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Neuropsychopharmacology : Official... Jun 2021Nonsuicidal self-injury (NSSI) is a prevalent and impairing behavior, affecting individuals with and without additional psychopathology. To shed further light on...
Nonsuicidal self-injury (NSSI) is a prevalent and impairing behavior, affecting individuals with and without additional psychopathology. To shed further light on biological processes that precede and result from NSSI acts, we built on previous cross-sectional evidence suggesting that the endogenous opioid system, and especially β-endorphin, is involved in the psychopathology of NSSI. This is the first study assessing salivary β-endorphin in daily life in the context of NSSI acts. Fifty-one female adults with repetitive NSSI participated over a period of 15 days in an ambulatory assessment study. Salivary β-endorphin was assessed before and after engagement in NSSI, during high urge for NSSI, and on a non-NSSI day. Furthermore, NSSI specific variables such as pain ratings, as well as method, severity, and function of NSSI were assessed. We found that β-endorphin levels immediately before an NSSI act were significantly lower than directly after NSSI. However, there was no difference between β-endorphin during high urge for NSSI and post NSSI measures. We found a positive association between severity of the self-inflicted injury and β-endorphin levels, but no significant association between β-endorphin levels and subjectively experienced pain. The results of the present study indicate that it is possible to assess salivary β-endorphin in daily life in the context of NSSI. Furthermore, our results provide a first indication that NSSI acts could be associated with a momentary increase of β-endorphin, and this might reinforce NSSI engagement. More research is needed to replicate and extend our findings on peripheral β-endorphin in daily life.
Topics: Adult; Cross-Sectional Studies; Female; Humans; Pain; Self-Injurious Behavior; beta-Endorphin
PubMed: 33398083
DOI: 10.1038/s41386-020-00914-2 -
Disease Markers 2016Background. Allergic rhinitis (AR) significantly impairs the quality of life of the patients; however, a questionnaire alone is an insufficient and subjective measure of...
Background. Allergic rhinitis (AR) significantly impairs the quality of life of the patients; however, a questionnaire alone is an insufficient and subjective measure of this condition. Obtaining an objective clinical assessment of the level of impairment will be valuable for its treatment. β-Endorphin is one of the most important mediators of both mental state and specific immunity. Thus, we investigated the possibility of using β-endorphin as a biomarker for evaluating the impairment level in AR. Methods. This study included 48 patients with AR and 32 healthy volunteers. The serum β-endorphin level was determined by enzyme immunoassay, and the serum-specific IgE and total IgE levels were determined by immunoblot assay. The Rhinoconjunctivitis Quality of Life Questionnaire (RQLQ) was used to assess the impairment level in the symptom duration. Results. The β-endorphin concentration was significantly decreased in AR patients compared to the healthy controls (p = 0.000, p < 0.05). There was significant negative correlation between the impairment level and serum β-endorphin level (correlation coefficient: -0.468; p = 0.001; p < 0.05), but there was no association between the serum β-endorphin and total IgE levels (p = 0.947, p > 0.05). Conclusion. β-Endorphin is a systemic biomarker that has the potential to assess the impairment level in AR and may therefore be a novel therapeutic target for the treatment of AR.
Topics: Adolescent; Adult; Aged; Biomarkers; Case-Control Studies; Female; Humans; Male; Middle Aged; Quality of Life; Rhinitis, Allergic; beta-Endorphin
PubMed: 27647946
DOI: 10.1155/2016/2025418 -
Fluids and Barriers of the CNS Jan 2015Beta-endorphin (β-END) is an opioid neuropeptide which has an important role in the development of hypotheses concerning the non-synaptic or paracrine communication of... (Review)
Review
Beta-endorphin (β-END) is an opioid neuropeptide which has an important role in the development of hypotheses concerning the non-synaptic or paracrine communication of brain messages. This kind of communication between neurons has been designated volume transmission (VT) to differentiate it clearly from synaptic communication. VT occurs over short as well as long distances via the extracellular space in the brain, as well as via the cerebrospinal fluid (CSF) flowing through the ventricular spaces inside the brain and the arachnoid space surrounding the central nervous system (CNS). To understand how β-END can have specific behavioral effects, we use the notion behavioral state, inspired by the concept of machine state, coming from Turing (Proc London Math Soc, Series 2,42:230-265, 1937). In section 1.4 the sequential organization of male rat behavior is explained showing that an animal is not free to switch into another state at any given moment. Funneling-constraints restrict the number of possible behavioral transitions in specific phases while at other moments in the sequence the transition to other behavioral states is almost completely open. The effects of β-END on behaviors like food intake and sexual behavior, and the mechanisms involved in reward, meditation and pain control are discussed in detail. The effects on the sequential organization of behavior and on state transitions dominate the description of these effects.
Topics: Animals; Behavior; Behavior, Animal; Cell Communication; Central Nervous System; Eating; Extracellular Space; Humans; Motivation; Pain; Reward; Sexual Behavior; beta-Endorphin
PubMed: 25879522
DOI: 10.1186/2045-8118-12-3 -
Cancer Research Feb 2012It is becoming increasingly clear that stressful life events can affect cancer growth and metastasis by modulating nervous, endocrine, and immune systems. The purpose of... (Review)
Review
It is becoming increasingly clear that stressful life events can affect cancer growth and metastasis by modulating nervous, endocrine, and immune systems. The purpose of this review is to briefly describe the process by which stress may potentiate carcinogenesis and how reducing body stress may prevent cancer growth and progression. The opioid peptide β-endorphin plays a critical role in bringing the stress axis to a state of homeostasis. We have recently shown that enhancement of endogenous levels of β-endorphin in the hypothalamus via β-endorphin neuron transplantation suppresses stress response, promotes immune function, and reduces the incidence of cancer in rat models of prostate and breast cancers. The cancer-preventive effect of β-endorphin is mediated through the suppression of sympathetic neuronal function, which results in increased peripheral natural killer cell and macrophage activities, elevated levels of anti-inflammatory cytokines, and reduced levels of inflammatory cytokines. β-endorphin inhibition of tumor progression also involves alteration in the tumor microenvironment, possibly because of suppression of catecholamine and inflammatory cytokine production, which are known to alter DNA repair, cell-matrix attachments, angiogenic process, and epithelial-mesenchymal transition. Thus, β-endorphin cell therapy may offer some therapeutic value in cancer prevention.
Topics: Animals; Cell Transplantation; Disease Progression; Humans; Neoplasms; Neurons; Neurosecretory Systems; Stress, Psychological; beta-Endorphin
PubMed: 22287549
DOI: 10.1158/0008-5472.CAN-11-3292 -
Biological Research For Nursing Jul 2019Osteoarthritis (OA) is the most common cause of pain in people aged 45 years, and the knee is the most commonly affected joint. There is a growing interest in...
Osteoarthritis (OA) is the most common cause of pain in people aged 45 years, and the knee is the most commonly affected joint. There is a growing interest in understanding the biological factors that influence pain among older adults, but few studies have examined the relationship between β-endorphin and experimental pain sensitivity in older adults with knee OA pain. The purpose of this study was to investigate the relationship between resting plasma levels of β-endorphin and experimental pain sensitivity. This study was a secondary analysis of data for 40 adults with knee OA pain in whom quantitative sensory testing was used to measure experimental sensitivity to heat- and mechanically induced pain. The mean age of the sample was 60 years ( = 9 years), and approximately half were female (53%). Regression analyses indicated that β-endorphin level was negatively related to pressure pain threshold (β = -17.18, = .02) and positively related to punctate mechanical pain (β = 17.13, = .04), after controlling for age, gender, and OA severity. We did not find a significant relationship between β-endorphin and heat pain tolerance. The results suggest that higher circulating levels of β-endorphin at rest are associated with increased sensitivity to mechanical pain in older adults with knee OA. These findings add to the literature regarding biological factors associated with pain sensitivity in older adults with chronic pain. Additional studies are needed to identify mediators of the relationship between β-endorphin and pain sensitivity in OA and other musculoskeletal pain conditions.
Topics: Aged; Female; Humans; Knee Joint; Male; Middle Aged; Osteoarthritis, Knee; Pain Measurement; Pain Threshold; Regression Analysis; Synovial Fluid; beta-Endorphin
PubMed: 31146541
DOI: 10.1177/1099800419853633 -
Nanoscale Dec 2021Functional amyloids are abundant in living organisms from prokaryotes to eukaryotes playing diverse biological roles. In contrast to the irreversible aggregation of most...
Functional amyloids are abundant in living organisms from prokaryotes to eukaryotes playing diverse biological roles. In contrast to the irreversible aggregation of most known pathological amyloids, we postulate that naturally-occurring functional amyloids are reversible under evolutionary pressure to be able to modulate the fibrillization process, reuse the composite peptides, or perform their biological functions. β-Endorphin, an endogenous opioid peptide hormone, forms such kinds of reversible amyloid fibrils in secretory granules for efficient storage and returns to the functional state of monomers upon release into the blood. The environmental change between low pH in secretory granules and neutral pH in extracellular spaces is believed to drive the reversible fibrillization of β-endorphin. Here, we investigate the critical role of a buried glutamate, Glu8, in the pH-responsive disassembly of β-endorphin fibrils using all-atom molecular dynamics simulations along with structure-based p prediction. The fibril was stable at pH 5.5 or lower with all the buried Glu8 residues protonated and neutrally charged. After switching to neutral pH, the Glu8 residues of peptides at the outer layers of the ordered fibrils became deprotonated due to partial solvent exposure, causing sheet-to-coil conformational changes and subsequent exposure of adjacent Glu8 residues in the inner chains. iterative deprotonation of Glu8 and induced structural disruption, all Glu8 residues would be progressively deprotonated. Electrostatic repulsion between deprotonated Glu8 residues along with their high solvation tendency disrupted the hydrogen bonding between the β1 strands and increased the solvent exposure of those otherwise buried residues in the cross-β core. Overall, our computational study reveals that the strategic positioning of ionizable residues into the cross-β core is a potential approach for designing reversible amyloid fibrils as pH-responsive smart bio-nanomaterials.
Topics: Amyloid; Amyloid beta-Peptides; Glutamic Acid; Hydrogen Bonding; Hydrogen-Ion Concentration; beta-Endorphin
PubMed: 34812835
DOI: 10.1039/d1nr05679d -
Pain Sep 2023The efficacy of acupuncture in treating pain diseases has been recognized in clinical practice, and its mechanism of action has been a hot topic in academic acupuncture...
The efficacy of acupuncture in treating pain diseases has been recognized in clinical practice, and its mechanism of action has been a hot topic in academic acupuncture research. Previous basic research on acupuncture analgesia has focused mostly on the nervous system, with few studies addressing the immune system as a potential pathway of acupuncture analgesia. In this study, we investigated the effect of electroacupuncture (EA) on the β-endorphins (β-END) content, END-containing leukocyte type and number, sympathetic neurotransmitter norepinephrine (NE), and chemokine gene expression in inflamed tissues. To induce inflammatory pain, about 200 µL of complete Frester adjuvant (CFA) was injected into the unilateral medial femoral muscle of adult Wistar rats. Electroacupuncture treatment was performed for 3 days beginning on day 4 after CFA injection, with parameters of 2/100 Hz, 2 mA, and 30 minutes per treatment. The weight-bearing experiment and enzyme-linked immunosorbent assay showed that EA treatment significantly relieved spontaneous pain-like behaviors and increased the level of β-END in inflamed tissue. Injection of anti-END antibody in inflamed tissue blocked this analgesic effect. Flow cytometry and immunofluorescence staining revealed that the EA-induced increase in β-END was derived from opioid-containing ICAM-1 + /CD11b + immune cells in inflamed tissue. In addition, EA treatment increased the NE content and expression of β2 adrenergic receptor (ADR-β2) in inflammatory tissues and upregulated Cxcl1 and Cxcl6 gene expression levels. These findings provide new evidence for the peripheral analgesic effect of acupuncture treatment by recruiting β-END-containing ICAM-1 + /CD11b + immune cells and increasing the β-END content at the site of inflammation.
Topics: Rats; Animals; beta-Endorphin; Intercellular Adhesion Molecule-1; Electroacupuncture; Neutrophils; Rats, Wistar; Pain; Analgesics; Acupuncture Analgesia
PubMed: 37027145
DOI: 10.1097/j.pain.0000000000002892 -
Current Diabetes Reports Jul 2022We are currently in the midst of a global opioid epidemic. Opioids affect many physiological processes, but one side effect that is not often taken into consideration is... (Review)
Review
PURPOSE OF REVIEW
We are currently in the midst of a global opioid epidemic. Opioids affect many physiological processes, but one side effect that is not often taken into consideration is the opioid-induced alteration in blood glucose levels.
RECENT FINDINGS
This review shows that the vast majority of studies report that opioid stimulation increases blood glucose levels. In addition, plasma levels of the endogenous opioid β-endorphin rise in response to low blood glucose. In contrast, in hyperglycaemic baseline conditions such as in patients with type 2 diabetes mellitus (T2DM), opioid stimulation lowers blood glucose levels. Furthermore, obesity itself alters sensitivity to opioids, changes opioid receptor expression and increases plasma β-endorphin levels. Thus, opioid stimulation can have various side effects on glycaemia that should be taken into consideration upon prescribing opioid-based medication, and more research is needed to unravel the interaction between obesity, glycaemia and opioid use.
Topics: Analgesics, Opioid; Blood Glucose; Diabetes Mellitus, Type 2; Epidemics; Humans; Obesity; beta-Endorphin
PubMed: 35593927
DOI: 10.1007/s11892-022-01473-0 -
Neurogastroenterology and Motility Nov 2019The gut immune, cannabinoid, and opioid systems constitute an integrated network contributing to visceral sensation and pain modulation. We aimed to assess the...
BACKGROUND AND AIMS
The gut immune, cannabinoid, and opioid systems constitute an integrated network contributing to visceral sensation and pain modulation. We aimed to assess the expression of the µ-opioid receptor (MOR), its ligand β-endorphin (β-END), and cannabinoid receptor-2 (CB ) in patients with irritable bowel syndrome (IBS) and asymptomatic controls (AC) and their correlation with sex and symptom perception.
METHODS
Mucosal biopsies were obtained from the left colon of 31 IBS patients (45% women) with predominant constipation (IBS-C, 9) or diarrhea (IBS-D, 10) or with mixed bowel habits (IBS-M, 12) and 32 AC (44% women) and processed for qRT-PCR, Western blotting, and immunohistochemistry.
KEY RESULTS
µ-opioid receptor and CB mRNA and protein expression and β-END protein levels were increased in patients with IBS compared to AC (all Ps=0.021). A significant sex by IBS interaction was found in relation to CB mRNA expression (P = .003) with women showing a markedly higher expression to men (P = .035). In contrast, in AC, men had higher expression than women (P = .033). β-END, MOR, and CB immunoreactivities (IR) were localized to CD4+T cells including EMR-1+ eosinophils and CD31+ T cells but not to mast cells.
CONCLUSIONS
The increased expression of MOR, β-END, and CB in the mucosa of IBS patients, where they are localized to immune cells, suggests that opioid and cannabinoid systems play an immune-related compensatory role in visceral pain in IBS patients. Further work is necessary to support this hypothesis.
Topics: Female; Humans; Intestinal Mucosa; Irritable Bowel Syndrome; Male; Receptor, Cannabinoid, CB2; Receptors, Opioid, mu; Sex Characteristics; beta-Endorphin
PubMed: 31336406
DOI: 10.1111/nmo.13688 -
Neuropharmacology Oct 2013Substantial evidence has implicated the endogenous opioid system in alcohol reinforcement. However, the role of each opioid peptide in alcohol reinforcement and,...
Substantial evidence has implicated the endogenous opioid system in alcohol reinforcement. However, the role of each opioid peptide in alcohol reinforcement and, particularly, reward is not fully characterized. In this study, using the conditioned place preference (CPP) paradigm as an animal model of reward, we determined the role of endogenous β-endorphin and enkephalins in the rewarding action of ethanol. Female mice lacking beta-endorphin and/or the proenkephalin gene as well as their respective wild-type controls were tested for baseline place preference on day 1, conditioned with ethanol versus saline on days 2-4 and were then tested under a drug-free state for postconditioning place preference on day 5. On each test day, mice were placed in the central neutral chamber and allowed to freely explore all three CPP chambers. The amount of time that mice spent in each chamber was recorded. We also studied the effect of naloxone, a non-selective opioid receptor antagonist, on ethanol CPP, in which wild-type mice were treated with saline or naloxone 10 min prior to ethanol or saline conditioning. Our results showed that the absence of β-endorphin or enkephalins alone failed to alter the acquisition of ethanol-induced CPP. However, the absence of both β-endorphin and enkephalins significantly reduced the CPP response. Interestingly, high but not low dose naloxone blunted ethanol CPP. These findings provide the first evidence illustrating that ethanol induces its rewarding action, at least in part, via a joint action of β-endorphin and enkephalins, possibly involving both mu and delta opioid receptors.
Topics: Animals; Choice Behavior; Conditioning, Psychological; Dose-Response Relationship, Drug; Enkephalins; Ethanol; Female; Mice; Mice, Knockout; Naloxone; Narcotic Antagonists; Protein Precursors; Reward; beta-Endorphin
PubMed: 23770261
DOI: 10.1016/j.neuropharm.2013.06.001