Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Normal corpus luteum function is determined by function in the follicular as well as the luteal phase. In the follicular phase adequate follicle-stimulating hormone (FSH) and oestrogen stimulation are required for granulosa cell mitosis and luteinizing hormone (LH) receptor synthesis. An increase in LH pulse frequency may also be necessary for adequate oestrogen synthesis and preparation of follicular cells for luteinization and secretion of progesterone. The nature of LH release may also influence luteal function and pre-ovulatory progesterone may increase the responsiveness of the follicle to gonadotrophins. The thecal vascular network becomes extensive around pre-ovulatory follicles and may influence access of gonadotrophins and/or the ability of follicular cells to respond to them. Further vascularization is an early feature of luteinization. Angiogenic factors are found in luteal tissue and prostacyclin increases luteal blood flow. The corpus luteum consists of large cells which secrete most of the progesterone and have prostaglandin F2 alpha receptors and small cells which are responsive to LH. In the luteal phase subnormal luteal function has not been associated with a reduction in LH concentration, pulse frequency or amplitude. The number and occupancy of LH receptors and adenylate cyclase activity do not appear to be altered by a reduction in luteal function. Low density lipoprotein provides the substrate and somatomedin C modulates among other hormones' influences, progesterone production. In addition to the cAMP second messenger system phosphatidyl inositol metabolism may also be associated with LH stimulation. Luteolysis is an active process; prostaglandin F2 alpha or lipoxygenase products and possibly an endogenous GnRH-like ovarian hormone may mediate it as also may oxytocin in some species.
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PMID:The corpus luteum. 328 62

Different changes in neurotransmitters were observed in patients with fibromyalgia. The aim of the study was to confirm the diagnosis fibromyalgia by determination of several of these substances. In 60 patients, who met the ACR classification criteria for fibromyalgia and in 20 sex and age matched controls the following estimations were made: serotonin (EIA), somatomedin C (RIA), calcitonin (RIA), prostaglandin E2 (EIA), oxytocin (RIA), ACTH (RIA), substance P (EIA), TSH (LIA), prolactin (LIA). In comparison to healthy controls, patients with fibromyalgia revealed significantly decreased levels of serotonin, somatomedin C, calcitonin, prostaglandin E2 and a significantly increased level of prolactin. No significant differences were found in the levels of ACTH, substance P and TSH. These results suggest that the diagnosis of fibromyalgia can be confirmed by various biochemical parameters, but further investigations must be carried out to value the diagnostic relevance of these findings.
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PMID:[Biochemical changes in fibromyalgia]. 876 46