Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Corticotropin releasing hormone (CRH), somatostatin (SRIF), and arginine vasopressin (AVP) concentrations were estimated using radioimmunoassay in the temporal and occipital cortices in postmortem brain from patients clinically and neuropathologically diagnosed as senile dementia of the Lewy body type (SDLT), senile dementia of the Alzheimer type (SDAT), and Parkinson's disease (PD) and from neurologically normal controls. The concentration of temporal and occipital neocortical CRH was diminished in both SDAT and SDLT compared to control values, whereas SRIF was reduced only in temporal cortex in both these conditions. In contrast, the concentrations of both CRH and SRIF were unaltered in PD. The concentrations of AVP in SDLT, SDAT, and PD were similar to those found in the control groups. The decrement in SRIF, but not CRH, was found to be correlated with some indices of severity of illness in SDAT; a similar but nonsignificant trend for SRIF was observed in SDLT.
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PMID:Neocortical concentrations of neuropeptides in senile dementia of the Alzheimer and Lewy body type: comparison with Parkinson's disease and severity correlations. 167 64

Corticotropin-releasing-factor-like immunoreactivity (CRF-LI) was measured in a number of subcellular fractions from rat brain using a highly sensitive and specific radioimmunoassay. CRF-LI was highly enriched in the crude synaptosomal/mitochondrial fraction (P2) relative to the homogenate, P1, S1, and S2 fractions. Separation of the P2 fraction into synaptosomal, myelin, and mitochondria-enriched subfractions on a rapid one-step sucrose gradient revealed that CRF-LI was present at higher concentration in the synaptosomal fraction than in the mitochondrial and myelin fractions. The distribution of CRF-LI paralleled that of synapsin, a synaptic vesicle marker phosphoprotein, but not that of pyruvate dehydrogenase, a mitochondrial phosphoprotein. These results are consistent with a nerve terminal localization of CRF and a potential role for this peptide as a central nervous system neurotransmitter.
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PMID:Subcellular distribution of corticotropin-releasing-factor-like immunoreactivity in rat central nervous system. 192 75

Corticotropin releasing factor (CRF) both stimulates ACTH secretion from the pituitary and inhibits secretion of growth hormone (GH) in adult rats through actions in the CNS. The purpose of the present study was to evaluate these pituitary and central actions of CRF in neonatal rats, in which the hypothalamo- pituitary adrenal (HPA) axis is relatively hypo-functional. The results of this study show that central or peripheral administration of CRF evokes a marked dose-related rise in serum corticosterone in 6-day old rats. The same doses of CRF stimulate, rather than inhibit GH secretion. These results suggest that CRF has unique central actions early in ontogeny.
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PMID:Corticotropin releasing factor stimulates growth hormone secretion in neonatal rats. 194 49

1. Corticotropin-stimulated lipolysis in adipocytes of rats, mice, hamsters, guinea pigs and rabbits. Melanotropins elicited high lipolytic activity only in guinea pig and rabbit adipocytes. Opiate peptides were active only in rabbit adipocytes. Pituitary and chorionic gonadotropins and somatotropin were lipolytic in guinea pig adipocytes. Other hormones tested including prolactin, somatostatin, substance P, neurotensin, angiotensin II, thyrotropin releasing hormone and pancreatic polypeptide were devoid of lipolytic activity in all of the adipocytes studied. 2. In the rabbit adipocytes gamma-melanotropin was lipolytic only at high doses. At these doses the peptide inhibited the lipolytic response to a high dose of corticotropin. 3. Lipolysis stimulated by vasoactive intestinal peptide and epinephrine in rat adipocytes was antagonized by insulin. The lipolytic hormones corticotropin, epinephrine, vasoactive intestinal peptide and secretin suppressed basal and insulin-stimulated lipogenesis.
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PMID:Studies on hormonal regulation of lipolysis and lipogenesis in fat cells of various mammalian species. 196 44

The sleep-wake effects of the proopiomelanocortin (POMC)-derived peptides, i.c.v. injected, are reported. Adrenocorticotropic hormone (ACTH, 1 microgram) induces an awakening effect, while its two derivatives, desacetyl-alpha-MSH (des-alpha-MSH, 1ng) and corticotropin-like intermediate lobe peptide (CLIP, 10 ng), are respectively able to increase slow wave sleep (SWS) and paradoxical sleep (PS); the hypnogenic effect of CLIP is also observed in hypophysectomized rats. Furthermore, two hypothalamic factors known to be involved in the control of POMC derivatives were also injected; MSH inhibiting Factor (MIF) does not influence the vigilance states, while Corticotropin Releasing Factor (CRF, 1 microgram) increases the waking state. Finally, some preliminary results, obtained with a restraint stress and suggesting a possible interrelation between stress, sleep and POMC derivatives, are discussed.
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PMID:Proopiomelanocortin (POMC)-derived peptides and sleep in the rat. Part 1--Hypnogenic properties of ACTH derivatives. 198 27

Corticotropin releasing factor, a 41 amino acid peptide, has been localized in climbing fibers and mossy fibers in the cat's cerebellar cortex. In the present study, corticotropin releasing factor was iontophoretically applied to Purkinje cells, isolated extracellularly, to assess the effect of this peptide on the firing rate of the neuron. By itself corticotropin releasing factor had little or no effect on cellular activity. However, this peptide potentiated the excitatory effects of aspartate and glutamate, the putative neurotransmitters of the climbing fiber and mossy fiber-parallel fiber systems, respectively. In addition, corticotropin releasing factor blocked the suppressive effects induced by the iontophoretic application of GABA. Finally, it shortened or eliminated the period of suppression produced by activation of climbing fibers in the cerebellar cortex. These data suggest that corticotropin releasing factor functions as a neuromodulator rather than as a neurotransmitter in cerebellar circuitry.
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PMID:Neuromodulatory effects of corticotropin releasing factor on cerebellar Purkinje cells: an in vivo study in the cat. 198 66

A specific double antibody radioimmunoassay (RIA) for human-Corticotropin-Releasing Hormone (hCRF) using an antibody to synthetic hCRF was established. This antibody allowed a usable range of 10 pg to 5 ng of CRF per ml in the assay. Comparing the efficiency of various plasma extraction procedures, the extraction with ice-cold methanol was found to be the most simple and rapid method with an extraction efficiency of more than 80%. The reliability of the radioimmunoassay was shown under physiological and pathophysiological conditions.
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PMID:Radioimmunoassay of corticotropin-releasing hormone. 209 59

N-Terminal (1-76) portion of proopiomelanocortin (hNT) was measured in normals, Addison's, Nelson's, Cushing's disease, and in dexamethasone suppressible hyperaldosteronism (DSH) by using a specific homologous RIA. Mean basal immunoreactive hNT level was 94.2 +/- 6 pg/ml (mean +/- SE) in normal subjects. In Cushing's disease hNT values were slightly but not significantly (121 +/- 26.5 pg/ml) higher. In patients with DSH the levels were within normal range while they were much higher in Addison's and Nelson's syndromes. A strong correlation was found between IR-hNT and ACTH in plasma of normal subjects and patients with different disorders of the pituitary-adrenal axis (r = 0.83, p less than 0.01). Corticotropin-Releasing-Hormone (CRH) test in Cushing's disease stimulated the release of both ACTH and IR-hNT, showing a slightly different pattern of secretion. Similar patterns of secretion were found for hNT and ACTH in various pituitary-adrenal abnormalities. Normal levels of hNT in DSH do not support a role of this peptide in the pathogenesis of the disorder. Measurement of hNT in plasma can provide an additional tool for the diagnosis of patients with various disorders of the hypothalamic-pituitary-adrenal axis.
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PMID:Pro-gamma-MSH levels in various disorders of pituitary-adrenal axis. 215 20

To assess whether neuroendocrine dysfunction is present in children with acquired immunodeficiency syndrome (AIDS) and growth failure, we evaluated the thyroid, adrenal, and growth hormone-insulin-like growth factor I (IGF-1) axes in nine children with AIDS and failure to thrive. Basal thyroid-stimulating hormone, free thyroxine, and triiodothyronine levels were normal in eight of the nine children and indicated primary hypothyroidism in one child; thyroxine levels were elevated in four and normal in five children. Thyroxine-binding globulin levels were elevated in all children. Serial measurements of thyroid-stimulating hormone, made hourly from 2 to 6 pm and from 10 pm to 2 am, revealed a flat diurnal rhythm of thyroid-stimulating hormone in six children, which may indicate early central hypothyroidism, and a normal nocturnal rise in the remaining three children. Basal plasma corticotropin and aldosterone levels were normal in all children, plasma renin levels were normal in three and elevated in six children, and cortisol levels were normal or elevated in all children. Corticotropin-stimulated cortisol levels exceeded 500 nmol/L (18 micrograms/dl) in all children except one, who was receiving treatment with ketoconazole. Thus adrenocortical function appeared to be grossly intact. The peak growth hormone responses to provocative testing was normal (greater than 7 ng/ml) in eight children and low in one child. The plasma level of insulin-like growth factor I was normal in eight of the nine children and low in one child. We conclude that growth failure in children with AIDS does not usually result from a recognized endocrine cause and that adrenal function is usually normal. However, endocrine deficiency may contribute to morbidity in some children with AIDS.
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PMID:Growth and neuroendocrine dysfunction in children with acquired immunodeficiency syndrome. 201 47

Corticotropin releasing factor (CRF), injected into the cerebral ventricles (i.c.v.) of rabbits, induced EEG limbic seizures, behavioural excitability, stereotyped behaviour and the tardive enhancement of hippocampal theta voltage and frequency. The beta-endorphin cleavage derivatives des-tyr-gamma-endorphin (DT gamma E) and des-enkephalin-gamma-endorphin (DE gamma E), when injected i.v. for 4 days prevented the EEG ictal seizures induced by CRF in the hippocampus of rabbits and partly prevented the tardive enhancement of theta wave amplitude and frequency. These results suggest the possibility that these peptides may have antiepileptogenic properties.
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PMID:Effects of endorphin derivatives on the EEG alterations induced by corticotropin releasing factor in the rabbit hippocampus. 227 3


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