Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of somatostatin (SRIF) on glucagon and insulin secretion was examined in fed and fasted sheep. This was related to changes in glucose production. Infusion of SRIF at 80 micrograms/h caused a marked reduction in plasma glucagon concentrations. However, the insulin response to SRIF infusion was not consistent; its concentrations decreased occasionally, but often did not change. The depression of glucagon was not associated with a significant reduction in blood glucose concentrations in either fed or fasted sheep, but was associated with a reduction in glucose production by 12--15%. The inhibitory effect of insulin on glucose production was not markedly increased by glucagon deficiency. Infusion of insulin at 1.17 U/h with SRIF decreased glucose production only an additional 10%. Thus, it appears that under basal conditions pancreatic hormonal influences on hepatic glucose production were relatively small in sheep. This implies that under normal conditions in sheep, substrate supply has a much greater impact on hepatic glucogenesis than do hormones.
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PMID:Effect of somatostatin suppression of glucagon secretion on glucose production in sheep. 49 97

The role of SRIF in starvation-induced inhibition of GH and insulin secretion was assessed by passive immunization with anti-SRIF serum. Six-hour secretory profiles obtained from chronically cannulated male rats deprived of food for 72 h showed marked suppression of GH secretory bursts and significant depression of plasma insulin levels. Administration of 1 ml SRIF antiserum (SRIF AS) iv to starved rats resulted in rapid (within 15 min) restoration of high amplitude GH pulses (600-800 ng/ml) and sighificant elevation of GH trough values. The mean 6-h GH level of starved SRIF, AS-treated rats (189.2 +/- 23.9 ng/ml) was significantly higher than that of starved, normal sheep serum-treated control animals (62.8 +/- 5.8 ng/ml) (P less than 0.005). In contrast to the effects on GH, plasma insulin levels in starved rats administered SRIF AS remained low. No significant difference was observed in the mean 6-h plasma insulin level of starved-SRIF, AS-treated rats when compared to starved, normal sheep serum-treated controls. These findings suggest that circulating SRIF is a physiological regulator of starvation-induced GH suppression but is not involved in mediating the inhibition of insulin.
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PMID:Antiserum to somatostatin reverses starvation-induced inhibition of growth hormone but not insulin secretion. 74 57

Cerebrospinal fluid (CSF) concentrations of immunoreactive corticotropin-releasing hormone (CRH) and somatostatin (SRIF) were measured in female psychiatric inpatients with DSM-III-R diagnoses of major depression, mania, generalized anxiety and somatization disorder. In addition, elderly patients with dementia disorders, with or without concomitant major depression, were also investigated. CSF SRIF was not significantly different among these groups; on the other hand, mean CSF CRH concentrations were significantly higher in major depression and in dementia with depression as compared with neurological controls with no psychiatric disorders. CSF CRH levels in mania, simple dementia, or anxiety or somatization disorder were not significantly different from the controls. Background physical or clinical variables did not account for the differences in CRH concentrations. It is concluded that CSF CRH elevation may be present in some patients with major depression independent of age and an underlying dementia disorder.
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PMID:Cerebrospinal fluid neuropeptides in mood disorder and dementia. 135 20

Immunoreactive corticotropin-releasing hormone (CRH) and somatostatin (SRIF) were measured in the cerebrospinal fluid (CSF) of 24 female in-patients, suffering from DSM-III-R major depression, both before and after antidepressant treatment. In the total group there were no significant differences between pre- and post-treatment CSF-CRH and SRIF concentrations despite satisfactory clinical improvement in each patient. However, there was a significant post-treatment reduction of the CSF-CRH concentration in the 15 patients who remained depression-free for at least 6 months following treatment, in contrast to the tendency for elevation in those 9 subjects who relapsed within 6 months. CSF-SRIF showed no similar pattern. High, or even increasing, CSF-CRH concentration during antidepressant treatment may indicate lack of normalization of an underlying process in major depression despite symptomatic improvement and predicted early relapse.
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PMID:CSF corticotropin-releasing hormone and somatostatin in major depression: response to antidepressant treatment and relapse. 135 99

Somatostatin (somatotropin release-inhibiting factor, SRIF) was originally discovered (1) during the purification of growth hormone-releasing factor from rat hypothalamus and was subsequently isolated and characterized (2) in 1972 from ovine hypothalamus. Since its initial characterization, SRIF has been shown to fulfill criteria for a neurotransmitter and to directly modulate neuronal activity as well as acting as an inhibitory factor regulating endocrine and exocrine secretion. Alterations in cerebrospinal fluid (CSF) concentrations of SRIF have been reported in several diseases exhibiting prominent cognitive dysfunction, including Alzheimer's disease (AD), major depression, Huntington's chorea, multiple sclerosis, schizophrenia and Parkinson's disease, while evidence for regional brain tissue concentration deficits in SRIF are more specific for AD. This mini-review will focus on the studies reporting alterations in CSF and postmortem tissue concentrations of SRIF in AD and depression.
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PMID:Somatostatin in Alzheimer's disease and depression. 135 21

Cerebrospinal fluid concentrations of corticotropin-releasing hormone (CRH), thyrotropin-releasing hormone (TRH) and somatostatin (SRIF) were measured in 77 female inpatients with moderate to extreme dementia and in 17 elderly female controls. Both multi-infarct (MID) and Alzheimer-type (SDAT) demented patients had equally elevated CSF CRH and TRH but not SRIF levels as compared with the controls. This elevation was, however, not seen in patients with simple dementia while it was most prominent in those exhibiting marked depressive symptoms. It is concluded that depression rather than dementia itself may be associated with CSF CRH and TRH elevation in elderly patients with cognitive impairment.
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PMID:Cerebrospinal fluid neuropeptides in dementia. 148 50

The effect of somatostatin-14 (SS-14) on gamma-aminobutyric acid (GABA)-mediated inhibitory neurotransmission in the dorsolateral septal nucleus (DLSN) was investigated using a submerged slice preparation and intracellular recording techniques. Somatostatin-14 applied by superfusion or by pressure ejection from micropipettes predominantly inhibited the intracellularly recorded fast inhibitory postsynaptic potential (fIPSP) and late hyperpolarizing potential (LHP) elicited by focal electrical stimulation of the DLSN. The decreases in LHP and fIPSP amplitude occurred at low concentrations of peptide, in the absence of appreciable changes in the passive-membrane properties of postsynaptic neurons, and outlasted the membrane hyperpolarizing effect produced by SS-14 at higher concentrations. The ability of SS-14 to modulate postsynaptic GABA receptor responses underlying the fIPSP and LHP were investigated by applying baclofen, a selective GABAB receptor agonist, and isoguvacine, a selective GABAA receptor agonist, by pressure ejection. Hyperpolarizing responses to GABAA and GABAB receptor stimulation were significantly decreased during superfusion of SS-14. Tetrodotoxin applied by superfusion blocked electrically evoked synaptic potentials but not the depressant effect of SS-14 on baclofen- or isoguvacine-induced hyperpolarization. Facilitation of the fIPSP or LHP by SS-14 also occurred but less frequently and consistently than the depressant action. Excitatory postsynaptic potentials and membrane response to NMDA or quisqualate appeared unaltered by bath-applied SS-14. These findings suggest a novel postsynaptic action of SS-14 leading to depression of synaptic responses mediated by GABAA and GABAB receptors. Synaptically released SS-14 in the DLSN may participate in modulation of feedforward and/or feedback inhibitory mechanisms coordinating DLSN function in the septo-hippocampal system.
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PMID:Somatostatin depresses GABA receptor-mediated inhibition in the rat dorsolateral septal nucleus. 197 66

In vitro assessment was made of the hormone-release capability of splenic pancreatic tissue 16 days after adult chickens had 99% of the pancreatic mass surgically removed. The objective of this study was to evaluate if the enlargement of the splenic lobe remnant after 99% pancreatectomy was attended by alterations in the responsivity of hormone release and, if so, were such changes reflective of all pancreatic hormones. After a 24-hr fast, splenic lobe tissue was obtained from young adult chickens on Postoperative Day 16, diced into 18-22 mg cubes, and incubated in vitro in media containing varying amounts of glucose with or without added somatostatin (SRIF). At 15-min intervals, the tissue cubes were transferred to fresh media and samples of each medium measured for insulin, glucagon, and APP. Viability of the tissue after 75 min was tested by tissue response to added 5 mM phenylalanine. The results obtained indicated that while total content of all four hormones (including SRIF) increased with tissue enlargement, the concentration of each decreased significantly except for SRIF, which remained at control levels. Further, the sensitivity of the B-cell in releasing insulin when confronted by a glucose challenge was not altered by previous pancreatectomy, while that of glucagon release from the A-cell was depressed. A-cell responsivity to SRIF does not appear to be adversely affected by previous 99% pancreatectomy. APP release was least affected by SRIF addition to the media, although depression by high glucose occurred. It is concluded that differential alterations occur in chicken pancreatic hormone-releasing cells as a result of 99% pancreatectomy. The efficacy in maintaining low, but still adequate, plasma I/G molar ratios (reported earlier) by the splenic remnant tissue either reflects a remarkable functional readjustment to surgical removal of 99% of the pancreatic mass in chickens or, alternatively, suggests the existence of extrapancreatic sources of insulin and glucagon, but not APP.
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PMID:In vitro release of pancreatic hormones following 99% pancreatectomy in the chicken. 256 76

The effects of plasma free fatty acids (FFA) and somatostatin-14 (S-14) on concentrations of plasma GH, glucagon and insulin were investigated in juvenile ducks. Oleic acid, S-14 or both were infused into 4- to 7-week-old birds and plasma GH, glucagon-like immunoreactivity (GLI), immunoreactive insulin (IRI) and FFA were measured. An increase in plasma GH and a decrease in GLI but no change in IRI was observed after infusion of 9 mg oleic acid/kg per min. A decrease in plasma GH, FFA and IRI and an increase in plasma GLI was seen after infusion of 800 ng S-14/kg per min. These effects of S-14 on IRI and GLI were abolished when S-14 was infused simultaneously with oleic acid. It is concluded that FFA have a direct stimulatory effect on GH secretion and an inhibitory effect on glucagon secretion. Somatostatin-14 directly inhibits the secretion of GH and its stimulatory effect on the secretion of glucagon is mediated by a depression in concentrations of plasma FFA. Finally, S-14 has no effect on plasma insulin when basal levels of plasma FFA are maintained.
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PMID:Control of plasma levels of growth hormone, glucagon and insulin in ducklings: roles of free fatty acids and somatostatin. 286 14

Somatostatin (SRIF) (6 nmol) given intracisternally (i.c.) into the alpha-chloralose anaesthetized rat has recently been shown to cause apnoea with a latency of 5-10 minutes (Kalia et al. 1984a). The apnoea produced by SRIF is very rapid, irreversible and leads to the death of the animal. In view of the existence of SRIF nerve cell bodies and terminals in medullary respiratory nuclei such as the ventral and ventrolateral subnuclei of the nucleus of the tractus solitarius (nTS) (Kalia et al. 1984b, Johanson et al. 1984), we have proposed the existence of somatostatinergic mechanisms in the respiratory nuclei of the medulla oblongata involved in mediating apnoeic conditions (Kalia et al. 1984a). In the present study, we have analysed whether the SRIF induced apnoea could be counteracted by a previous i.c. administration of the highly selective alpha 2-adreno-receptor blocking agent RX 781094 (2-(2-(I,4 benzodioxanyl]2-imi-dazoline HCl) (Doxey et al. 1983), or an opiate receptor blocking agent such as naloxone. Thus, both alpha 2-adrenoreceptor agonists and opiates induce respiratory depression, and opiates in high doses cause apnoea (Bolme et al. 1974, Hassen et al. 1982, Sitsen et al. 1982). In addition, catecholamine (CA) and enkephalin immuno-reactive nerve terminal networks exist in high densities within the nucleus tractus solitarius (nTS) of the medulla oblongata and may therefore interact with somatostatin nerve terminals in regulation of respiratory activity (Kalia et al. 1984b).
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PMID:Somatostatin induced apnoea: prevention by central and peripheral administration of the opiate receptor blocking agent naloxone. 286 86


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