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)

It was admitted that human beta-MSH was responsible for the hyper-pigmentation observed in some syndromes associated with ACTH hypersecretion. beta-LPH was a pituitary polypeptide, containing the entire sequence of beta-MSH in its fragment 37-58, and the physiological role of which remained unknown. alpha-MSH and CLIP (Corticotrophin-like Intermediary Peptide) were thought to be specific of certain species possessing a distinct pituitary pars intermedia. Recent data give new insight upon some of these conceptions. beta-MSH seems not to exist in man; it is almost established now that plasma "Immunoreactive beta-MSH" (IR-beta-MSH) is in fact beta- and/or gamma-LPH. In chronic renal failure plasma IR-beta-MSH is elevated because of a decreased plasma disappearance rate, whereas ACTH is normal. Good evidence suggests that both LPH and ACTH are synthesized in the same pituitary cell within a common polypeptidic precursor. Endogenous peptides with morphinomimetic activity (Endorphins) have been isolated from brain and hypophysis; they are all made up of different fractions of beta-LPH-C-terminal fragment 61-91; It is likely that they represent a new class of brain neurotransmitters involved in some functions of the central nervous system, structural similarities suggest that beta-LPH may be the biosynthetic precursor of Endorphins, however such a hypothesis remains to be clearly demonstrated.
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PMID:[Recent data on the group of melanotropic and lipotropic pituitary hormones (MSH-LPH) and on the brain morphinomimetic peptides (endorphins)]. 21 12

An analysis of the factors that influence the increase in plasma immunoreactive beta-melanocyte-stimulating hormone (beta-MSH) concentration in chronic renal failure showed that: (a) the increase correlated with the increase in serum creatinine concentrations; (b) beta-MSH was not cleared from the plasma by haemodialysis; (c) beta-MSH concentrations increased with length of time on dialysis and increased further after bilateral nephrectomy but there was no further increase with time; (d) beta-MSH levels decreased to normal after renal transplantation; and (e) beta-MSH was excreted in urine only when plasma levels rose to well above those of chronic renal failure (in Nelson's syndrome). These findings suggest that the kidney regulated plasma beta-MSH by a non-excretory mechanism and is the major site of beta-MSH metabolism.
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PMID:Role of the kidney in regulating plasma immunoreactive beta-melanocyte-stimulating hormone. 76 7

beta-endorphin (BE) and other opioid peptides participate significantly in the development of the uremic syndrome. In patients with chronic renal failure (CRF) an elevated serum BE level and lack of a twenty-four-hour BE-secretory pattern were found. In 14 patients with CRF on conservative treatment with serum creatinine above 500 mumol/l and in 14 healthy subjects serum BE was evaluated after intravenous insulin injection. An adequate hypoglycemia was obtained in every subject. Basel serum BE concentration was significantly higher in patients with CRF than in healthy subjects and correlation positively with creatinine. After 60 min. from insulin injection in both groups the peak BE level was observed here after 120 min. it returned to the initial values. The curve of BE concentration in patients with CRF ran significantly higher than in healthy subjects. A total secretory answer of the pituitary measured by the area over basel value of BE was similar in both groups. It seems that BE secretion by the corticotropic cells of the pituitary is unchanged in patients with CRF. Impaired BE elimination by the kidneys is probably responsible for hyper-beta-endorphin levels in those patients.
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PMID:[Levels of beta-endorphin in serum of patients with chronic renal failure on conservative treatment during insulin-induced hypoglycemia stimulation testing]. 130 70

The fasting plasma levels of 10 vasoactive regulatory peptides were measured by radioimmunoassay in 23 stable patients with chronic renal failure receiving regular hemodialysis treatment (RDT) and compared with those of healthy controls. The plasma concentrations of arginine vasopressin, atrial natriuretic peptide, beta-endorphin, methionine-enkephalin, motilin, neuropeptide Y, substance P, and vasoactive intestinal peptide were increased. The plasma level of calcitonin gene-related peptide was not statistically different from that of the controls. The plasma concentration of gamma 2-melanocyte-stimulating hormone was lowered in the RDT-patients. The arterial blood pressure correlated with the plasma levels of motilin and neuropeptide Y. We conclude that patients with chronic renal failure receiving RDT have increased concentrations of 8 out of 10 measured vasoactive regulatory peptides. The elevated levels of vasoactive peptides may contribute to the adaptation of the cardiovascular system to impaired renal function.
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PMID:Plasma levels of vasoactive regulatory peptides in patients receiving regular hemodialysis treatment. 137 31

In 7 patients with end stage renal failure, anterior pituitary function was tested by simultaneous application of maximally effective doses of the hypothalamic releasing peptides, corticotropin-releasing hormone, growth hormone-releasing hormone, thyrotropin-releasing hormone and gonadotropin-releasing hormone, and compared to 8 normal controls. In addition to the pituitary hormones, plasma cortisol, thyroxine and testosterone concentrations were measured. To test for possible effects of treatment with recombinant human erythropoietin (rhu-EPO), all patients with chronic renal failure were studied again after partial correction of anemia by treatment with erythropoietin. Before initiation of rhu-EPO treatment, plasma concentrations of follicle-stimulating hormone were significantly elevated and the thyroid-stimulating hormone and prolactin responses to thyrotropin-releasing hormone blunted when compared to normal controls. Treatment with rhu-EPO induced a significant increase in plasma ACTH and follicle-stimulating hormone concentrations. All other pituitary functions remained unchanged. Thus, the general improvement in well-being, working capacity and sexual activity cannot be attributed to hormonal changes.
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PMID:Effect of recombinant human erythropoietin on anterior pituitary function in patients on chronic hemodialysis. 166 42

The fasting plasma levels of corticotropin-releasing hormone (CRH), delta sleep-inducing peptide (DSIP), beta-endorphin (beta-END), methionine-enkephalin (m-ENK), beta-lipotropin (beta-LPH), and alpha-melanocyte-stimulating hormone (alpha-MSH) were measured by radioimmunoassay in 22 stable patients with chronic renal failure on regular hemodialysis treatment and compared with those of 10 healthy controls. The plasma concentrations of DSIP, beta-END, m-ENK, beta-LPH, and alpha-MSH were increased. The plasma level of CRH was not different from that of the controls. The elevated plasma levels of endogenous opioid peptides and DSIP may contribute to the uremic syndrome, although this must be further elucidated.
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PMID:Elevated plasma levels of opioid peptides and delta sleep-inducing peptide but not of corticotropin-releasing hormone in patients receiving chronic hemodialysis. 166 74

We investigated the effect of exogenous ovine corticotropin-releasing hormone (oCRH) on plasma levels of adrenocorticotropic hormone (ACTH) and cortisol in 24 chronic renal failure patients: 8 nondialysis (NDCRF), 8 on hemodialysis (HD), and 8 on continuous ambulatory peritoneal dialysis (CAPD). In all groups the acute administration of oCRH caused a further increase (less pronounced in NDCRF patients) in the already elevated levels of cortisol. Following oCRH administration, plasma ACTH rose significantly in CAPD patients, but there was a blunted response of the hormone in the NDCRF and HD groups. The patterns of the ACTH and cortisol response in the last two groups, resemble those observed in chronic stress. We conclude that the hypothalamic-pituitary-adrenal axis in chronic uremic patients, retains the ability to respond to exogenous oCRH. Patients on CAPD, however, display a better, identical to normal response, which can be due to less chronic stress and/or to the more effective clearance of uremic toxins.
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PMID:Pituitary adrenal responsiveness to corticotropin-releasing hormone in chronic uremic patients. 196 5

To investigate possible abnormalities of the hypothalamic-pituitary axis in patients with chronic renal failure on dialysis, we have examined the effects of insulin-induced hypoglycemia on the adrenal steroid responses. In normal subjects, plasma aldosterone and cortisol concentrations increase significantly in response to hypoglycemia, with good correlation. In the patients with end-stage renal disease (ESRD) however, insulin-induced hypoglycemia fails to elicit significant increases in the plasma cortisol and aldosterone levels. To test the adrenal responsiveness to adrenocorticotropin (ACTH), we administered ACTH to both groups. Plasma cortisol and aldosterone responses are similar in both groups suggesting that the adrenal responsiveness to ACTH is not impaired. We also investigated the responsiveness of the renin-angiotensin-aldosterone system in response to volume contraction by hemofiltration in patients with ESRD. Neither plasma renin activity nor plasma aldosterone concentration change significantly following such contrived volume contraction. These results reveal several endocrinologic abnormalities in the patients with ESRD on chronic hemodialysis.
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PMID:Aldosterone response to insulin-induced hypoglycemia in hemodialysis patients. 254 16

The recently described human corticotropin-releasing factor was administered to eight patients with chronic renal failure in order to assess hypothalamic-pituitary-adrenocortical (HPA) function. Acute administration of corticotropin-releasing factor lead to a diminished increase of the basally elevated levels of ACTH and beta-endorphin immunoreactivity in patients on chronic hemodialysis. Basal plasma cortisol concentration was normal in end-stage renal disease; however, considering the corresponding elevated ACTH concentrations, cortisol levels were inadequately low. Thus, the hypothalamus as well as the adrenal gland seems to contribute to the alterations in HPA function observed in patients with chronic renal failure; involvement of the pituitary gland and effects of metabolic alterations cannot be ruled out.
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PMID:Abnormalities in the hypothalamic-pituitary-adrenocortical axis in patients with chronic renal failure. 302 34

In 72 patients with end-stage renal failure and 70 healthy subjects, the influence of blockade of opioid receptors by naloxone on secretion of prolactin, lutropin (LH), follitropin (FSH), adrenocorticotropin (ACTH), somatotropin (HGH), insulin (IRI), glucagon (IR-G), parathyroid hormone (PTH) and calcitonin (CT) was studied. Administration of naloxone stimulated luliberin-induced LH and FSH secretion quantitatively equally in patients and controls. Blockade of opioid receptors was followed by a less marked suppression of chlorpromazine-induced prolactin secretion but by a higher response of hypoglycemia-induced ACTH secretion in uremic patients than in controls. In addition, a less marked suppressive effect of naloxone was noted on hypoglycemia-induced HGH secretion in chronic renal failure as compared with controls. Blockade of opioid receptors improved significantly glucose tolerance and glucose-induced insulin secretion in uremic patients and suppressed nearly completely glucagon secretion response during the second phase of a glucose tolerance test. Finally, administration of naloxone was followed by a blunted response of Ca-induced CT secretion and suppression of PTH. Data presented in this paper suggest the existence of hyperendorphinism in end-stage renal failure.
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PMID:Effects of naloxone administration on endocrine abnormalities in chronic renal failure. 303 7


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