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

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

The purpose of this study was to elucidate the phenotypic conditions in the sella turcica/pituitary gland complex in human trisomy 18 fetuses. Fourteen human fetuses with gestational ages from 12 to 39 weeks were included in the study. Normal fetuses at corresponding ages were used as controls. Whole body and special radiographic examination was undertaken before the midsagittal cranial base block, including the pituitary gland, was excised and analyzed histologically and immunohistochemically (keratin wide spectrum [KWS], thyroid-stimulating hormone [TSH], and neurophysin [Nph]). In all trisomy 18 fetuses, TSH-positive adenopituitary tissue was present in the sella and in greater or lesser amounts pharyngeally. The neurohypophysis was Nph-positive and located normally in the sella turcica. The adenohypophyseal tissue reacted either KWS-faint or KWS-negative, whereas KWS-positive reaction occurs in normal fetuses. This circumstance might suggest an altered cytoskeletal structure of the surface ectoderm in the pituitary placode in trisomy 18. The sella turcica was malformed in all the fetuses. Very broad craniopharyngeal canals were observed in some of the fetuses. Because endocrine disorders occur in many congenital malformations, it is essential in future studies to chart the sella turcica/pituitary gland region systematically in different genotypes.
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PMID:Pituitary gland and sella turcica in human trisomy 18 fetuses. 950 72

m-Chlorophenylpiperazine (m-CPP), a serotonin (5-HT) agonist with some selectivity for the 5-HT2C receptor subtype, which is widely used to examine 5-HT receptor function in human subjects, has been found to induce oxytocin and thyrotropin (TSH) responses in rodents. This study examined whether m-CPP had any effect on plasma oxytocin, TSH and aldosterone concentration in healthy volunteers using a double-blind, placebo-controlled crossover design. Plasma adrenocorticorticotropic hormone (ACTH) and cortisol responses, two generally accepted markers of m-CPP-induced 5-HT receptor activation, were measured in parallel. Male subjects (n=7) received placebo, 0.25 and 0.5 mg/kg oral m-CPP. In female subjects (n=5), the effects of placebo and 0.25 mg/kg m-CPP were studied. After placebo, given in the morning, ACTH, cortisol, TSH and aldosterone concentrations decreased over time. m-CPP 0.25 mg/kg avoided decreases in ACTH, cortisol and TSH concentrations; these responses were significant. At the dose of 0.5 mg/kg, m-CPP caused increase in ACTH, cortisol, TSH and aldosterone concentrations. Significant plasma oxytocin responses were found in female subjects only; thus this effect of m-CPP was statistically significantly gender dependent. Other responses to m-CPP were similar in male and female subjects. The present results suggest that there are clear differences, including dose and gender-dependent dissociations, among the 5-HT receptor agonist m-CPP-induced neuroendocrine responses.
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PMID:Gender-dependent dissociation between oxytocin but not ACTH, cortisol or TSH responses to m-chlorophenylpiperazine in healthy subjects. 960 May 79

A group of 17 consecutive regularly menstruating women who gained at least 5 kg the previous year (Group 1) was compared with a control group of similar age, parity and social class (Group 2). Galactorrhea was observed in 6/17 women from group 1 and in 1/16 women from group 2 (chi 2 4.571; p < .05). Average morning prolactin levels were higher in group 1 (8.15 +/- 4.92 micrograms/l) than in group 2 (5.29 +/- 2.48 micrograms/l; p < .05). The two groups were similar in their morning thyroxin, triiodothyronine, TSH, estradiol, cortisol, gastrin, cholecystokinin, somatostatin, oxytocin, insulin and IGF-1 levels. Leptin levels were significantly higher in group 1 than in group 2 (18.85 +/- 10.63 micrograms/l vs. 10.15 +/- 6.38 micrograms/l; p < .02) but this difference could be attributed exclusively to the higher body mass index (BMI) of group 1 (MANCOVA). Analysis of the distribution of basal prolactin levels in group 1 revealed a skewed distribution due to the presence of six outliers (Barnett and Lewis test associated with Mahalanobis distance) whose values were higher than the highest value found in group 2. These outliers were henceforth considered as subgroup 1a, and the remnant patients in group 1 as subgroup 1b. Besides the expected difference in basal prolactin levels between subgroups 1a and 1b (13.72 +/- 3.69 and 5.12 +/- 1.81 micrograms/l, respectively) and the higher frequency of galactorrhea in group 1a (4/6 vs. 2/11; p < .05) no other differences were observed in clinical or basal biochemical parameters. Following domperidone (10 mg, i.v.) the percentual increase in prolactin (delta Prl 20'/Prl 0') was significantly lower in group 1 than in group 2 (23.9 + 15.2 vs. 37.0 +/- 21.2; p < .05). In absolute values, the prolactin rise in subgroup 1a (100.7 +/- 45.5 micrograms/l) was significantly lower (p < .02) than that of subgroup 1b (157.3 +/- 50.3 micrograms/l) and group 2 (152.7 +/- 34.5 micrograms/l). Group 1 (and each one of its two sub-groups) also differed from group 2 in a higher incidence of meaningful life-events the year preceding the study. This study confirms previous observations that recent weight gain in women is preceded by important life-events and is associated with galactorrhea and increased prolactin levels in a number of them. Besides, it provides evidence that the increased prolactin levels are due to reduced hypothalamic dopaminergic tone.
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PMID:Rapid weight gain, at least in some women, is an expression of a neuroendocrine state characterized by reduced hypothalamic dopaminergic tone. 992 49

The adipose tissue signals to the brain via its secretory products. However, it is unknown whether the brain itself can directly contact the fat tissue. In order to test this hypothesis, the adipocytic expression of receptors for pituitary hormones and hypothalamic peptides was investigated. Besides FSH- and LH-receptors, adipocytes do express the specific receptors for ACTH, TSH, GH, prolactin, oxytocin and the three receptor subtypes for vasopressin. Thus, the adipose tissue might no longer be regarded as an inert and steady tissue but as a fast acting player downstream of and under the control of the brain. Based on this, the potential existence and clinical impact of a hypothalamic-pituitary-adipose axis should further be investigated.
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PMID:Hypothesis paper Brain talks with fat--evidence for a hypothalamic-pituitary-adipose axis? 1604 Jan 19

Adiponectin plays important roles in the control of energy homeostasis and autonomic function through peripheral and central nervous system actions. The paraventricular nucleus (PVN) of the hypothalamus is a primary site of neuroendocrine (NE) and autonomic integration, and, thus, a potential target for adiponectin actions. Here, we investigate actions of adiponectin on parvocellular PVN neurons. Adiponectin influenced the majority (65%) of parvocellular PVN neurons, depolarizing 47%, whereas hyperpolarizing 18% of neurons tested. Post hoc identification (single-cell RT-PCR) after recordings revealed that adiponectin depolarizes NE-CRH neurons, whereas intracerebroventricular injections of adiponectin in vivo caused increased plasma ACTH concentrations. Adiponectin also depolarized the majority of TRH neurons, however, NE-TRH neurons were unaffected, in accordance with in vivo experiments showing that intracerebroventricular adiponectin was without effect on plasma TSH. In addition, bath administration of adiponectin also depolarized both preautonomic TRH and oxytocin neurons. These results show that adiponectin acts in the central nervous system to coordinate NE and autonomic function through actions on specific functional groups of PVN neurons.
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PMID:Adiponectin depolarizes parvocellular paraventricular nucleus neurons controlling neuroendocrine and autonomic function. 1894 98

Opioid abuse has increased in the last decade, primarily as a result of increased access to prescription opioids. Physicians are also increasingly administering opioid analgesics for noncancer chronic pain. Thus, knowledge of the long-term consequences of opioid use/abuse has important implications for fully evaluating the clinical usefulness of opioid medications. Many studies have examined the effect of opioids on the endocrine system; however, a systematic review of the endocrine actions of opioids in both humans and animals has, to our knowledge, not been published since 1984. Thus, we reviewed the literature on the effect of opioids on the endocrine system. We included both acute and chronic effects of opioids, with the majority of the studies done on the acute effects although chronic effects are more physiologically relevant. In humans and laboratory animals, opioids generally increase GH and prolactin and decrease LH, testosterone, estradiol, and oxytocin. In humans, opioids increase TSH, whereas in rodents, TSH is decreased. In both rodents and humans, the reports of effects of opioids on arginine vasopressin and ACTH are conflicting. Opioids act preferentially at different receptor sites leading to stimulatory or inhibitory effects on hormone release. Increasing opioid abuse primarily leads to hypogonadism but may also affect the secretion of other pituitary hormones. The potential consequences of hypogonadism include decreased libido and erectile dysfunction in men, oligomenorrhea or amenorrhea in women, and bone loss or infertility in both sexes. Opioids may increase or decrease food intake, depending on the type of opioid and the duration of action. Additionally, opioids may act through the sympathetic nervous system to cause hyperglycemia and impaired insulin secretion. In this review, recent information regarding endocrine disorders among opioid abusers is presented.
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PMID:The effects of opioids and opioid analogs on animal and human endocrine systems. 1990 33

Accumulating evidence clearly indicates both thyroid hormone and estrogen have a pivotal role in bone metabolism. Pituitary hormones, TSH and FSH, regulate circulating levels of thyroid hormone and estrogen, respectively. Recent works raise a possibility that either TSH or FSH also has its own direct effects on bone cells involved in bone resorption and formation. More recently, it is suggested that oxytocin and vasopressin are also involved in bone metabolism. However, several investigations of genetically manipulated model mice and clinical data from patients with certain diseases have provided inconsistent results. Thus, we need more data that answer the question whether or not each pituitary hormone is physiologically and pathophysiologically involved in controlling bone metabolism in human.
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PMID:[Control of bone remodeling by nervous system. Possible roles of pituitary hormones for bone metabolism]. 2112 38

Accumulating evidence clearly indicates both thyroid hormone and estrogen have a pivotal role in bone metabolism. Pituitary hormones, TSH and FSH, regulate circulating levels of thyroid hormone and estrogen, respectively. Recent works raise a possibility that either TSH or FSH also has its own direct effects on bone cells involved in bone resorption and formation. More recently, it is suggested that oxytocin and vasopressin are also involved in bone metabolism. However, several investigations of genetically manipulated model mice and clinical data from patients with certain diseases have provided inconsistent results. Thus, we need more data that answer the question whether or not each pituitary hormone is physiologically and pathophysiologically involved in controlling bone metabolism in human.
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PMID:[Possible involvement of pituitary hormones in bone metabolism]. 2335 86

Bone remodeling is determined by function of two basic cell forms--bone resorbing osteoclasts and bone formation activating osteoblasts. Both cells are under control of a variety of endogenic and environmental factors, which ensure balance between bone resorption and bone formation. This article reviews the neuro-hormonal factors with osteoanabolic (central isoform of serotonin, melatonin, cannabinoids, beta 1 adrenergic system, oxytocin, ACTH and TSH) or osteocatabolic effects (neuropeptide Y, neuromedin U, beta2 adrenergic system). The dual effects of the beta-adrenergic system, serotonin and leptin are also discussed. The goal of studies focused on neuro-skeletal interaction is to synthesize new molecules, which can modify osteo-anabolic or osteo-catabolic pathways.
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PMID:[Neuro-skeletal biology and its importance for clinical osteology]. 2339 Aug 67


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