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)

1. The nocturnal secretion of plasma ACTH and serum cortisol and their responses to ovine corticotropin-releasing hormone (oCRH) were studied in acutely abstinent alcoholic and normal men. 2. Nocturnal cortisol secretion was similar in alcoholic and normal men, but nocturnal ACTH secretion tended to be decreased during the early morning hours (0600h-0900h) in alcoholic men. ACTH, but not cortisol, responses after oCRH administration tended to be attenuated in alcoholic men. CLUSTER ANALYSIS showed that the changes were not due to alterations in ACTH pulse frequency, amplitude, or interpulse interval. 3. The data suggest an intrinsic defect in response to CRH by the pituitary corticotroph cell, possibly due to genetic vulnerability or to the toxic effects of prolonged alcohol abuse.
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PMID:Adrenal function in abstinent alcoholic men. 166 2

If untreated, alcohol abuse, which often results from alcohol craving, causes major metabolic abnormalities, altered life-styles, lost productivity, and eventually death. Biochemical mechanisms that may contribute to alcohol craving include the stress response of the hypothalamic-pituitary adrenal axis, the endogenous opiate beta-endorphin system, neurotransmitter synthesis and release, hypoglycemia, and nutrient deficiencies. The macronutrient ratio of meals, the resulting insulin response, and nutrient blood levels can affect amino acid and nutrient transport across the blood-brain barrier. Researchers have reported that animals increase alcohol intake when fed nutrient-deficient diets or after stressful experience. A pilot study was designed to assess the effects of nutrition therapy added to a traditional rehabilitation program based on the 12-step program of Alcoholics Anonymous. One study group received traditional therapy; the other study group received traditional therapy and nutrition therapy consisting of modified menus and individualized nutrition counseling. Patients who received nutrition therapy reported significantly fewer hypoglycemic symptoms, lower sugar intake, less alcohol craving as well as significantly greater nutrient intakes; a greater number abstained from alcohol. These findings indicate that nutrition therapy can aid in the recovery from alcoholism.
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PMID:Alcohol craving in rehabilitation: assessment of nutrition therapy. 201 94

Alcoholism and alcohol abuse are serious health problems. Alcohol is known to influence the activity of a number of biological systems, for example the hormonal and neuronal systems. One of the biological systems whose activity is greatly influenced by alcohol is the endogenous opiate system. Alcohol modifies the function of both opiate receptors and opioid peptides. In fact it has been proposed that many of the effects of ethanol are mediated by its effects on the endogenous opiate system. This review will present results from various laboratories on the effects of acute and chronic ethanol treatments on various species, and on the release, biosynthesis and post-translational processing of the endorphins, enkephalins and dynorphins, the three known families of endogenous opioid peptides. Furthermore, the effect of acute and chronic ethanol consumption on the beta-endorphin system in man, and the possible implications of the functional activity of the endogenous opiate system for the genetic predisposition to alcoholism will be discussed.
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PMID:The effect of ethanol on the biosynthesis and regulation of opioid peptides. 265 84

The authors administered 100 micrograms human corticotropin-releasing hormone (h-CRH) to alcohol-dependent subjects after short-term abstention from alcohol abuse and observed that these patients released significantly less adrenocorticotrophic hormone (ACTH) than a control group. Cortisol responses were also blunted, but this effect was less pronounced. These findings indicate that hypercortisolism in alcohol withdrawal is driven by a central neurotransmitter/receptor disturbance rather than by peripheral alterations.
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PMID:Response of ACTH and cortisol to human corticotropin-releasing hormone after short-term abstention from alcohol abuse. 284 Sep 77

Endogenous opioid peptides are known to be involved in the alcohol tolerance and dependence following alcohol abuse. However, the cellular mechanisms involved in the ethanol tolerance and dependence are not well established. We have previously shown that low concentrations of ethanol stimulate immunoreactive beta-endorphin (IR-beta-EP) release from the cultured hypothalamic neurons and that chronic ethanol exposure desensitizes these neurons to ethanol challenges. In this study, we determined the IR-beta-EP response to increasing doses of ethanol during the desensitizing phase of moderate ethanol doses to test whether the cultured IR-beta-EP-secreting neurons develop tolerance to ethanol following constant exposure. We also determined IR-beta-EP responses following withdrawal from chronic ethanol challenge and compared the IR-beta-EP secretory response to various doses of ethanol in ethanol-naive and ethanol-preexposed cultures. The IR-beta-EP responses to increasing doses of ethanol (50-150 mM) were markedly reduced in the cultures preexposed to a 50 mM dose of ethanol when compared with those that were naive to ethanol. The ethanol-exposed cultures showed hypersecretion of IR-beta-EP after removal from 48 hr of constant ethanol, as compared with ethanol-naive cultures. When ethanol-preexposed cultures were challenged with various doses of ethanol 4 days after ethanol withdrawal, the cultures showed higher IR-beta-EP secretory responses than did the ethanol-naive cultures. These data suggest that IR-beta-EP secretory neurons in primary cultures develop tolerance to chronic ethanol, show withdrawal response after removal of chronic ethanol exposure, and develop sensitization following repeated ethanol challenges.
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PMID:Effects of chronic alcohol on immunoreactive beta-endorphin secretion from hypothalamic neurons in primary cultures: evidence for alcohol tolerance, withdrawal, and sensitization responses. 769 50

Certain neuroendocrine abnormalities (e.g., blunted plasma adrenocorticotropic hormone [ACTH] response to corticotropin-releasing hormone [CRH] administration and blunted serum TSH response to thyrotropin-releasing hormone [TRH] administration) are common in alcoholic patients. It was the objective of this study to evaluate whether they are centrally mediated: that is, whether they are secondary to increased activity of CRH and/or TRH neurons. We evaluated the nocturnal secretion (2200 hours to 1000 hours, q 15 min) of plasma ACTH, serum cortisol, and serum TSH, and their responses to the combined administration of CRH and TRH, in 28 acutely abstinent alcoholic (age range: 32 to 57 years; mean: 42.4 years) and 19 normal men (age range: 21 to 52 years; mean: 32.1 years). To assess the validity of administering CRH and TRH simultaneously, we gave 10 additional abstinent alcoholic men (age range: 36 to 53 years; mean: 45.8 years), in random order and at least 4 days apart, either CRH, TRH, placebo, or CRH plus TRH. Nocturnal ACTH, cortisol, and TSH secretion, as well as cortisol and TSH responses after CRH plus TRH administration, were similar in alcoholic and normal men. However, ACTH peak responses to CRH plus TRH were reduced in the alcoholic men (p < 0.05). The ACTH, but not cortisol, response was greater after combined CRH plus TRH administration than after CRH alone (p < .002). The blunted ACTH response does not appear to be the result of increased endogenous CRH activity, because all parameters of nocturnal ACTH pulsatility were normal in the alcoholics. It rather appears to be secondary to an intrinsic defect in the CRH responsiveness of the pituitary corticotroph, possibly due to genetic vulnerability or to the toxic effects of prolonged alcohol abuse.
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PMID:Thyroid and adrenal dysfunction in abstinent alcoholic men: locus of disturbance. 830 25

The circadian secretion of beta-endorphin, adrenocorticotropic hormone (ACTH), and cortisol was evaluated in 14 non-cirrhotic alcoholic men after 7 and 28 days of abstinence and in 12 sex- and age-matched normal subjects. A significant decrease in plasma levels of beta-endorphin, reduced ACTH levels, and increased cortisol levels were observed in samples taken at 08.00 h, 12.00 h, 18.00 h, and 23.00 h both after 7 and 28 days of abstinence. These data suggest the presence of a strong negative feedback on pro-opiomelanocortin synthesis by cortisol hypersecretion in abstinent alcoholics, which might be due to long-term stimulation of adrenal function by alcohol. The decreased plasma beta-endorphin levels might predispose to relapse in alcohol abuse.
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PMID:Beta-endorphin, adrenocorticotropic hormone and cortisol secretion in abstinent alcoholics. 940 8

Opioid drugs play important roles in the clinical management of pain, as well as in the development and treatment of drug abuse. The mu opioid receptor is the primary site of action for the most commonly used opioids, including morphine, heroin, fentanyl, and methadone. By sequencing DNA from 113 former heroin addicts in methadone maintenance and 39 individuals with no history of drug or alcohol abuse or dependence, we have identified five different single-nucleotide polymorphisms (SNPs) in the coding region of the mu opioid receptor gene. The most prevalent SNP is a nucleotide substitution at position 118 (A118G), predicting an amino acid change at a putative N-glycosylation site. This SNP displays an allelic frequency of approximately 10% in our study population. Significant differences in allele distribution were observed among ethnic groups studied. The variant receptor resulting from the A118G SNP did not show altered binding affinities for most opioid peptides and alkaloids tested. However, the A118G variant receptor binds beta-endorphin, an endogenous opioid that activates the mu opioid receptor, approximately three times more tightly than the most common allelic form of the receptor. Furthermore, beta-endorphin is approximately three times more potent at the A118G variant receptor than at the most common allelic form in agonist-induced activation of G protein-coupled potassium channels. These results show that SNPs in the mu opioid receptor gene can alter binding and signal transduction in the resulting receptor and may have implications for normal physiology, therapeutics, and vulnerability to develop or protection from diverse diseases including the addictive diseases.
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PMID:Single-nucleotide polymorphism in the human mu opioid receptor gene alters beta-endorphin binding and activity: possible implications for opiate addiction. 968 28

Teenage drinking continues to be a major problem in industrialized countries, where almost 35% of alcohol drinkers are under 16 years old. In the present paper we studied the effects of acute alcohol intoxication (AAI) on the pituitary-gonadal (PG) axis hormones, and the possible contribution of pituitary-adrenal (PA) axis hormones, beta-endorphin (BEND), and prolactin (PRL) to the alcohol-induced dysfunction of PG axis hormones. Blood samples were drawn from adolescents that arrived at the emergency department with evident behavioral symptoms of drunkenness (AAI) or with nil consumption of alcohol (controls [C]). Our results demonstrated that AAI produces in adolescents a high increase in plasma PRL, ACTH, and cortisol (F), and a contradictory behavior of testosterone (T) according to gender: plasma T was increased in females and decreased in males. ACTH and PRL correlated positively with F, dehydroepiandrosterone-sulphate (DHEAS) and T in females, which suggests that PRL and ACTH could synergistically stimulate adrenal androgen production. In contrast, the decrease in T and increase in BEND in males suggests that AAI could have an inhibitory effect on testicular T, perhaps mediated by BEND. The hormones studied are involved in the development of secondary sexual characteristics and the growth axis during adolescence. The deleterious effects of alcohol abuse should be made known to adolescents and the appropriate authorities.
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PMID:Effects of acute alcohol intoxication on pituitary-gonadal axis hormones, pituitary-adrenal axis hormones, beta-endorphin and prolactin in human adolescents of both sexes. 1095 41

Fifteen 3,4-methylenedioxymethamphetamine (MDMA, 'ecstasy') users who did not have other drug dependencies or prolonged alcohol abuse and 15 control subjects were studied. All the subjects were exposed to the same psychosocial stressor (Stroop Color-Word Interference Task, public speaking and mental arithmetic in front of an audience) 3 weeks after MDMA discontinuation. Plasma concentrations of adrenocorticotropic hormone (ACTH) and cortisol were measured immediately before the tests began and at their end, 30 min later. Growth hormone (GH) responses to the dopaminergic agonist bromocriptine and psychometric measures (Tridimensional Personality Questionnaire, Minnesota Multiphasic Personality Inventory, Buss-Durkee Hostility Inventory) were also obtained 4 weeks after MDMA discontinuation for the same subjects. ACTH and cortisol basal levels were significantly higher in ecstasy users than in control subjects. In contrast, ACTH and cortisol responses to stress were significantly blunted in MDMA users. The sensitivity of dopamine D2 receptors, reflected by GH responses to bromocriptine challenge, was reduced in MDMA users compared with controls. The responsiveness of the hypothalamic-pituitary-adrenal (HPA) axis (ACTH and cortisol delta peaks) correlated directly with GH areas under curves in response to bromocriptine, and inversely with psychometric measures of aggressiveness and novelty seeking. No correlation was found between hormonal measures and the extent of MDMA exposure. Reduced D2 receptor sensitivity, HPA basal hyperactivation and reduced responsiveness to stress may represent a complex neuroendocrine dysfunction associated with MDMA use. The present findings do not exclude the possibility that dopamine dysfunction partly predated MDMA exposure.
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PMID:Hypothalamic-pituitary-adrenal axis responses to stress in subjects with 3,4-methylenedioxy-methamphetamine ('ecstasy') use history: correlation with dopamine receptor sensitivity. 1452 43


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