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)

A bidirectional interaction exists between the electrophysiological and neuroendocrine components of sleep. The first is represented by the nonrapid eye movement sleep (NREMS) and rapid eye movement sleep (REMS) cycles, the latter by distinct patterns of the secretion of various hormones. Certain hormones (neuropeptides and steroids) play a specific role in sleep regulation. Changes in their activity contribute to the pathophysiology of sleep disorders. A reciprocal interaction of the peptides growth hormone-releasing hormone (GHRH) and corticotropin-releasing hormone (CRH) plays a key role in sleep regulation. GHRH promotes growth hormone secretion and, at least in males, NREMS, whereas CRH impairs NREMS, promotes REMS and stimulates the secretion of adrenocorticotropic hormone and cortisol. Changes in the CRH:GHRH ratio in favor of CRH contribute to impaired sleep, elevated cortisol secretion and blunted GH levels during depression and normal aging. However, in women, GHRH exerts CRH-like effects. Galanin, ghrelin and neuropeptide Y are other sleep-promoting peptides, whereas somatostatin impairs sleep. A decline of orexin activity causes narcolepsy. In addition to CRH overactivity, hypercortisolism appears to be involved in the pathophysiology of sleep- electroencephalogram (EEG) changes in depression. Various neuroactive steroids exert specific effects on sleep. The changes of sleep EEG in women after the menopause are related to the decline of estrogen and progesterone. Furthermore, sleep-EEG changes in dwarfism, acromegaly, Addison's disease, Cushing's disease, brain injury, sleep apnea syndrome, primary insomnia, prolactinoma and dementia appear to be related to changes in the activity of peptides and steroids.
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PMID:Roles of peptides and steroids in sleep disorders. 3075 93

Prolonged remission of hypercortisolism with steroidogenesis inhibitors has been described in patients with ectopic adrenocorticotropic hormone (ACTH) syndrome. The anti-proliferative and pro-apoptotic effect of ketoconazole in human cancer cells was previously suggested. The aim of this study was to explore the effects of ketoconazole on ACTH-producing and non-ACTH-producing neuroendocrine tumor (NET) cell lines. The effects of ketoconazole alone, and in combination with somatostatin analogs, were evaluated in two human cell lines: DMS-79 (ectopic ACTH-producing small cell lung carcinoma) and BON-1 (human pancreatic NET). Total DNA measurement, apoptosis, cell cycle, chromogranin A (CgA)/proopiomelanocortin (POMC) expression by qRT-PCR, serotonin, CgA, and ACTH secretion assays were performed. In both cell lines, ketoconazole significantly suppressed cell growth and colony formation in a dose and time-dependent manner. The effect in DMS-79 was primarily cytotoxic, while it was more apoptotic in BON-1 cells. Ketoconazole also induced increase in G0/G1 phase in both cell lines and arrest in phase G2/M of BON-1 cells. Ketoconazole did not affect the secretion of serotonin, CgA, ACTH, or the mRNA expression of CgA and POMC. Decreased serotonin secretion was observed after the combination treatment with pasireotide. These results suggest a direct effect of ketoconazole on cell proliferation, apoptosis, and cell cycle in both ACTH- and non-ACTH-producing NET cells.
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PMID:Effects of Ketoconazole on ACTH-Producing and Non-ACTH-Producing Neuroendocrine Tumor Cells. 3110 72


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