beta-endorphin and Nelson-Syndrome

Topics: ACTH Syndrome, Ectopic; Anorexia Nervosa; beta-Endorphin; Biomarkers; Depression; Diagnostic Techniques, Endocrine; Humans; Hypopituitarism; Mass Spectrometry; Nelson Syndrome; Pituitary ACTH Hypersecretion; Radioimmunoassay; Radioligand Assay; Reference Values; Specimen Handling

The effect of LH-RH (25 micrograms as a single i.v. bolus) on plasma corticotropin (ACTH) levels and beta-endorphin-like immunoreactivity was studied at 30 and 60 min in eight women with Nelson's syndrome. Plasma ACTH concentrations increased in three of them, while beta-endorphin-like immunoreactivity, measured in six cases, rose significantly at 30 min in all the patients under investigation. In the control group containing seven women with Nelson's syndrome, placebo (0.9% sodium chloride) administration did not induce any significant changes in ACTH concentrations or in beta-endorphin-like immunoreactivity. Our results suggest that a paradoxical stimulatory influence of LH-RH on pituitary Nelson's adenomas may play an important role in the adenoma hormonal activity and, perhaps, growth. Such an effect could be responsible for a rapid development of some pituitary neoplasms during pregnancy.

Topics: Adenoma; Adrenalectomy; Adrenocorticotropic Hormone; Adult; Animals; beta-Endorphin; Endorphins; Female; Gonadotropin-Releasing Hormone; Humans; Middle Aged; Nelson Syndrome; Pituitary Neoplasms; Placebos; Rabbits; Radioimmunoassay

Topics: Adult; beta-Endorphin; Cognition; Cushing Syndrome; Emotions; Endorphins; Humans; Middle Aged; Naloxone; Nelson Syndrome; Nociceptors

We wished to discriminate between the opioid peptide beta-endorphin (beta-EP) and its non-opioid precursor beta-lipotrophin (beta-LPH) in normal subjects and patients with ACTH-related disorders.. We produced monoclonal antibodies to beta-EP and beta-LPH for the development of two-site immunoradiometric assays (IRMAs) which specifically quantitate beta-EP and beta-LPH.. Samples were obtained from patients with a range of ACTH-related disorders and compared with 18 normal subjects. Peptide levels were also compared in six patients with Cushing's syndrome undergoing bilateral inferior petrosal sinus sampling with corticotrophin releasing hormone administration.. In the beta-EP IRMA, antibody 6B2, specific for beta-EP 18-27, is radiolabelled and antibody 2E10, recognizing beta-EP 1-5, is coupled to Sephacryl S-300 as solid phase. The IRMA is specific for beta-EP (beta-LPH cross-reacts < 0.02%), has a detection limit of 1.4 +/- 0.7 pmol/l (n = 7) and has a within-assay coefficient of variation of < 10% between 4.9 and 1200 pmol/l. In the beta-LPH IRMA, antibody 6B2, which recognizes an epitope common to beta-LPH and beta-EP, is radiolabelled and paired with solid-phase antibody 5C11 which recognizes beta-LPH 39-56. The binding site of this antibody ensures that beta-EP cannot be measured in the beta-LPH assay. The detection limit is 0.8 +/- 0.1 pmol/l (n = 9) and the within-assay coefficient of variation is < 10% at concentrations 1.7-870 pmol/l.. In normal subjects, beta-EP and beta-LPH levels were < 1.4-1.7 pmol/l (< 5-6 ng/l) and 2.5-6.7 pmol/l (29-77 ng/l) at 0930 h and < 1.4-1.7 pmol/l (< 5-6 ng/l) and 1.9-4.5 pmol/l (22-49 ng/l) at 1600 h, respectively. In patients with ACTH-related pathologies concentrations of beta-EP and beta-LPH paralleled those of ACTH. The ratio of beta-LPH:beta-EP in plasma varied between 3.2:1 and 38:1 in these patients demonstrating that beta-LPH is the major circulating peptide derived from the C-terminal of pro-opiomelanocortin in man. However, in two patients undergoing bilateral inferior petrosal sampling with corticotrophin releasing hormone for diagnosis of Cushing's disease beta-EP concentrations increased rapidly during the first 5 minutes of the test, resulting in a sharp decrease in the beta-LPH: beta-EP ratio. These results suggest that beta-EP is preferentially released in response to acute corticotrophin releasing hormone stimulation.. It is concluded that two-site IRMAs for beta-EP and beta-LPH provide an easy approach to study the dynamic changes in processing of beta-LPH to beta-EP.

Topics: ACTH Syndrome, Ectopic; Addison Disease; Adolescent; Adrenocorticotropic Hormone; Adult; Animals; Antibodies, Monoclonal; beta-Endorphin; beta-Lipotropin; Cushing Syndrome; Drug Stability; Endocrine System Diseases; Female; Humans; Immunoradiometric Assay; Male; Middle Aged; Nelson Syndrome; Reference Values; Sensitivity and Specificity

Topics: Addison Disease; Adult; beta-Endorphin; Cushing Syndrome; Female; Humans; Hypopituitarism; Infant, Newborn; Male; Nelson Syndrome; Pituitary Function Tests; Pregnancy; Radioimmunoassay; Radioligand Assay; Reference Values

Topics: Adrenocorticotropic Hormone; Adult; beta-Endorphin; Female; Humans; Indomethacin; Male; Middle Aged; Nelson Syndrome; Pituitary Neoplasms; Radioimmunoassay

Topics: Adolescent; Adult; Anorexia Nervosa; beta-Endorphin; Cushing Syndrome; Endorphins; Humans; Middle Aged; Nelson Syndrome; Radioimmunoassay

Tissues from 12 human corticotropin-secreting adenomas, obtained during surgery for Cushing's disease (CD, ten cases) or Nelson's Syndrome (NS, two cases), were exclusively mechanically dispersed. Single cells and cell aggregates were plated on extracellular matrix derived from bovine corneal endothelia. Functional responses to physiological stimuli were analyzed by measuring human beta-endorphin (beta h-EP) immunoreactivity (IR) by radioimmunoassay in the culture medium. All adenomas responded with stimulated secretory activity to arginine vasopressin (AVP), corticotropin-releasing factor (CRF), or both. Cortisol higher than 10(-8) M suppressed basal secretion and CRF- or AVP-stimulated beta h-EP-IR secretion. There was no consistent difference in response of the cells when cultured in medium containing 10% fetal calf serum (FCS) or in serum-free conditions. A change of cells from serum to serum-free conditions usually resulted in 10%-50% reduction in the basal secretion level that remained stable for at least 2 weeks and, in one case (NS), 10 weeks. In cells maintained in medium supplemented with 5% serum obtained from the respective patients 40 min after adenoma removal, basal secretion was suppressed to 60% of the baseline level in a 10% FCS control. Long-term incubation with CRF (10(-9) M) showed sustained stimulation of hormone secretion. No remarkable cell proliferation was observed under basal conditions or during long-term, low-dose incubation with cholera toxin (10(-12) M) in two cases (CD), or CRF (10(-9) M) in two cases (NS, CD). Parallel beta-EP-IR and adrenocorticotropin secretion was verified in selected cases.

Topics: Adenoma; Adrenocorticotropic Hormone; Arginine Vasopressin; beta-Endorphin; Corticotropin-Releasing Hormone; Culture Techniques; Cushing Syndrome; Endorphins; Extracellular Matrix; Humans; Hydrocortisone; Nelson Syndrome; Pituitary Neoplasms

Pituitary carcinoma is defined as a malignant pituitary tumour associated with blood- or lymph-borne metastases. Cushing's disease is frequently present in patients with this condition. After adrenalectomy for Cushing's disease, a 37-year-old man developed Nelson's syndrome resulting from a pituitary carcinoma with metastases to the spinal cord, cauda equina, heart, liver, and pancreas. The primary tumour and its metastases showed immunocytochemical staining for ACTH, beta-lipotrophin, and variably for beta-endorphin and alpha-melanocyte stimulating hormone (alpha-MSH). A coincidental glioblastoma was also present. Nine cases of Cushing's disease associated with pituitary carcinoma, including the present patient, are documented in the literature. The case reported is only the second in which immunohistochemical staining of the primary pituitary tumour and its metastases was performed, and the first in which ACTH-related peptides, in addition to ACTH itself, were demonstrated in the carcinoma cells.

Topics: Adrenalectomy; Adrenocorticotropic Hormone; Adult; beta-Endorphin; beta-Lipotropin; Brain Neoplasms; Cushing Syndrome; Endorphins; Glioma; Humans; Male; Melanocyte-Stimulating Hormones; Nelson Syndrome; Neoplasms, Multiple Primary; Pituitary Neoplasms; Pro-Opiomelanocortin

Sixty-one pituitary corticotroph adenomas from 47 patients with Cushing's disease, 10 with Nelson's syndrome, and four eucorticoid patients were studied by light microscopy, immunoperoxidase, and electron microscopy. Seventy nine percent of all tumors and 70% of Nelson's cases were microadenomas, sometimes minute. A contiguity between the posterior lobe and the adenoma was seen in ten cases. Spontaneous infarction of the tumor with remission of Cushing's syndrome occurred in one case. Light microscopy revealed that the adenoma cells were basophilic and contained PAS-positive granules also staining with Herlant tetrachrome and lead-hematoxylin. The granules stained positively with antiserum to adrenocorticotrophic hormone (ACTH), beta-lipotropic hormones (beta-LPH) and beta-endorphin. The most characteristic ultrastructural finding was the presence of perinuclear bundles of microfilaments found in all our cases. Oncocytic changes were seen in three tumors. Four silent corticotroph adenomas, two of them originally microadenomas that had enlarged to enclosed adenomas while being treated with bromocriptine for hyperprolactinemia and one a large diffuse invasive tumor, did not differ in their microscopic, immunocytological, or ultrastructural features.

Topics: Adenoma, Basophil; Adolescent; Adrenocorticotropic Hormone; Adult; Aged; beta-Endorphin; beta-Lipotropin; Child; Cushing Syndrome; Endorphins; Female; Humans; Hydrocortisone; Male; Microscopy, Electron; Middle Aged; Nelson Syndrome; Pituitary Gland; Pituitary Neoplasms

Molecular forms of immunoreactive adrenocorticotropin (ACTH), beta-lipotropin (beta-LPH) (beta-endorphin (beta-END), human NH-2-terminal (hNT) of pro-opiomelanocortin (POMC), and gamma-3-melanotropin (gamma-3-MSCH) were studied in plasma, CSF and urine of a patient with Nelson's syndrome by molecular sieving and concanavalin A (Con A)-sepharose chromatography. In the culture tumor medium of the tumor cells, and in the plasma and CSF, these compounds were found mainly in forms corresponding in molecular weight to the authentic peptides, with the exception of gamma-3-MSH. Stimulation of the pituitary tumor by synthetic ovine corticotropin-releasing factor (CRF 1-41) caused a 171-468% increase in vivo (60 min) and 453-953% increase in vitro (3h incubation) in the levels of POMC derived peptides; it increased the relative amount of beta-END in vivo, and that of beta-LPH in vitro. Molecular sieving chromatography of urine samples revealed that beta-LPH and hNT are extensively degraded by the kidney. By contrast, ACTH showed no significant renal degradation before the removal of the pituitary adenoma. However, following pituitary surgery, only smaller fragments of immunoreactive (IR) ACTH were detected in the urine. These results suggest no major abnormal metabolic pathway for POMC in Nelson's syndrome, although the proportions of various peptides derived from the precursor could be different in vivo from those after in vitro incubation under basal conditions and during CRF stimulation. The results also indicate differences in the renal handling of ACTH in POMC hypersecretory states.

Topics: Adrenocorticotropic Hormone; beta-Endorphin; beta-Lipotropin; Body Fluids; Chromatography; Concanavalin A; Endorphins; Female; Humans; Middle Aged; Nelson Syndrome; Peptide Fragments; Peptides; Pituitary Neoplasms; Pro-Opiomelanocortin; Radioimmunoassay

In 14 cases of ACTH-producing pituitary adenomas (8 cases of Cushing's disease and 6 cases of Nelson's syndrome) dispersed cells prepared from adenoma tissue were incubated in a superfusion or static incubation system and investigated for ACTH, beta-endorphin (beta-EP) and beta-lipoprotein (beta-LPH) production. Effects of cortisol and lysine vasopressin (LVP) were evaluated. During the superfusion a qualitatively parallel secretory pattern is obtained for all hormones. Quantitatively, however, the response to LVP stimulation is more pronounced for beta-endorphin-like immunoreactivity (beta-LPH/beta-EP-IR) causing ACTH/beta-LPH/beta-EP-IR ratios to change throughout single experiments. beta-EP/beta-LPH ratios, however, which were estimated by means of Sephadex G-50 gel chromatography at various key points of the superfusion, were constant for each tumor, although variable between different adenomas, ranging from 0.68 to 2.0. The results suggest neither a differential control for the secretion of the peptides investigated within individual tumors nor a direct effect of cortisol or LVP on pro-opiomelanocortin processing. Summarizing clinical data and in vitro findings such as secretory behavior or hormone ratios, we can find no characteristic differences between Nelson's syndrome and Cushing's disease.

Topics: Adenoma; Adrenocorticotropic Hormone; beta-Endorphin; Cushing Syndrome; Endorphins; Humans; In Vitro Techniques; Lipoproteins, LDL; Lypressin; Nelson Syndrome; Pituitary Neoplasms; Pro-Opiomelanocortin

beta-Endorphin31, beta-endorphin1-27, and their alpha-N-acetyl derivatives were specifically separated by ion exchange chromatography from human beta-endorphin-'like' material obtained from extracts and culture media of corticotropic adenomas and extract of plasma from Nelson's syndrome and ectopic ACTH/LPH syndrome. Studies with pituitary-derived materials have shown that human beta-endorphin1-31 was the major form and human beta-endorphin1-27 a minor form. No other peptide was detected. In plasma from the ectopic ACTH-LPH syndrome human beta-endorphin1-31 was the only detected peptide. In 2 such patients with chronic elevation of human beta-endorphin1-31 the pain sensitivity threshold was normal and naloxone induced no modification, suggesting that circulatory human beta-endorphin has no effect on the central nervous system.

Topics: ACTH Syndrome, Ectopic; Adenoma; beta-Endorphin; beta-Lipotropin; Chemical Phenomena; Chemistry; Chromatography, Ion Exchange; Cushing Syndrome; Endorphins; Humans; Nelson Syndrome; Paraneoplastic Endocrine Syndromes; Pituitary Neoplasms

The effects of bromocriptine, a dopamine agonist, and cyproheptadine, a serotonin antagonist, on basal and corticotropin-releasing factor (CRF)-stimulated ACTH release were investigated in a 40-year-old female patient with Nelson's syndrome. Oral administration of either bromocriptine (2.5 mg) or cyproheptadine (8 mg) caused a marked drop in plasma ACTH levels. Intravenous administration of synthetic ovine (o) CRF (50 micrograms) produced an exaggerated response of plasma ACTH. Short-term (3-week) treatment with either bromocriptine (7.5 mg/day) or cyproheptadine (12 mg/day) resulted in a marked suppression of basal ACTH release. Furthermore, a blunted response of plasma ACTH to oCRF was observed after short-treatment with either drug. However, after a longer period of treatment with cyproheptadine (18-week), plasma ACTH levels rose again and hyperresponsiveness to oCRF was restored to the pretreatment levels. These data indicate that synthetic oCRF is a potent secretagogue for ACTH release in a patient with Nelson's syndrome. It is suggested that bromocriptine and cyproheptadine are effective drugs in reducing basal and CRF-stimulated ACTH release, possibly acting at the pituitary level in this case. However, the apparent refractoriness after chronic treatment with cyproheptadine may limit its therapeutic use in the present case.

Topics: Adrenocorticotropic Hormone; Adult; Basal Metabolism; beta-Endorphin; Bromocriptine; Corticotropin-Releasing Hormone; Cyproheptadine; Endorphins; Female; Gonadotropin-Releasing Hormone; Humans; Lypressin; Nelson Syndrome; Pituitary Neoplasms; Thyrotropin-Releasing Hormone

The effects of ovine CRF, lysine vasopressin (LVP), and their interrelationships, and rat hypothalamic extract (HME), on ACTH and beta-endorphin release by human pituitary tumor cells from two patients with Nelson's syndrome and one with Cushing's disease and on ACTH and cortisol secretion in vivo were studied. In cultured pituitary tumor cells, both LVP and CRF greatly stimulated ACTH and beta-endorphin release at maximally active concentrations of 0.1 microM and 10 nM, respectively. At these concentrations, the combination of the two substances had an additive or synergistic effect on hormone release. Low concentrations of HME potentiated and/or were synergistic with CRF-mediated ACTH release. In vivo, the combination of CRF (1 microgram/kg) and LVP (10 pressor units) induced greater ACTH release than the sum of the responses to CRF and LVP alone. This synergistic effect of CRF plus LVP concerned only ACTH release, while cortisol release after CRF plus LVP was equivalent to the sum of the maximal increments in this hormone after CRF and LVP alone. The peak levels of cortisol after a combination of CRF and LVP probably reflect the maximum stimulatory capacity of the adrenal cortex. These data support the concept that in man, both ovine CRF and vasopressin are corticotropin-releasing factors which act synergistically. Both substances might well regulate, at the pituitary level, the responsiveness of the pituitary-adrenal axis to stimuli reaching the hypothalamus. A test using ovine CRF and LVP together might provide a better index of total pituitary ACTH reserve than one using the two compounds separately.

Topics: Adrenocorticotropic Hormone; Animals; beta-Endorphin; Corticotropin-Releasing Hormone; Cushing Syndrome; Drug Synergism; Endorphins; Female; Humans; Hydrocortisone; Hypothalamus; In Vitro Techniques; Lypressin; Nelson Syndrome; Pituitary Gland; Pituitary Neoplasms; Rats; Sheep; Tissue Extracts

Dispersed corticotrophic cells of 3 patients with Nelson's syndrome were studied in tissue culture for up to 25 days. During this culture period a parallel decrease with time was seen in ACTH and beta-endorphin-like immunoreactivity ( LIR ) release. A concomitant decline was observed for intracellular hormones. The time course of hormone release showed a parallel secretion of ACTH and beta-endorphin- LIR up to 8 h. Both the release of ACTH and beta-endorphin LIR were stimulated by 0.1 microM lysine vasopressin (LVP) in all three adenoma cell cultures. Dexamethasone (0.1 and 1 microM) suppressed basal hormone secretion for 4 h. Synthetic ovine corticotrophin-releasing factor (CRF) at 10 and 100 nM stimulated the secretion of ACTH and beta-endorphin LIR maximally. This stimulation was higher than observed with maximal stimulative concentration of LVP (0.3 microM). The CRF-mediated hormone secretion was calcium-dependent. Dexamethasone (0.1 microM) blocked the stimulating effect of 10 nM CRF completely. Gel-filtration chromatography demonstrated the cells to secrete both beta-lipotrophin (beta-LPH) and beta-endorphin. The ratio of beta-LPH to beta-endorphin released remained constant upon stimulation by LVP and CRF. HPLC studies demonstrate the possibility that several beta-endorphin fragments, including alpha-endorphin and gamma-endorphin, were secreted by cells from a Nelson tumour. CRF caused a simultaneous parallel stimulation of the release of these peptides.

Topics: Adenoma; Adrenocorticotropic Hormone; beta-Endorphin; Cells, Cultured; Chromatography, Gel; Chromatography, High Pressure Liquid; Corticotropin-Releasing Hormone; Dexamethasone; Endorphins; Female; Humans; Lypressin; Nelson Syndrome; Pituitary Neoplasms; Time Factors

The response of pituitary adenomas obtained surgically from patients with Cushing's disease of Nelson's syndrome to synthetic ovine corticotropin-releasing factor (CRF), vasopressins, somatostatin-28, dexamethasone, 3-isobutylmethylxanthine or high [K+] was examined in vitro by measuring the amount of pro-opiomelanocortin (POMC)-derived peptides secreted into the culture medium. CRF did not stimulate the secretion of adrenocorticotropin-, beta-endorphin-, or gamma 3-melanotropin-like peptides from the pituitary adenomas at concentrations ranging from 1 x 10(-13) M to 1 x 10(-7) M whereas vasopressins, 3-isobutyrl-methylxanthine and high [K+] increased, while somatostatin-28 and dexamethasone suppressed, the secretion of these POMC-derived peptides. These findings suggest that either the pituitary ACTH-producing tumors have lost their receptors to CRF or their post-receptor mechanism to CRF is not functional.

Topics: Adenoma; Adolescent; Adrenocorticotropic Hormone; Adult; beta-Endorphin; Cells, Cultured; Corticotropin-Releasing Hormone; Cushing Syndrome; Dexamethasone; Endorphins; Female; Humans; Male; Melanocyte-Stimulating Hormones; Nelson Syndrome; Pituitary Neoplasms; Somatostatin; Somatostatin-28; Vasopressins

This is a report of the development, calibration, and validation of a series of techniques required to measure beta-endorphin (beta-END)-like immunoreactivity in human plasma, including sieve and affinity chromatography. The RIA, which uses the antibody Brenda, is very sensitive (IC50 = 5-15 fmol/tube at a final concentration of 1:40,000). The extraction process, which uses the Sep-Pak C18 cartridge (Waters Associates, Inc.), is simple and rapid and has a recovery rate of more than 90%. It extracts proopiomelanocortin, beta-lipotropin, and beta-END. Physiological validation was provided by the measurement of beta-END-like immunoreactivity in a pool of plasma of normal humans (2.25 fmol/ml plasma), two pregnant women at term (9.5 and 10.75 fmol/ml), and one patient with Nelson's disease (2 pmol/ml plasma).

Topics: Animals; Antibody Specificity; beta-Endorphin; beta-Lipotropin; Chromatography, Affinity; Chromatography, Gel; Chromatography, High Pressure Liquid; Endorphins; Female; Humans; Male; Nelson Syndrome; Pituitary Gland; Pituitary Hormones, Anterior; Pregnancy; Pro-Opiomelanocortin; Protein Precursors; Radioimmunoassay; Rats; Specimen Handling

To clarify whether various neuropeptides found in the hypothalamus act directly on a pituitary adenoma causing Nelson's syndrome, we examined the influence of these peptides on the secretion of immunoreactive ACTH, beta-endorphin, and melanotropins, the proopiomelanocortin (POMC)-derived peptides, by the cultured pituitary adenoma from a patient with Nelson's syndrome. Results showed that somatostatin-14 and somatostatin-28 suppressed the secretion of POMC-derived peptides by the adenoma and that somatostatin-28 was as potent as somatostatin-14. Other neuropeptides such as arginine vasopressin, vasoactive intestinal polypeptide, and oxytocin stimulate the secretion of POMC-derived peptides. Substance P, TRF, Met-enkephalin and Leu-enkephalin were also found to modulate the secretion of POMC-derived peptides. This suggests that the adenoma may have multiple receptors to various neuropeptides.

Topics: Adenoma; Adrenocorticotropic Hormone; Arginine Vasopressin; beta-Endorphin; beta-Lipotropin; Culture Techniques; Endorphins; Humans; Melanocyte-Stimulating Hormones; Nelson Syndrome; Peptides; Pituitary Neoplasms; Somatostatin

Human ACTH-producing tumor and plasma have been examined by gel filtration and ion exchange chromatography to detect the possible presence of reported multiple forms of immunoreactive beta-endorphin (I-EP) Ion exchange chromatography of I-EP obtained from gel filtration showed four components of I-EP [two major peaks in the positions of EP-(1-31) and EP-(1-27) and two minor peaks in the positions of N-acetyl EP-(1-31) and N-acetyl EP-(1-27)] in two ectopic ACTH-producing lung cancers, and two components of I-EP [the major peak in the position of EP-(1-31) and minor peak in the position of N-acetyl EP-(1-31) in an ectopic ACTH-producing thyroid cancer. Only a single peak in the position of EP-(1-31) was present in plasma from a patient with Nelson's sindrome and a patient with Addison's disease, in the pituitary adenomas from six patients with Cushing's disease, and in the nontumorous pituitary tissues from a patient with Cushing's disease and a patient with acromegaly. These data suggest that the posttranslational processing of EP in human pituitary is different from that in the ectopic ACTH-producing tumor.

Topics: Addison Disease; Adenoma; Adrenocorticotropic Hormone; beta-Endorphin; Chromatography, Gel; Chromatography, Ion Exchange; Cushing Syndrome; Endorphins; Humans; Lung Neoplasms; Nelson Syndrome; Pituitary Gland; Pituitary Neoplasms; Radioimmunoassay; Thyroid Neoplasms

Using a sensitive and precise radioimmunoassay for human beta-endorphin, we have demonstrated the sustained secretion of opioid peptides from human pituitary tumour cells. Pituitary tumour tissue obtained from a patient with Nelson's syndrome was maintained in continuous monolayer culture and secreted both beta-lipotropin and beta-endorphin, with predominance of the latter. This is compatible with the idea that the beta-endorphin in normal human serum is secreted as such despite the predominance of beta-lipotropin compared with beta-endorphin in the anterior pituitary.

Topics: beta-Endorphin; beta-Lipotropin; Cells, Cultured; Chromatography, Gel; Endorphins; Humans; Male; Nelson Syndrome; Pituitary Gland, Anterior; Pituitary Neoplasms; Radioimmunoassay; Time Factors

Topics: Adrenocorticotropic Hormone; Adult; beta-Endorphin; Endorphins; Female; Humans; Nelson Syndrome; Pituitary Neoplasms