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)

In a double-blind placebo-controlled crossover study of ten patients with multiple sclerosis, we found amantadine hydrochloride therapy to be effective in improving fatigability in six. Administration of the drug was associated with significantly higher levels of beta-endorphin-beta-lipotropin and responders had significantly higher levels than nonresponders. Lactate levels were significantly higher and pyruvate levels lower in nonresponders. Amantadine given for fatigue to patients with multiple sclerosis is associated with measurable changes in levels of metabolites and peptides in the circulation.
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PMID:Amantadine, fatigue, and multiple sclerosis. 297 70

A patient with ectopic adrenocorticotrophic hormone (ACTH) production from a neuroendocrine tumour of the nasal roof is presented. By indirect immunoperoxidase techniques the tumour cells were shown to be distinctly positive for ACTH and beta-endorphin but negative for other peptides derived from pro-opiomelanocortin. Neither corticotropin releasing hormone (CRF) found in some tumours associated with ectopic Cushing's syndrome, nor gastrin immunoreactivity, which coexists with ACTH in normal rat pituitary and in rat and human gastrointestinal cells, were demonstrable in the tumour. A review of other, previously recognized locations of CRF/ACTH producing tumours is given to increase the awareness of the ectopic Cushing's syndrome, which may lack the classical features and is characterized by fulminant clinical course, extreme fatigue, weakness, pale facial swelling, oedema and hypokalaemic alkalosis.
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PMID:Cushing's syndrome due to an ACTH-producing neuroendocrine tumour in the nasal roof. 298 19

Serum beta-endorphin levels during a graded exercise test to exhaustion. Med. Sci. Sports Exerc., Vol. 19, No. 2, pp. 78-82, 1987. Nine untrained college age males completed a graded exercise protocol to maximal capacity on a bicycle ergometer to determine if there was a relationship between intensity of exercise and serum beta-endorphin (beta-EP) levels. Subjects fasted for 12 h and abstained from physical activity at least 24 h prior to testing. Subjects completed the Multiple Affect Adjective Check List prior to and following exercise to ascertain if psychological state would be associated with beta-EP levels. The initial workload was 150 kilopond meters and was increased 150 kilopond meters every 3 min until VO2max or leg fatigue occurred. Expired gases were continuously analyzed, and a venous blood sample was drawn from an indwelling catheter during the final 30 s of each stage and 5-min post-exercise. beta-EP levels were determined from serum using a radioimmunoassay technique and corrected for cross-reactivity with beta-lipotropin using affinity chromatography. Resting beta-EP levels were 25.3 +/- 4.1 pg X ml-1 and did not demonstrate significant changes during any stage of exercise. A correlation analysis (r = 0.30) revealed no significant relationship between exercise intensity and beta-EP levels. Following exercise, beta-EP levels were significantly increased compared to resting values (38.8 +/- 4.8 pg X ml-1). In addition, psychological state was unaffected by exercise despite significant increases in recovery beta-EP levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum beta-endorphin levels during a graded exercise test to exhaustion. 357 52

The endogenous opioids seem likely to be assigned a significant role in the integrated hormonal and metabolic response to exercise. This article reviews the present evidence on exercise and the endogenous opioids, and examines their involvement in a number of widely disparate physiological processes. In considering the role of individual opioid peptides, it is important to remember that many of the tools and techniques now used are still relatively crude. Most studies have demonstrated that serum concentrations of endogenous opioids, in particular beta-endorphin and beta-lipotrophin, increase in response to both acute exercise and training programmes. Elevated serum beta-endorphin concentrations induced by exercise have been linked to several psychological and physiological changes, including mood state changes and 'exercise-induced euphoria', altered pain perception, menstrual disturbances in female athletes, and the stress responses of numerous hormones (growth hormone, ACTH, prolactin, catecholamines and cortisol). Many reports have described a role for the endorphin response as seen during exercise and have used the opioid receptor antagonist, naloxone, to investigate and verify the degree of involvement of the opioids. However, whether the observed increases in peripheral endorphin concentrations are sufficient to cause immediate mood changes, create menstrual cycle dysfunction or alter pain perception is still not resolved. A relatively new implication for the endorphins and associated changes with exercise is in ventilatory regulation. A number of studies have suggested that endogenous opioids depress ventilation and may, therefore, play a role in ventilatory regulation by carbon dioxide, hypoxia and exercise. It may also be possible that during exercise, the perception of fatigue is modulated by an increase of endogenous opioids.
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PMID:Endorphins and exercise. 609 Dec 17

In order to investigate the effects of long-term exercise training on brain endorphin systems, and the latter's possible effects on the hypothalamic-pituitary-gonadal axis, female Wistar rats were subjected to daily treadmill running. A sedentary control group was also employed. After 8 weeks of training, and just prior to sacrifice, one-half of each group received a final fatiguing bout of exercise. Thus the final four groups consisted of a trained-fatigued (TF), trained-nonfatigued (TN), control-fatigued (CF), and control-nonfatigued (CN) group. Regional brain levels of beta-endorphin (beta E), methionine enkephalin and leucine enkephalin (LE) were assayed with independent RIAs from the nucleus accumbens, cortex, caudate-putamen, septum, amygdala, anterior and posterior hypothalamus, substantia nigra and ventral tegmentum. Diestrus serum levels of luteinizing hormone (LH), follicle stimulating hormone and prolactin (PRL) were also determined. Fatiguing resulted in a decrease in serum LH levels as well as an increase in beta E content in the nucleus accumbens, and LE content in the ventral tegmentum. Finally, TF animals exhibited less LE in the amygdala than the TN rats. Taken together, these changes in brain endorphins may indicate an acute, fatigue-running modulation of the hypothalamic-pituitary-gonadal axis.
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PMID:Effects of exercise training on brain opioid peptides and serum LH in female rats. 609 22

The adrenocorticotropin fragment ACTH/MSH 4--10 (0.1 ug/kg IP) effectively modulates the neuromuscular responses of 9 to 15 day old rats. Muscle (extensor digitorum longus) contraction amplitude is increased, fatigue is delayed and muscle half-relaxation time is shortened during 20 min of continuous in situ stimulation of a branch of the deep peroneal nerve (square wave shocks 10 Hz, duration 0.5 msec, strength supermaximal). No effect on contraction time is seen. There is no facilitation or change in any contraction parameter in rats older than two weeks (16 to 40 days) indicating that these older animals, like normal adult rats, are unaffected by the peptide. Immature rats, however, are even more sensitive than hypophysectomized adult rats [29] to the ameliorative action of ACTH/MSH 4-10. This early sensitivity to ACTH/MSH 4--10 corresponds to important developmental changes occurring in nerve and muscle during the most critical period in postnatal development, the first two weeks.
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PMID:Neuromuscular response of the immature rat of ACTH/MSH 4--10. 627 Jun 35

Familial glucocorticoid resistance (FGR) is a rare hereditary disorder characterized by hypercortisolism and the absence of stigmata of Cushing's syndrome. The inability of glucocorticoids to exert their effects on target tissues is compensated for by increases in circulating corticotropin (ACTH) and cortisol, the former causing excess secretion of both adrenal androgens and adrenal steroid-biosynthesis intermediates with salt-retaining activity. There is considerable variability in the clinical presentations of FGR ranging from asymptomatic, to isolated chronic fatigue and to hypertension with or without hypokalemic alkalosis or to hyperandrogenism, or both. In women, hyperandrogenism can result in acne, hirsutism, menstrual irregularities, oligoanovulation, and infertility; in men it may lead to infertility and in children to precocious puberty. The reported molecular defects in FGR, such as point mutations and a microdeletion of the glucocorticoid receptor (GR) gene, cause partial resistance by, respectively, compromising the function of the GR or decreasing its intracellular concentration in glucocorticoid target tissues. Complete glucocorticoid resistance is believed to be incompatible with life in humans. Hence, the glucocorticoid resistance cases reported have been partial and of variable degree. The extreme variability in the clinical manifestations of the disorder can, additionally, be explained by differing sensitivity of target tissues to mineralocorticoids or androgens or both, and perhaps by different biochemical defects of the glucocorticoid receptor, causing selective resistance of certain glucocorticoid responses in specific tissues. Isolated tissue-resistance from a somatic mutation of the GR in a corticotropinoma from a patient with Nelson's syndrome was also found, suggesting that this may be a mechanism of tumorigenesis. There is additional evidence that defects of GR function can appear surreptitiously in a variety of clinical conditions, suggesting that glucocorticoid resistance in humans may be involved in the pathogenesis and/or clinical picture of a plethora of disease states, of which FGR is the archetype.
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PMID:Glucocorticosteroid resistance in humans. Elucidation of the molecular mechanisms and implications for pathophysiology. 782 90

Tourette's syndrome (TS) is a complex inherited neuropsychiatric disorder that is characterized by multiple motor and phonic tics. Stress-related fluctuations in symptom severity and medication responsiveness are common, and patients often report that tics are worsened by fatigue, emotional trauma, and anxiety. We examined the effects of lumbar puncture (LP) stress on plasma adrenocorticotropin (ACTH) and cortisol, urinary catecholamines, and self- and clinician ratings of anxiety in 13 medication-free TS patients and 10 normal controls, ages 17 to 41 years. The TS patients secreted significantly more ACTH than the normal controls in response to the stress of the lumbar puncture. Compared to the controls the TS patients had significantly greater postLP mean and postLP peak ACTH levels. The TS patients also excreted significantly more norepinephrine in the 20 hr preceding the lumbar puncture and reported higher levels of anxiety before and during the procedure than the controls. In addition, urinary norepinephrine excretion of the TS patients was significantly correlated with clinician ratings of tic severity. The results were not related to current levels of depression and anxiety. Taken together, these findings suggest that a subset of TS patients may be characterized by heightened reactivity of the hypothalamic-pituitary-adrenal axis and related noradrenergic sympathetic systems.
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PMID:Enhanced stress responsivity of Tourette syndrome patients undergoing lumbar puncture. 808 Sep 1

We report a young female case of alcoholic liver injury accompanied with various metabolic and endocrinological disorders. A 29 year-old woman was admitted because of general fatigue and hyperlipidemia. She was a heavy drinker. Laboratory data on admission revealed liver dysfunction and hyperlipidemia (type II b) with a quite high serum gamma-glutamyltranspeptidase (gamma GTP) level. The microscopic finding of the liver biopsy specimen showed fatty metamorphosis and ballooning of hepatocytes, and she was diagnosed as heavy alcoholic liver injury. The endocrinological examination revealed the elevated plasma cortisol level, though the urinary 17-hydroxycorticoids (17-OHCS) and 17-ketosteroids (17-KS) excretion and the plasma adrenocorticotropic hormone (ACTH) level were reduced. Cortisol secretion showed the normal circadian rhythm and the normal response to ACTH provocation. The levels of plasma triiodothyronine (T3), thyroxine (T4), and thyroid stimulating hormone (TSH) were also reduced. These endocrinological and metabolic disorders were normalized in company with recovery of the liver function by temperance, diet therapy and nutritional education. Thus, these abnormalities were considered to be resulted from the alcoholic liver injury and the effect of the ethanol to the hypothalamic-pituitary system.
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PMID:[Alcoholic liver injury accompanied with various metabolic and endocrinological disorders--a case report]. 822 58

Glucocorticoid resistance results from the partial, albeit apparently generalized, inability of glucocorticoids to exert their effects on target tissues. The condition is associated with compensatory increases in circulating pituitary corticotropin and cortisol, with the former causing excess secretion of both adrenal androgens and adrenal steroid biosynthesis intermediates with salt-retaining activity. The manifestations of glucocorticoid resistance vary from chronic fatigue (perhaps a result of glucocorticoid deficiency in the central nervous system) to various degrees of hypertension with or without hypokalemic alkalosis or hyperandrogenism, or both, caused by increased cortisol and other salt-retaining steroids and adrenal androgens, respectively. In women, hyperandrogenism can result in acne, hirsutism, menstrual irregularities, oligoanovulation, and infertility; in men, it may lead to infertility and in children, to precocious puberty. Different molecular defects, such as point mutations or a microdeletion of the highly conserved glucocorticoid receptor gene, alter the functional characteristics or concentrations of the intracellular receptor and appear to cause glucocorticoid resistance. The extreme variability in the clinical manifestations of glucocorticoid resistance and its mimicry of many common diseases can be explained by the overall degree of glucocorticoid resistance, differing sensitivity of target tissues to mineralocorticoids or androgens or both, and perhaps different biochemical defects of the glucocorticoid receptor, with selective resistance of certain glucocorticoid responses in specific tissues. The various different symptoms of classic glucocorticoid resistance and the theoretical potential of this condition to appear surreptitiously emphasize the importance of the glucocorticoid receptor in the pathogenesis of human disease.
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PMID:Syndromes of glucocorticoid resistance. 818 39


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