenized meal; no significant change in gastric acid secretion; no change in the overall postprandial pancreatic enzyme outputs, but a delay of lipase secretion; no change in the early bile salt postprandial output, but a reduced bile salt secretion from the second postprandial hour onwards; no significant change in carbohydrate and lipid duodenal absorption; and a significantly greater postcibal gastrin release. The mechanisms for these effects of alcohol on upper digestive tract function remain to be clarified.
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PMID:Effect of ethanol ingestion on postprandial gastric emptying and secretion, biliopancreatic secretions, and duodenal absorption in man. 370 25

To assess the possible influence of alcoholism on serotonergic control of growth hormone (GH) secretion, 6 mg of the 5-HT1D serotonergic receptor agonist, sumatriptan, was injected subcutaneously in a group of nine normal controls (aged 32 to 49 years) and in nine age-matched nondepressed male alcoholic subjects after 10 to 25 days of abstinence from alcohol. During the same period, subjects were also tested with GH-releasing hormone ([GHRH] 1 microgram/kg body weight in an intravenous [i.v.] bolus) and L-arginine, which releases GH from somatostatin inhibition (50 g in 50 mL normal saline over 30 minutes) to determine whether GH secretion in response to alternate secretagogues is preserved in alcoholics. A control test with administration of normal saline instead of drug treatments was also performed. Plasma GH levels were recorded over 2 hours in all tests. Administration of placebo did not change plasma GH levels in any subject. Similar GH responses were observed in normal controls and alcoholic subjects when GHRH or arginine were administered. A significant GH increase was observed in normal controls after sumatriptan injection; in contrast, GH secretion was not modified by sumatriptan administration in alcoholic patients. These data show that alcoholism is associated with an impairment in the serotonergic-stimulatory regulation of GH secretion, whereas GH responses to direct pituitary stimulation with GHRH or to release from somatostatinergic inhibition with arginine appear to be preserved in alcoholics.
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PMID:Alcoholism abolishes the growth hormone response to sumatriptan administration in man. 878 27

Alcoholism is sometimes associated with a blunted thyroid-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH; peak minus baseline < 5 mIU/liter), despite basal TSH and thyroid hormone levels within the normal range. In light of the inhibitory effect of somatostatin on TSH secretion, we examined whether this condition is caused by an increased hypothalamic somatostatinergic tone in alcoholic subjects. To answer this question, 16 euthyroid male alcoholics (aged 38 to 50 years) with normal [n = 8; normal responder alcoholics (NRAs)] or blunted [n = 8; low responder alcoholics (LRAs)] TSH response to TRH were selected in a preliminary TRH test (200 micrograms in an intravenous bolus). In addition, 8 age- and weight-matched normal men were tested with TRH and used as normal controls (NCs). NCs and alcoholic patients showed similar basal serum TSH, free triiodothyronine, and free thyroxine levels. All subjects were tested again with TRH, 60 min after treatment with 180 mg of pyridostigmine orally. According to selection criteria, NCs and NRA groups showed similar TSH responses to TRH, whereas TRH-induced TSH rise was strikingly lower in LRAs than in NCs and the NRA group. Pyridostigmine did not change the basal levels of TSH in any group, whereas it enhanced in a similar manner the TRH-induced TSH rise in the NC and NRA groups. No significant change in the TSH response to TRH was observed in LRA patients after pyridostigmine treatment. These data argue against the possibility that an enhanced somatostatinergic tone is responsible for the blunted TSH response to TRH observed in some alcoholic patients. This phenomenon might be attributed to alcohol-related defects of stimulated pituitary thyrotroph secretory capacity in some individuals, possibly due to genetic vulnerability and/or the toxic effects of prolonged alcohol abuse.
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PMID:Effect of pyridostigmine on the thyroid-stimulating hormone response to thyrotropin-releasing hormone in abstinent alcoholics. 934 94

Whereas oral or intraduodenal ethanol causes a moderate stimulation of pancreatic bicarbonate and enzyme output, intravenous ethanol inhibits basal and hormonally stimulated pancreatic exocrine secretion in humans, dogs, cats, pigs, rabbits, and rats. This inhibition could be mediated by inhibitory cholinergic mechanisms or be the result of a direct cellular effect of ethanol. In vitro investigations have specified several signaling molecules that may be involved in the action of ethanol on stimulus-secretion coupling in the exocrine pancreas, including cyclic adenosine monophosphate, intracellular calcium, and cholecystokinin and somatostatin receptors. In difference to pure ethanol solutions and distilled spirits, beer strongly stimulates pancreatic enzyme output, probably by nonalcoholic fermentation products. During chronic alcoholism, the ethanol-induced inhibition is replaced by an enhanced enzyme output that causes intraductal protein precipitation. In vitro investigations suggest that this increase is reversible after alcohol withdrawal. The occurrence of protein precipitates is considered to be a crucial step in the development of chronic alcoholic pancreatitis in humans. Other ethanol-induced secretory alterations that may contribute to the development of alcoholic pancreatitis are a decreased secretion of trypsin inhibitor, an increased cholinergic tone, and changes in the concentration of lithostathine.
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PMID:A review: acute and chronic effects of ethanol and alcoholic beverages on the pancreatic exocrine secretion in vivo and in vitro. 980 44

When alcohol is a large proportion of daily nutrient energy, the network of signals for energy homeostasis appears to adapt with abnormal patterns of sleep and growth hormone (GH) release along with gradual acquisition of an addictive physical dependency on alcohol. Early relapse during treatment of alcoholism is associated with a lower GH response to challenge, perhaps reflecting an altered balance of somatostatin (SS) to somatropin releasing hormone (GHRH) that also affects slow wave sleep (SWS) in dependent patients. Normal patterns of sleep have progressively shorter SWS episodes and longer rapid eye movement (REM) episodes during the overall sleep period, but the early sleep cycles of alcoholics have truncated or non-existent SWS episodes, and the longer REM episodes occur in early cycles. During SWS delta wave activity, the hypothalamus releases GHRH, which causes the pituitary to release GH. Alcohol-dependent patients have lower levels of SWS power and GH release than normal subjects, and efforts to understand the molecular basis for this maladaptation and its relation to continued alcohol dependence merit encouragement. More needs to be learned about the possibility of decreasing alcohol dependency by increasing SWS or enhancing GHRH action.
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PMID:Alcohol, slow wave sleep, and the somatotropic axis. 1045 61

Dysregulation of the monoaminergic systems is likely a sufficient but not a necessary cause of depression. A wealth of data indicates that neuropeptides, e.g., NPY, CRH, somatostatin, tachykinins and CGRP play a role in affective disorders and alcohol use/abuse. This paper focuses on NPY in etiology and pathophysiology of depression. Decreased peptide and mRNA NPY were found in hippocampus of both the genetic, e.g., the FSL strain, and environmental rat models of depression, e.g., chronic mild stress and early life maternal separation paradigms. Rat models of alcoholism also show altered NPY. Furthermore, NPY is also reduced in CSF of depressed patients. Antidepressive treatments tested so far (lithium, topiramate, SSRIs, ECT and ECS, wheel running) increase NPY selectively in rat hippocampus and in human CSF. Moreover, NPY given icv to rat has antidepressive effects which are antagonized by NPY-Y1 blockers. The data support our hypothesis that the NPY system dysregulation constitutes one of the biological underpinnings of depression and that one common mechanism of action of antidepressive treatment modalities may be effects on NPY and its receptors. In a novel paradigm, early life maternal separation was superimposed on "depressed" FSL and control rats and behavioral and brain neurochemistry changes observed in adulthood. The consequences were more deleterious in genetically vulnerable FSL. Early antidepressive treatment modulated the adult sequelae. Consequently, if these data are confirmed, the ethical and medical question that will be asked is whether it is permissible and advisable to consider prophylactically treating persons at risk.
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PMID:Search for biological correlates of depression and mechanisms of action of antidepressant treatment modalities. Do neuropeptides play a role? 1757 54


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