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)

Two patients with AIDS are described who developed acral hyperpigmented macules of the fingers, palms and soles, buccal mucosa and genitalia, associated with longitudinal melanonychia. These pigmentary changes seemed to be independent of zidovudine and were associated in one with diffuse melanoderma and elevated levels of alpha-MSH. Histological and ultrastructural studies showed an increase of the dendrites and pigmentation of the melanocytes and few melanosomes in the keratinocytes.
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PMID:Acral hyperpigmented macules and longitudinal melanonychia in AIDS patients. 131 50

Intracerebroventricular (i.c.v.) infusion of glycosylated recombinant gp120, the envelope protein of human immunodeficiency virus, in various doses (100 ng to 4 micrograms) resulted in detection of interleukin 1 (IL-1) activity in a high percentage (61%; 33 of 54) of rat brains, whereas IL-1 was very rarely detected in brains of animals infused with several control substances (4%; 1 of 28). To detect IL-1, clarified glial lysate of diencephalon plus brainstem was subjected to gel exclusion chromatography and fractions were assessed for thymocyte stimulation. IL-1 was seen 2, 6, and 24 hr postinfusion. i.c.v. gp120 also produced known effects of IL-1 in brain, elevating steroid concentration in plasma and decreasing cellular immune responses [natural killer (NK) cell activity and mitogenic response to Con A] of blood and splenic lymphocytes. When gp120 was infused together with alpha-melanocyte-stimulating hormone (20 ng), which blocks many biological actions of IL-1, gp120 no longer elevated steroids or decreased NK cell activity. After intravenous gp120, IL-1 was not found in brain or plasma, indicating that stimulation of IL-1 in brain by i.c.v. gp120 was not due to gp120 affecting infiltrating cells from blood or to elevated circulating IL-1. That induction of IL-1 in brain might have resulted from lipopolysaccharide (LPS) in the gp120 solution was ruled out by studies showing that (i) heating of the infusion solution, which does not affect the capacity of LPS to induce IL-1, eliminated the ability of gp120 infusion to induce brain IL-1, and (ii) gp120 induced IL-1 in brains of LPS-resistant C3H/HeJ mice. Injection of gp120 directly into the hippocampus stimulated IL-1 more readily than i.c.v. infusion. Thymocyte stimulation produced by active fractions of gp120-infused brains was blocked by monoclonal antibody to IL-1 receptors. These findings indicate that elevation of IL-1 in brain can result from infection with human immunodeficiency virus and may be responsible for certain abnormalities (e.g., elevated activity of pituitary-adrenal axis) seen in AIDS patients.
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PMID:Human immunodeficiency virus glycoprotein (gp120) infused into rat brain induces interleukin 1 to elevate pituitary-adrenal activity and decrease peripheral cellular immune responses. 166 89

Seven young cats were injected with feline leukemia virus (FeLV); six of them became viremic. All of the viremic cats developed AIDS-related symptoms, i.e. lymphopenia, neutropenia, thymic atrophy, and wasting syndrome, along with an altered pituitary and adrenocortical function. These symptoms closely resemble human AIDS induced by HIV. It was discovered that, after 2 weeks of infection, the average amount of plasma adrenocorticotropic hormone (ACTH) detected in the infected cats was reduced by 29% in comparison with that before the infection. In contrast to the second week, the fifth week of infection showed a 94% increase of plasma ACTH which then dropped back down to 38% after the sixth and seventh weeks. This opposing biphasic pattern of change was also observed in the plasma cortisol content of the infected cats. The amount of change in plasma cortisol did not correlate with the detected increase in plasma ACTH, indicating a weak adrenal response to pituitary action.
AIDS 1990 Dec
PMID:Induction of feline immunodeficiency syndrome by feline leukemia virus: pituitary and adrenocortical dysfunctions. 196 24

Three groups of male homosexuals: AIDS (n = 19), HIV seropositive (n = 15), and seronegative partners of seropositive subjects (n = 15), were compared to a heterosexual seronegative control group (n = 13). Twice daily evaluations (8 A.M. and 5 P.M.) of plasma levels of beta-endorphin, ACTH, and cortisol were done by radioimmunoassay. Seropositive subjects and their seronegative partners showed similar levels of neurohormones: 1. An elevation in the ACTH/beta-endorphin ratio in the plasma, (C = 0.69 +/- 0.84, AIDS = 0.44 +/- 0.32, S+ = 0.42 +/- 0.28, and S- = 0.42 +/- 0.5); 2. A loss of normal relationship of the coupling ACTH/total cortisol, (C = 0.00035 +/- 0.00028, AIDS = 0.00042 +/- 0.0034, S+ = 0.00074 +/- 0.00068, and S- = 0.00072 +/- 0.0008. Neuroendocrinological disorders have been observed in HIV-infected subjects and in their seronegative partners. These could be related to their sexual behavior, as well as to the HIV infection. If this last hypothesis is confirmed, the ACTH/beta-endorphin and ACTH/cortisol ratios may be seen as possible early signs of HIV infection.
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PMID:ACTH/beta-endorphins and ACTH/cortisol ratios as early biological markers in HIV infection. 196 59

Suramin is a polyanionic compound which has been used in the treatment of trypanosomiasis and acquired immunodeficiency syndrome (AIDS), while preliminary success has been reported in the treatment of cancer. However, suramin also causes adrenal insufficiency. We have previously reported that suramin selectively inhibited corticotropin (ACTH)-stimulated corticosterone release by dispersed adrenal cells in a dose-dependent manner via a direct interaction with the ACTH molecule. The present study was undertaken in order to investigate the effect of suramin on hormone release by dispersed rat anterior pituitary cells. Suramin at a concentration of 100 microM inhibited both basal and secretagogue-stimulated ACTH release by cells cultured in minimal essential medium (MEM) only, while it had no effect on ACTH release by cells cultured in MEM + 10% fetal calf serum (FCS) or MEM + 0.1% bovine serum albumin (BSA). In addition, suramin also caused a parallel decrease of prolactin (PRL) and growth hormone (GH) release by cells cultured in MEM only, suggesting a toxic, rather than a selective effect of suramin on anterior pituitary cells cultured in MEM only. In addition, suramin potentiated the effect of thyrotropin-releasing hormone (TRH) on PRL release by cells cultured in MEM + 10% FCS and suppressed the inhibitory effect of dopamine (DA) on PRL release by cells cultured in MEM + 10% FCS and in MEM + 0.1% BSA. Comparable suppressive effects of suramin on growth hormone-releasing hormone (GHRH)-stimulated and somatostatin (SRIH)-inhibited GH release were found in cells cultured in MEM + 0.1% BSA but not in cells cultured in MEM + 10% FCS.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of suramin on hormone release by cultured rat anterior pituitary cells. 198 Aug 98

Alterations in the circadian time structure of the secretion of several hormones were investigated in 13 male patients infected with human immunodeficiency virus (HIV). Seven were asymptomatic (classified CDC II, according to the criteria of the Atlanta Centers for Disease Control), and 6 had acquired immunodeficiency syndrome (CDC IV). Ten healthy males volunteered as controls. Plasma levels of dehydroepiandrosterone (DHEA) and its sulfate (DHEA-S), cortisol, testosterone, ACTH, and beta-endorphin were determined by RIA in blood samples obtained every 4 h from 0830-0830 h the next morning. Data were analyzed both by two-way analysis of variance and the cosinor method. Circadian rhythms were statistically validated for each of the six hormones in each of the three groups of subjects. Compared with the control subjects, mesors (24-h adjusted means) were significantly higher for cortisol and lower for DHEA, DHEA-S, and ACTH (P less than 0.001 for all four hormones) in all HIV-infected patients. Plasma testosterone mesors were similar in controls and CDC II patients, but decreased significantly in the CDC IV patient group (P less than 0.05). Analysis of the circadian rhythms of plasma hormone levels clearly indicated an altered adrenal hormonal state in HIV-infected male patients, even during the asymptomatic period of the infection. For instance, plasma cortisol at 0430 h was more than twice as high in HIV-infected patients as it was in time-qualified controls. Although patients already had elevated plasma cortisol and lowered adrenal androgen levels at this stage, hypogonadism was not observed, as gauged by plasma testosterone concentrations. We speculate that the primary hormonal defect in HIV-infected patients is increased cortisol secretion resulting from circadian-varying stimulation of the adrenal cortex by a factor other than pituitary ACTH. This factor might be a stimulating substance secreted primarily by infected immune cells. Excess cortisol would lower adrenal androgen secretion by shifting adrenal steroid biosynthesis toward glucocorticoids and decreasing pituitary ACTH secretion via a negative feedback mechanism.
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PMID:Circadian variations in plasma levels of hypophyseal, adrenocortical and testicular hormones in men infected with human immunodeficiency virus. 230 20

In a review of 74 autopsy cases of acquired immune deficiency syndrome (AIDS), the incidence of cytomegalovirus (CMV) infection was found in 50% (37 cases). Of these 37 cases the adrenal glands were affected by CMV in 84%. The authors analyzed the histologic features of 30 of these 37 cases of CMV adrenalitis by grading the CMV inclusions, inflammation and necrosis (CMV score), focal versus diffuse involvement, and the degree of fibrosis (fibrosis score). The clinical data were not significant except for sodium to potassium ratio (Na:K), which was less than 30 in 11 cases. Focal CMV adrenalitis had low CMV and fibrosis scores and Na:K ratio higher than 30, whereas diffuse adrenalitis had high CMV and fibrosis scores and Na:K ratio less than 30. Adrenocorticotropic hormone (ACTH) stimulation tests performed in three patients revealed normal or elevated baseline cortisol levels with a blunted response after stimulation. The authors conclude that the adrenal gland is the most frequently affected organ in AIDS with CMV infection. ACTH tests on a larger number of selected cases of AIDS are needed for further evaluation of functional status of adrenal glands. Selection criteria for the test should include evidence of CMV infection from any site and a low Na:K ratio.
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PMID:Cytomegaloviral adrenalitis and adrenal insufficiency in AIDS. 216 75

The finding of endocrine gland lesions at pathological examination in AIDS and reports of several cases of endocrine disease in patients with this syndrome have prompted us to study endocrine functions in 63 patients (51 men, 12 women) with HIV-1 infection. According to the Center for Disease Control (CDC) classification system, 13 of these patients were stage CDC II, 27 stage CDC III and 23 stage CDC IV. We explored the adrenocortical function (ACTH, immediate tetracosactrin test) and the thyroid function (free T3 and T4 levels, TRH on TSH test) in all 63 patients. The hypothalamic-pituitary-gonadal axis (testosterone levels, LHRH test) and prolactin secretion (THR test) were explored in the 51 men. The results obtained showed early peripheral testicular insufficiency at stage CDC II and early pituitary gland abnormalities with hypersecretion of ACTH and prolactin also at stage CDC II. On the other hand, adrenocortical and pituitary abnormalities were not frequently found. The physiopathology of the endocrine abnormalities observed in HIV-1-infected patients remains unclear, but one may suspect that it involves interleukin-1 since this protein factor has recently been shown to stimulate the corticotropin-releasing hormone secretion and to act directly on the glycoprotein capsule of the virus (gp 120) whose structure is similar to that of some neurohormones.
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PMID:[Endocrine abnormalities in HIV infections]. 216 75

To assess whether neuroendocrine dysfunction is present in children with acquired immunodeficiency syndrome (AIDS) and growth failure, we evaluated the thyroid, adrenal, and growth hormone-insulin-like growth factor I (IGF-1) axes in nine children with AIDS and failure to thrive. Basal thyroid-stimulating hormone, free thyroxine, and triiodothyronine levels were normal in eight of the nine children and indicated primary hypothyroidism in one child; thyroxine levels were elevated in four and normal in five children. Thyroxine-binding globulin levels were elevated in all children. Serial measurements of thyroid-stimulating hormone, made hourly from 2 to 6 pm and from 10 pm to 2 am, revealed a flat diurnal rhythm of thyroid-stimulating hormone in six children, which may indicate early central hypothyroidism, and a normal nocturnal rise in the remaining three children. Basal plasma corticotropin and aldosterone levels were normal in all children, plasma renin levels were normal in three and elevated in six children, and cortisol levels were normal or elevated in all children. Corticotropin-stimulated cortisol levels exceeded 500 nmol/L (18 micrograms/dl) in all children except one, who was receiving treatment with ketoconazole. Thus adrenocortical function appeared to be grossly intact. The peak growth hormone responses to provocative testing was normal (greater than 7 ng/ml) in eight children and low in one child. The plasma level of insulin-like growth factor I was normal in eight of the nine children and low in one child. We conclude that growth failure in children with AIDS does not usually result from a recognized endocrine cause and that adrenal function is usually normal. However, endocrine deficiency may contribute to morbidity in some children with AIDS.
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PMID:Growth and neuroendocrine dysfunction in children with acquired immunodeficiency syndrome. 201 47

The studies have clearly demonstrated that binding sites for opioid peptides, beta-endorphin, and methionine-enkephalin exist on T lymphocytes. beta-Endorphin appears to be immunodepressant, whereas methionine-enkephalin is immunostimulant. Both in vitro and in vivo studies have shown that methionine-enkephalin can influence some immune functions. Since in vitro modification of immune function requires very low concentrations, it is reasonable to believe that methionine-enkephalin plays a physiological role in the immune system. Although not well established, methionine-enkephalin appears to activate T lymphocytes via opioid receptors and triggers a series of intracellular signals leading to the activation of receptors for interleukin-2 (IL-2), OKT10, and active sheep T red blood cell receptors. Methionine-enkephalin enhances the activity of NK cells and induces the production of IL-2, which in turn may recruit and activate other T-cell subsets like CD3 and CD4. Methionine-enkephalin also enhances mitogen-induced proliferation of lymphocytes. Since preliminary studies with methionine-enkephalin in ARC patients have provided beneficial effects by the improvements in their symptoms, it will be worthwhile to extend these observations to a larger number of patients with ARC and AIDS. Finally, it appears that some endogenous opioid peptides and their analogs, in addition to methionine-enkephalin, may provide therapeutic benefits not only in ARC and AIDS but also in other immunodeficient states.
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PMID:Opioid peptides, receptors, and immune function. 217 24


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