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)

The effects of lesions of the suprachiasmatic (SCN) and paraventricular nuclei (PVN) of the hypothalamus on photoperiodic responses were examined in adult Siberian hamsters. SCN lesions reduced nocturnal water intake in long days, whereas PVN lesions increased body weight and food intake in both short and long days. SCN or PVN lesions blocked short-day-induced decreases in body, fat pad, and testes weights and in food intake. Serum prolactin (PRL), but not follicle-stimulating hormone, levels were increased. The distribution of immunostained neurons and fibers for gonadotropin-releasing hormone (GnRH), beta-endorphin, arginine vasopressin (AVP), and vasoactive intestinal polypeptide (VIP) resembled that of other rodent species. Short-day exposure reduced AVP staining in lateral septum, medial amygdala, and bed nucleus of the stria terminalis but not in the PVN of the thalamus or the SCN. Short-day-exposed hamsters had fewer beta-endorphin-positive arcuate nucleus cells and tended to have fewer GnRH-positive preoptic cells than long-day controls. VIP staining was unaffected by photoperiod. Most day length effects on immunostaining were eliminated by either lesion. These results establish the importance of the SCN and PVN in the photoperiodic control of several seasonal responses in Siberian hamsters.
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PMID:Suprachiasmatic and paraventricular control of photoperiodism in Siberian hamsters. 189 44

Interleukin 1 alpha (IL-1 alpha), a powerful endogenous pyrogen released from monocytes and macrophages by bacterial endotoxin, stimulates corticotropin, prolactin, and somatotropin release and inhibits thyrotropin release by hypothalamic action. We injected recombinant human IL-1 alpha into the third cerebral ventricle, to study its effect on the pulsatile release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) in conscious, freely moving, ovariectomized rats. Intraventricular injection of 0.25 pmol of IL-1 alpha caused an almost immediate reduction of plasma LH concentration; this decrease was statistically significant 20 min after injection and occurred through a highly significant reduction in the number of LH pulses, with no effect on pulse amplitude. In contrast, there was no change in pulse frequency but a small significant elevation in amplitude of FSH pulses. Intraventricular injection of the diluent had no effect on gonadotropin release. The results provide further evidence for separate hypothalamic control mechanisms for FSH and LH release. To determine the mechanism of the suppression of LH release, mediobasal hypothalamic fragments were incubated in vitro with IL-1 alpha (10 pM) and the release of LH-releasing hormone (LHRH) and prostaglandin E2 into the medium was measured by RIA in the presence or absence of norepinephrine (50 microM). IL-1 alpha reduced basal LHRH release and blocked LHRH release induced by norepinephrine. It had no effect on the basal release of prostaglandin E2; however, it completely inhibited the release of PGE2 evoked by norepinephrine. To evaluate the possibility that IL-1 alpha might also interfere with the epoxygenase pathway of arachidonic acid metabolism, epoxyeicosatrienoic acids were also measured. IL-1 alpha had no effect on the content of epoxyeicosatrienoic acids in the hypothalamic fragments as measured by gas chromatography and mass spectrometry. In conclusion, IL-1 alpha suppresses LH but not FSH release by an almost complete cessation of pulsatile release of LH in the castrated rat. The mechanism of this effect appears to be by inhibition of prostaglandin E2-mediated release of LHRH.
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PMID:Interleukin 1 alpha inhibits prostaglandin E2 release to suppress pulsatile release of luteinizing hormone but not follicle-stimulating hormone. 190 15

Breast cyst fluid (BCF) and plasma levels of beta-endorphin (beta-EP), oestradiol (E2), progesterone (P), luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), prolactin (PRL) and cortisol were assayed radiochemically in a group of 10 premenopausal women aged 45-50 years suffering from gross cystic breast disease. The concentration of beta-EP (fmol/ml) in BCF (17.6 +/- 4.6 S.E.) was over four times higher than that in plasma (4.2 +/- 0.5 S.E.). The level of E2 was 41 times higher (1738.2 +/- 350.5 S.E. pg/ml) and that of P was 47 times higher (65.47 +/- 8.25 S.E. ng/ml) in BCF than in plasma. The significantly increased values of beta-EP, E2 and P in BCF and the identification of beta-EP in the cyst-lining epithelium indicated that local synthesis occurs. Growth factor-like properties of beta-EP and E2 are responsible for the propagation of cystic changes. The autonomous formation and activity of beta-EP, E2 and P in cystic formations were not correlated with LH, FSH, TSH and cortisol levels, which were significantly higher in plasma than in BCF. The concentration of PRL in BCF was not significantly higher than that in plasma. Moreover, the plasma concentrations of testosterone, androstenedione, thyroxine, triiodothyronine, thyroxine-binding globulin and sex-hormone-binding globulin were within the normal ranges. In this study we demonstrated synergism between beta-EP and steroid hormones which encourages the development of gross cystic disease in premenopausal women.
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PMID:Breast cyst fluid concentrations of beta-endorphin, steroids and gonadotrophins in premenopausal women with gross cystic disease. 192 35

Hypothalamic pituitary functions were studied in 25 patients before and 6 months after cranial irradiation with or without radiosensitizing chemotherapy for nasopharyngeal carcinoma. The estimated average total dose was 5,000 cGy to the hypothalamus and pituitary gland. The radiosensitizing chemotherapy used was endoxan, 4900 +/- 873 mg and/or methotrexate 113 +/- 30 mg. All patients had normal pituitary function before radiotherapy. Six months after radiotherapy, there was a significant increase in baseline serum thyrotropin (TSH) and follicle-stimulating hormone (FSH) levels. The TSH response to thyrotropin-releasing hormone (TRH) was significantly increased, suggesting primary hypothyroidism due to neck irradiation. The peak serum TSH response to TRH became delayed in 21 patients, suggesting a defect in TRH release. In male patients who did not receive radiosensitizing chemotherapy, the FSH response to luteotropic hormone-releasing hormone (LHRH) increased while the luteinizing hormone (LH) response decreased. But in male patients who also received radiosensitizing chemotherapy, both the FSH and LH responses to LHRH increased. The adrenocorticotropic hormone (ACTH) response to ovine corticotropin-releasing hormone (CRH) did not change, while the integrated cortisol response increased. The growth hormone (GH) response to growth hormone-releasing hormone (GRH) did not change. The GH response to insulin tolerance test (ITT) increased and may be explained by the more severe hypoglycemia induced by the same dosage of insulin after radiotherapy or the recovery from the previous wasting caused by radiotherapy. There was no significant increase in serum prolactin. In conclusion, we demonstrated impairment of the hypothalamus-pituitary-endocrine gland axes as early as 6 months after cranial irradiation with or without chemotherapy.
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PMID:Early effects of cranial irradiation on hypothalamic pituitary function. 197 95

The hypothesis was tested that corticotropin-releasing factor (CRF) is involved in the inhibition of gonadotropin secretion during chronic hyperprolactinemia. Two models of hyperprolactinemia were used, namely inoculation with the prolactin (PRL)-secreting tumor 7315b and implantation of isogenic pituitary glands. Gonadectomized, adrenalectomized male rats received a testosterone capsule and a corticosterone pellet and were inoculated subcutaneously with tumor 7315b. Similar rats without tumor served as controls. The rats were studied 3-4 weeks later while anesthetized with urethane. Plasma testosterone and corticosterone were similar in the two groups of rats. Compared to controls, the tumor-bearing rats had significantly higher plasma levels of PRL (100-fold increase) and adrenocorticotropin (ACTH; 3-fold increase), whereas plasma luteinizing hormone (LH) and follicle-stimulating hormone (FSH) had significantly decreased to 15 and 40%, respectively. CRF release into hypophysial stalk plasma was higher in rats with tumor 7315b than in controls (298 +/- 23 vs. 197 +/- 28 pg/h), and hypothalamic CRF content had increased from 3.0 +/- 0.3 to 4.3 +/- 0.3 ng. Male rats received 3 pituitary glands under the kidney capsule. Sham-operated rats served as controls. They were studied 5-7 weeks later while anesthetized with urethane. Compared to controls, pituitary-grafted rats had larger adrenals (49 +/- 4 vs. 34 +/- 2 mg), higher plasma PRL (156 +/- 18 vs. 52 +/- 8 ng/ml), ACTH (0.46 +/- 0.05 vs. 0.22 +/- 0.02 ng/ml) and corticosterone (455 +/- 39 vs. 268 +/- 14 ng/ml), and lower plasma levels of LH (21 +/- 2 vs. 41 +/- 6 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence for the involvement of corticotropin-releasing factor in the inhibition of gonadotropin release induced by hyperprolactinemia. 210 70

Brain beta-endorphin (beta-EP) plays an important role in regulating the hypothalamus-pituitary-gonadal axis activity. Cerebrospinal fluid (CSF) beta-EP levels seem to reflect the central rather than pituitary secretion. With the aim to correlate the changes of plasma estradiol (E2), progesterone, luteinizing hormone (LH) and follicle-stimulating hormone with brain beta-EP, CSF levels of beta-EP were measured in 15 normally cycling and 15 postmenopausal women. CSF beta-EP levels in post-menopausal women were lower than in fertile women. A positive correlation between plasma E2 and CSF beta-EP level was found in all women. In fertile women CSF beta-EP levels were inversely correlated to plasma gonadotropin levels. These results showed that CSF beta-EP levels differ between fertile and postmenopausal women and are correlated with plasma LH and E2, suggesting a strong linkage between central beta-EP levels and pituitary-gonadal axis hormones.
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PMID:Relationship between cerebrospinal fluid beta-endorphin and plasma pituitary-gonadal hormone levels in women. 213 50

To investigate the role of progesterone (P) in the early follicular phase, the antiprogesterone effect of RU486 was examined in five normally cycling women monitored by daily hormonal levels during three consecutive cycles (control, treatment, and recovery). In addition, luteinizing hormone (LH) pulse characteristics were assessed by frequent blood sampling (10 minutes for 10 hours) on day 3 of the control and the corresponding day of treatment cycles. Administration of RU486 (3 mg/kg, orally) for the first 3 days of the menstrual cycle did not significantly alter the length of the follicular phase (13.4 +/- 1.7 to 15.2 +/- 1.3 days), the LH surge, or the luteal phase length (12.2 +/- 0.5 to 12.6 +/- 0.7 days). The intermenstrual length of the treatment cycle (29.8 +/- 1.9 days) did not differ from the control (27.6 +/- 1.8 days) or recovery cycles (29.6 +/- 2.5 days). Integrated secretion of P and estradiol (E2) did not vary during the luteal phase of the control, treatment, or recovery cycles. During RU486 treatment, LH pulse frequency, pulse amplitude, and mean LH were not altered. Whereas mean E2 levels were significantly decreased from 150.5 +/- 15.1 to 110.1 +/- 7.0 pmol/L, follicle-stimulating hormone, P, adrenocorticotropin hormone, and cortisol were not significantly altered. Thus, in spite of the transient decrement in E2 secretion during RU486 treatment, the integrity of the ovulatory menstrual cycle was maintained. We conclude that administration of the antiprogesterone RU486 at the dose used during the first 3 days of the follicular phase does not perturb menstrual cyclicity.
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PMID:Effects of the antiprogesterone RU486 in the early follicular phase of the menstrual cycle. 215 36

In order to examine the effect of glucocorticoids on the menstrual cycle of rhesus monkeys, cortisol was injected twice daily during the follicular phase. This cortisol treatment did not alter basal gonadotropin secretion but blocked the normal follicular rise of estrogens, the gonadotropin surge and the luteal rise of progesterone, and delayed the onset of the next cycle. In a second study, estradiol benzoate (E2B) was injected on the sixth day following the start of menstrual bleeding either with or without concurrent adrenocorticotropic hormone (ACTH) treatment. E2B injection was able to stimulate surges of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) whether or not the animals had been treated with ACTH. These data suggest that, the action of cortisol, the final mediating step in the hypothalamic-pituitary-adrenal axis, occurs at the level of the gonads versus the pituitary in the rhesus monkey. While the pituitary response to endogenous gonadotropin-releasing hormone or exogenous E2B stimulation appears to remain unaffected, normal folliculogenesis is disrupted, preventing the follicular secretion of estrogens and the subsequent gonadotropin surges. The effects of corticosteroids are temporary, with normal cycling returning when plasma corticosteroids return to basal concentrations, albeit after a delay.
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PMID:Influence of the hypothalamic-pituitary-adrenal axis on the menstrual cycle and the pituitary responsiveness to estradiol in the female rhesus monkey (Macaca mulatta). 215 8

We evaluated six patients in whom a diagnosis of Sheehan's syndrome had been made. The plasma levels of the following hormones were measured: basal thyroxine (T4), estradiol and cortisol; and also follicle-stimulating hormone (FSH), luteinizing hormone (LH), growth hormone (GH), thyrotropin (TSH), prolactin (PRL) and adrenocorticotropic hormone (ACTH), basally and after acute challenge with LH releasing hormone (LHRH), GRF (1-29)NH2 or insulin hypoglycemia, TSH releasing hormone (TRH) and lysine-8-vasopressin, respectively. Two patients underwent chronic LHRH stimulation by pulsatile subcutaneous administration with infusion pump. In 4 cases, computed tomography (CT) was performed although cranial X-ray study was normal. A severe and generalized pituitary involvement was found in all patients, 3 of whom had diabetes mellitus. Probably, more insidious cases go unnoticed. The presence of asymptomatic partial empty sella (ES) in all the CTs that were carried out raises the possibility that it is another evolutive feature of SS.
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PMID:[Relations between Sheehan's syndrome and empty sella turcica. A functional study apropos of 6 cases]. 217 69

Tumor necrosis factor-alpha (TNF-alpha) is secreted by activated monocytes and other immune cells. This paper reports studies on the effects of TNF-alpha on the releases of pituitary hormones such as luteinizing hormone (LH), follicle-stimulating hormone, prolactin (PRL) and adrenocorticotropic hormone (ACTH). The addition of recombinant human TNF-alpha (rTNF-alpha) to cultures of pituitary cells resulted in significantly increased releases of gonadotropins, PRL, and ACTH for up to 30 min, but not later. rTNF-alpha, like GnRH, also stimulated the release of bioactive LH. In addition, rTNF-alpha induced production of an interleukin-6 (IL-6)-like molecule by pituitary cells. As IL-6 induces the releases of multiple hormones from pituitary cells, our data suggest that rTNF-alpha may stimulate the releases of multiple pituitary hormones through IL-6 production as well as by its direct action on pituitary cells.
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PMID:Induction by tumor necrosis factor-alpha of rapid release of immunoreactive and bioactive luteinizing hormone from rat pituitary cells in vitro. 217 54


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