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)

Pituitary cells from hamsters bearing diethylstilbestrol induced renal adenocarcinomas were cultured in vitro. Dispersed cells in plastic dishes were viable for up to two weeks in Dulbecco's modified Eagle's medium supplemented with 17.5% of 6:1 horse serum to fetal calf serum. The secretion of alpha-melanocyte stimulating hormone and prolactin into the medium were measured by radioimmunoassay. The concentrations of both were elevated by day 3 in the medium from the hyperplastic pituitaries obtained from the estrogen treated, tumor bearing hamsters. Neither DES (10(-8)M) nor tamoxifen (10(-7)M) influenced the secretion of either hormone and neither altered either cell number or DNA synthetic activity as measured by thymidine incorporation. The secretion of hormones and the growth of the pituitary cells were, however, decreased by charcoal treatment of the serum. The results suggest that the elevation of serum alpha-MSH and prolactin observed in DES implanted hamsters is due to pituitary secretion of the hormones but that DES probably does not act directly on the pituitary to control the secretion.
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PMID:Melanocyte-stimulating hormone and prolactin secretion in cell culture of estrogen-induced pituitary tumors in the hamster. 664 94

Genetically obese mice (C57BL/6J-ob/ob), fed ad libitum, demonstrated a precipitous increase in the spontaneous death rate after 50 weeks. The first signs of morbidity were a ruffled hair coat and a progressive motor ataxia. Necropsy revealed that obese mice had pale and fatty livers, urolithiasis and grossly distended bladders. Microscopically, the hepatocellular changes observed in all aged obese mice included: a loss of orientation of hepatocytes, an enormous variability in the size of both hepatocytes and their nuclei, and an extensive deposition of both large and small lipid droplets, confirmed by an increase content of triacylglycerols. A subacute-to-chronic, multifocal, necrotizing hepatitis was also present. Kidneys from aged obese mice contained hypertrophied glomeruli and increased PAS-stained material. Tubular dilation with compaction of the tubular cells was also seen. There were no significant alterations in the microanatomy or mineralization of femurs from obese mice, yet there was a significant increase in plasma alkaline phosphatase activity. In obese mice at 62-63 weeks of age, hyperglycemia was present even in spite of hyperinsulinemia. Pituitary immunoreactive ACTH and its molar ratio to pituitary immunoreactive beta-endorphin were also increased in obese mice at this age. Even though the etiology of the decreased lifespan of genetically obese mice remains uncertain, the possibility is discussed that an overall defect in the central nervous system may be involved.
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PMID:Hormonal, metabolic and morphologic studies of aged C57BL/6J obese mice. 673 67

Most neuropeptides can now be assayed in human cerebrospinal fluid (CSF). Some, such as beta-endorphin and arginine vasopressin, seem to be secreted directly into CSF. Others may reach CSF from plasma either by passage through the blood-brain barrier or by absorption through the circumventricular organs, which lack a blood-brain barrier. The role of neuropeptides in CSF is still unclear. Thyrotropin-releasing hormone, somatostatin, arginine vasopressin, angiotensin II, substance P, vasoactive intestinal polypeptide, beta-endorphin, gastrin, and cholecystokinin are all present in assayable quantities in human CSF. Their functions in this fluid are liable to be as diverse as their functions elsewhere in the body. The release of hypothalamic releasing factors into the CSF may be part of the pathway of pituitary hormone release. Pituitary hormones may function in CSF as part of a feedback loop from the hypothalamus. Other neuropeptides may affect receptors in the central nervous system far away from their release site. Intraventricular neuropeptide injection, anatomical and physiological ablation experiments, receptor studies, and neurobiological techniques now being developed will allow a more complete understanding of CSF neuropeptide function in the future.
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PMID:Neuropeptides in cerebrospinal fluid. 675 95

Pituitary and central beta-endorphin have been implicated in the regulation of food intake. It has been suggested that an elevation in hypophyseal beta-endorphin represents the genetic defect in the obese mutant Zucker rat. Both pituitary and central beta-endorphin systems appear to interact with dopamine. We have therefore examined hypophyseal, hypothalamic, and basal forebrain levels of beta-endorphin in the obese Zucker rat, its lean littermate, and lean littermates sustaining neurotoxic lesions of the A10 dopamine cell group in the ventral mesencephalon. The obese mutant exhibits elevated pituitary, but not central, beta-endorphin levels relative to lean littermates. A10 lesions result in a marked increase in both pituitary and hypothalamic beta-endorphin levels, and tend to decrease the amount of the peptide in the basal forebrain. These lesions do not result in either increased food intake or body weight. These data therefore suggest that elevated pituitary beta-endorphin levels do not mediate obesity in the Zucker rat, and also demonstrate that both central and pituitary beta-endorphin are modulated by a dopamine system originating in the ventral mesencephalon.
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PMID:Mesencephalic dopamine modulation of pituitary and central beta-endorphin: relation to food intake regulation. 686 61

Pituitary intermediate lobe melanocyte-stimulating hormone (MSH) is responsible for normal skin darkening in amphibians. Light-background adapted frogs (Rana pipiens) injected with naloxone and placed on black backgrounds maintain melanophore indices and pituitary cytology characteristic of light-background adaptation. In vitro and in vivo experiments showed that naloxone hydrochloride did not have a direct effect on skin melanophores or on the neurointermediate lobe. These data suggest that naloxone acts at the level of the central nervous system to inhibit the mechanism(s) responsible for release of MSH when light-background adapted frogs are placed on a dark background. Release of MSH, known to be tonically inhibited by the hypothalamus, may be modulated by opiate receptor-dependent mechanisms.
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PMID:Naloxone prevents dark-background adaptation in amphibians. 696 64

Immunoreactive alpha-MSH was measured in plasma, pituitary and brain of male and female rats on the day of birth and at intervals afterwards up to 55-70 days of age. Plasma alpha-MSH concentrations on the day of birth were 528 +/- 111 pg/ml and 406 +/-167 pg/ml in female and male rats, respectively. Plasma alpha MSH concentrations then fell and remained low until the onset of sexual maturity when they again rose reaching 406 +/- 38 pg/ml in 70 day old females and 312 +/- 46 pg/ml in 55 day old males. Pituitary alpha-MSH concentrations also changed with age and in male rats generally reflected the changes in plasma alpha-MSH concentrations. In females, on the other hand, pituitary alpha-MSH concentrations showed a gradual increase with age. Concentrations of alpha-MSH in the hypothalamus and brain increased with age and as with plasma and pituitary reached peak values in sexually mature animals. These findings are consistent with the idea that both pituitary and brain alpha-MSH have a role in sexually mature rats. Although alpha-MSH may have a role in sexual behaviour there was no evidence of any change in brain alpha-MSH throughout the estrous cycle.
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PMID:Changes in plasma, pituitary and brain alpha-MSH content in rats from birth to sexual maturity. 719 72

Pituitary opioid peptides levels, measured by guinea-pig ileum bioassay, have been evaluated in rats given single intracerebroventricular injections of alpha-methyl-p-tyrosine (4 mg/rat) or phentolamine (40 microgram/kg). Phentolamine produces an immediate rise in corticosteroid levels and an increase in pituitary endorphin content after 20 min. alpha-Methyl-p-tyrosine does not affect the pituitary endorphin levels, even if its effectiveness as a stressing agent is demonstrated by serum corticosterone increase and by reduced hypothalamic norepinephrine concentration. Repeated steroid treatment results in a decrease of serum corticosterone levels and of pituitary opioid activity. Such a decrease is mainly due to the reduction of beta-endorphin content, as shown by gel filtration analysis of pituitary extracts. It is suggested that the pituitary endorphin system, like ACTH, is under negative direct or indirect regulatory control of glucocorticoids. The adrenergic inhibitory tonus on pituitary opioid peptides, however, requires further confirmation.
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PMID:Role of adrenergic blocking agents and glucocorticoids on the regulation of pituitary opioid peptides levels. 722 9

Although plasma levels of Met-enkephalin and beta-endorphin are elevated in patients suffering from liver failure, it is not known whether central nervous system (CNS) opioidergic neurotransmission is altered in these patients. Such changes may contribute to the motor dysfunction, psychiatric abnormalities and CNS depression observed in hepatic encephalopathy (HE). Therefore, Met- and Leu-enkephalin, dynorphin A and beta-endorphin levels were measured in discrete brain regions and plasma from thioacetamide-treated rats in Stages II to IV of HE. Pituitary and plasma beta-endorphin, Met- and Leu-enkephalin concentrations increased with the severity of HE by 50 to 290%. Pituitary and brainstem dynorphin A levels increased whereas plasma levels decreased in rats with thioacetamide-induced fulminant hepatic failure. Both striatal Met- and Leu-enkephalin levels increased and hypothalamic concentrations decreased in HE. Concurrent with the increase in striatal Met-enkephalin levels was a 26 to 48% decrease in the density of striatal and hypothalamic delta receptors. No change in either the density or affinity of radioligand binding to mu or delta receptors was observed in the CNS. Finally, administering (+/-)-naloxone (5 and 10 mg/kg) or (+/-)-naltrexone (5-15 mg/kg), but not (+)-naloxone (10 mg/kg), significantly increased the motor activity of rats with Stage III HE. Whereas elevated plasma levels of opioid peptides may play a role in the peripheral manifestations of hepatic failure (ascites and hypotension), increased CNS levels of these peptides may be involved in the neuropsychiatric abnormalities characteristic of HE. Thus, opioid antagonists may be effective in ameliorating some of the neurological manifestations of HE.
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PMID:Brain and plasma levels of opioid peptides are altered in rats with thioacetamide-induced fulminant hepatic failure: implications for the treatment of hepatic encephalopathy with opioid antagonists. 771 65

Diagnostic advances have resulted in earlier and more frequent recognition of pituitary tumors. Pituitary tumors cause problems owing to the hormones they secrete or the effects of an expanding sellar mass--hypopituitarism, visual field abnormalities, and neurologic deficits. Prolactin-secreting tumors (prolactinomas), which cause amenorrhea, galactorrhea, and hypogonadism, constitute the most common type of primary pituitary tumors, followed by growth hormone-secreting tumors, which cause acromegaly, and corticotropin-secreting tumors, which cause Cushing's syndrome. Hypersecretion of thyroid-stimulating hormone, the gonadotrophins, or alpha-subunits is unusual. Nonfunctional tumors currently represent only 10% of all clinically diagnosed pituitary adenomas, and some of these are alpha-subunit-secreting adenomas. Insights into the pathogenesis and biologic behavior of these usually benign tumors have been gained from genetic studies. We review some of the recent advances and salient features of the diagnosis and management of pituitary tumors, including biochemical and radiologic diagnosis, transsphenoidal surgery, radiation therapy, and medical therapy. Each type of lesion requires a comprehensive but individualized treatment approach, and regardless of the mode of therapy, careful follow-up is essential.
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PMID:Pituitary tumors. Current concepts in diagnosis and management. 774

This study compared plasma concentrations of adrenocorticotropin (ACTH) and cortisol in young men (N = 10, mean age 24.4 years), young women (N = 10, mean age 25.4 years), old men (N = 8, mean age 81.6 years) and old women (N = 8, mean age 83.5 years) under basal resting conditions and after stimulation with either human corticotropin-releasing hormone (hCRH, 100 micrograms iv) or a combined injection of hCRH (100 micrograms) and arginine vasopressin (VP, 0.5 IU iv). Basal secretion of cortisol did not differ among groups, but basal concentrations of ACTH were diminished in young women (p < 0.01), indicating an enhanced adrenal sensitivity to ACTH in these subjects. Pituitary responses to hCRH did not differ between young men and women. However, responses to hCRH/VP were stronger in the young females (p < 0.01), suggesting an enhanced pituitary responsiveness to the augmenting effect of VP on ACTH release in this group. Pituitary-adrenal secretory responses were greater in old than in young men after sole injection of hCRH (p < 0.05) and even more so after combined injection of hCRH/VP (p < 0.01). In old women, pituitary-adrenal secretory responses were also greater than in young women (p < 0.05). But, in particular for responses to hCRH/VP, these effects were less distinct than within the men. Results indicate an enhancing effect of age on pituitary responsiveness to the hypothalamic secretagogues hCRH and VP, modulated by the subject's gender.
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PMID:Effects of age and gender on pituitary-adrenocortical responsiveness in humans. 778 10


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