Plasma Β-endorphin Levels Research Articles

Neuroendocrine effects of a single bout of functional and core stabilization training in women with chronic nonspecific low back pain: A crossover study.

Exercise‐induced hypoalgesia (EIH) is characterized as the pain reduction after an exercise session and it seems to be related to the release of plasma β‐endorphin. In this sense, the core stabilization training (CT) has been suggested for patients with chronic nonspecific low back pain (CNSLBP), but it is unclear whether it induces EIH. Patients with CNSLBP have neuromotor dysfunctions that can affect the performance of functional tasks, thus, performing functional training (FT) could improve motor control and promote EIH, since functional training uses multi‐joint exercises that aim to improve the functionality of actions performed in daily life. EIH is usually assessed using quantitative sensory tests (QST) such as conditioned pain modulation, pressure pain threshold, and temporal summation. Thus, the sum of parameters from quantitative sensory tests and plasma β‐endorphin would make it possible to understand what the neuroendocrine effects of FT and CT session are. Our study compared the acute effect of CT and FT on the EIH and plasma β‐endorphin release, and correlated plasma β‐endorphin with quantitative sensory testing in patients with CNSLBP. Eighteen women performed two training sessions (CT and FT) with an interval of 48 h between sessions. EIH was assessed by QST and plasma β‐endorphin levels. Results showed that only FT significantly increased plasma β‐endorphin (FT p < 0.01; CT p = 0.45), which correlated with pain pressure threshold (PPT) and conditioned pain modulation (CPM). However, QST values were not different in women with CNSLBP after CT or FT protocols. Plasma β‐endorphin correlated with PPT and CPM, however, the same did not occur with a temporal summation.

The effects of conventional, warm and cold acupressure on the pain perceptions and beta-endorphin plasma levels of primiparous women in labor: A randomized controlled trial

ObjectiveThis study was performed to determine the impact of different acupressure procedures, performed on women's hands during labor, on β-endorphin plasma levels and labor pain perception. DesignRandomized controlled experimental trial Setting and ParticipantsThis study was conducted with 140 pregnant women in the delivery rooms of a university research and training hospital and a state hospital in a province in the Black Sea Region of Turkey. MethodsThis study was conducted with three experimental groups (who had conventional, warm and cold acupressure on their LI4 acupressure point) and one control group (no acupressure). Each group included 35 pregnant women. The data were collected using a personal information form, the Labor Intervention Follow-up Form, the Visual Analog Scale (VAS) and the Verbal Category Scale (VCS). Its main outcomes were the women's labor pain perceptions and β-endorphin plasma levels. ResultsThe experimental and control groups had homogeneous introductory characteristics. The experimental groups had significantly higher mean VAS and VCS posttest scores than the control group (p<0.001). The experimental groups’ mean posttest β-endorphin plasma levels were also significantly higher (p<0.05). ConclusionIn this study, conventional, warm and cold acupressure reduced the women's labor pain and increased their β-endorphin plasma levels. Midwives can use acupressure to reduce labor pain.

Anxiety enhances pain in a model of osteoarthritis and is associated with altered endogenous opioid function and reduced opioid analgesia.

Negative affect, including anxiety and depression, is prevalent in chronic pain states such as osteoarthritis (OA) and associated with greater use of opioid analgesics, potentially contributing to present and future opioid crises. We tested the hypothesis that the interaction between anxiety, chronic pain, and opioid use results from altered endogenous opioid function. A genetic model of negative affect, the Wistar-Kyoto (WKY) rat, was combined with intra-articular injection of monosodium iodoacetate (MIA; 1 mg) to mimic clinical presentation. Effects of systemic morphine (0.5-3.5 mg·kg-1) on pain behaviour and spinal nociceptive neuronal activity were compared in WKY and normo-anxiety Wistar rats 3 weeks after MIA injection. Endogenous opioid function was probed by the blockade of opioid receptors (0.1-1 mg·kg-1 systemic naloxone), quantification of plasma β-endorphin, and expression and phosphorylation of spinal mu-opioid receptor (MOR). Monosodium iodoacetate-treated WKY rats had enhanced OA-like pain, blunted morphine-induced analgesia, and greater mechanical hypersensitivity following systemic naloxone, compared with Wistar rats, and elevated plasma β-endorphin levels compared with saline-treated WKY controls. Increased MOR phosphorylation at the master site (serine residue 375) in the spinal cord dorsal horn of WKY rats with OA-like pain (P = 0.0312) indicated greater MOR desensitization. Reduced clinical analgesic efficacy of morphine was recapitulated in a model of high anxiety and OA-like pain, in which endogenous opioid tone was altered, and MOR function attenuated, in the absence of previous exogenous opioid ligand exposure. These findings shed new light on the mechanisms underlying the increased opioid analgesic use in high anxiety patients with chronic pain.

How do Spinal Stabilization Exercises Relieve Back Pain? An Analysis of Potential Mechanisms of Analgesia Effected at Muscular, Spinal Cord and Supraspinal Levels

STUDY OBJECTIVE Spinal stabilization exercises have emerged as an effective treatment for low back pain (LBP), but the mechanism of analgesia obtained through these exercises is unknown. The objective of the present research was to derive viable hypotheses for this pain relief based on previously validated analgesic mechanisms. METHODS A literature review was conducted by first considering commonly known methods of both exogenous and endogenous pain control, and then selecting for deeper analysis those mechanisms which could conceivably be operative during the self-generated, low amplitude movements involved in spinal stabilization exercises. The three chosen analgesic processes were related to perfusion, gate control, and endogenous analgesia. RESULTS Mechanism 1: Increased Perfusion Muscle contraction is known to increase perfusion of muscle tissue, leading to increased nutrient delivery and removal of waste products, and ischemia caused by atherosclerosis causes pain in multiple tissues including muscle. The lumbar blood supply derives from the abdominal aorta/lumbar artery system and blockages in this system have been linked to LBP. Gentle stabilization exercises targeting the core which activate these muscles may thus increase perfusion and thereby lessen pain related to ischemia. Mechanism 2: Gate Control-Mediated Analgesia Since Melzack and Wall first proposed the Gate Control Theory, the existence of multiple specific pain-inhibiting circuits linking dorsal horn laminae has been confirmed. Recent studies support a role for muscle spindles and golgi tendon organs in “closing the gate” to pain sensations, via muscle contraction. Pain relief during contract-relax and resistance exercises has been achieved in at least 3 studies, possibly through activation of these receptors. This process may explain in part the achievement of pain relief obtained after a short course of spinal stabilization exercises. Mechanism 3: Exercise-Induced Analgesia Exercise Induced analgesia (EIA) works through multiple endogenous systems that decrease pain perception, including the opioidergic, serotonergic, noradrenergic, endocannabinoid, and nitrergic systems. Numerous studies have shown EIA occurs with aerobic exercise in both humans and animals. The role of EIA in analgesia during isometric and core stabilization exercises is starting to be explored, including findings that both plasma β-endorphin and serotonin levels increase after core exercises. CONCLUSIONS The manner in which spinal stabilization exercises achieve analgesia is unknown. The vascular, gate-control, and exercise-mediated mechanisms outlined above are known to elicit an analgesic effect, and could conceivably be evoked by the gentle, low amplitude movements of these exercises. Rigorous, prospective research on perfusion of the muscles involved in core stabilization, the activation of muscle proprioceptive pathways in dorsal horn pain synapses, and plasma levels of key hormones during and after core stabilization exercises, would help support or refute the existence of this link.

Comparative study between electroacupuncture at Neima point and Neiguan (PC 6) and epidural nerve block for preemptive analgesia in patients undergoing thoracic surgery

To compare the clinical effect between electroacupuncture (EA) at Neima point and Neiguan (PC 6) and epidural nerve block for preemptive analgesia in patients undergoing thoracic surgery. Sixty patients with elective radical esophagectomy were randomly divided into a group A, a group B and a control group, 20 cases in each group. The patients in the group A were treated with injection of 20 mL 0.375% ropivacaine at epidural space 30 min before anesthesia induction, followed by normal anesthesia during operation; the patients in the group B were treated with 30 min EA at bilateral Neima point and Neiguan (PC 6) before anesthesia induction, followed by normal anesthesia during operation; the patients in the control group were treated with general anesthesia alone. Patient-controlled intravenous analgesia was applied for all the patients. The mean arterial pressure (MAP) and heart rate (HR) were recorded at the following time points: before acupuncture/epidural puncture (T0), skin incision (T1), extubation (T2) and 2 h after operation (T3); the dosage of anesthetics and extubation time were recorded; the plasma levels of β-endorphin (β-EP), 5-hydroxytryptamine (5-HT) and prostaglandin E2 (PGE2) were measured at the following time points: T0, T3, 12 h after operation (T4), 24 h after operation (T5) and 48 h after operation (T6). Visual analogue scale (VAS) was used to evaluate the analgesic effect. The MAP at T1 and T2 in the group A was lower than that in group B and control group (P<0.05), and HR at T1 and T2 was lower than that in control group (P<0.05). The MAP and HR at T1 and T2 in the group B were lower than those in the control group (P<0.05). The dosage of remifentanil in the group A and group B was lower than that in the control group (P<0.05), and extubation time was earlier than that in the control group (P<0.05). The content of β-EP at T4, T5 and T6 in the group B was higher than that in the group A and control group (P<0.05); the contents of 5-HT and PGE2 at T3, T4 and T5 in the group A and group B were lower than those in the control group (P<0.05). The VAS scores at T3, T4 and T5 in the group A and group were lower than those in the control group (P<0.05). The preemptive analgesia of EA at Neima point and Neiguan (PC 6) and epidural nerve block could both provide effective perioperative analgesia for thoracic surgery. The EA could better maintain intraoperative hemodynamics and has less physiological disturbance.

Plasma B-endorphin and cortisol profiles around periparturient period in Friesian Cattle suffering from reproductive disorders in Egypt

The present study aimed to determine plasma β-endorphin and cortisol concentrations in cattle with reproductive disorders (dystocia and retained placenta) and weakness body condition score during periparturient period. Stress may cause an overproduction of beta-endorphins and free radicals. Twenty multiparous Friesian cows weighing 400–650 kg aged 6-10 years and between (3-8) parities at late pregnancy period was used for two months before parturition. From ten days before the expected birth date the birth canal of each animal was monitored by rectal and vaginal palpations, and the body temperature was checked daily to predict the probable time of parturition. Animals were divided into four groups according to parturition disorders’ five animals in each one. First group delivered spontaneously at term with no obstetrical assistance(A), second group delivery was at term but was accompanied by dystocia(B), third group delivery was at term but was accompanied by retained placenta(C), and fourth group delivery was at term but animals showed weakness body condition score (D). Results illustrated that Plasma β-endorphin level in Friesian cattle during pregnancy state increased gradually through gestation period. It reaches its highest level during the third trimester due to stressful state. Also, it reaches its peak at zero time of parturition by appearing its analgesic action. Meanwhile, it decreases gradually towards re-establishment of ovarian cycle. Generally, cows suffering reproductive disorders had a clear impact on blood plasma β-endorphin concentration around parturition process.

The Relationship Between Course of Illness and β-Endorphin Plasma Levels in Patients with Schizophrenia.

ObjectiveExtensive investigations have been conducted into predictors of schizophrenia outcome. The heterogeneity of the illness implies that many factors should be taken into account. Some studies have reported the relationship between increased β-endorphin concentration and predominant negative symptoms.MethodsWe included 77 outpatients with schizophrenia and 74 healthy controls. Data referring to duration and course of illness, hospitalization number and treatment were collected on the basis of clinical interviews and medical documentation analysis. The β-endorphin concentrations were assessed once in all participants, at the onset of the study.ResultsA chronic course of illness was found in 44 of the 77 schizophrenics. Patients with schizophrenia, especially those with a chronic course of illness, revealed significantly higher β-endorphin concentrations than those with an episodic course and controls (mean 29.70 vs 19.86 pmol/L; p=0.0001). Increased levels of β-endorphin were related to longer duration of illness (R=0.294, p=0.009) and frequent psychiatric hospitalization (R=0.346, p=–0.002).ConclusionEndorphins may be potential biological predictors of persistent negative symptoms and final outcome in schizophrenia.

Cough Suppression during Flexible Bronchoscopy Using Transcutaneous Electric Acupoint Stimulation: A Randomized Controlled Study.

Background and Objective. Transcutaneous electric acupoint stimulation (TEAS) is recommended for its sedative and analgesic effects. We sought to evaluate the effect of TEAS on cough suppression during flexible bronchoscopy (FB) and explore the underlying mechanism. Methods. In this single-center, randomized, single-blind, parallel-controlled study, we randomized 100 patients scheduled for FB into two equal groups treated with or without TEAS (TEAS group and control group). Patients in the TEAS group received 30 min of stimulation at the Hegu (LI4), Neiguan (PC6), and Lieque (LU7) points before FB. The control group underwent the same procedure, but without stimulation. The primary outcome was the intraoperative cough score determined by the bronchoscopist. The secondary outcomes were patient-reported discomfort scores and other procedural parameters. Results. Compared with the controls, patients who received TEAS preconditioning had lower cough scores (P=0.0027) and requirement of lidocaine and fentanyl (P < 0.05) and significantly higher postprocedural plasma β-endorphin levels (P=0.0367). There were no intergroup differences in discomfort scores, midazolam dosage, rate of premature termination, oxygen requirement, sedation level, airway assistance, oxygen saturation, lowest oxygen saturation level, heart rate, plasma substance-P levels, and rate of complications after 24 h. The total procedure duration, time for passage of the bronchoscope through the vocal cords, and systolic and diastolic blood pressure levels were less in the TEAS group than in the control group (P=0.033, 0.039 and <0.05, respectively). Conclusion. The combination of midazolam and TEAS was superior to midazolam alone for cough suppression during FB, probably due to increased plasma β-endorphin levels. This trial is registered with ChiCTR1800016612 at chictr.org.cn/index.aspx.

Examination of pain threshold and neuropeptides in patients with acute suicide risk

IntroductionOne of the main challenges in suicide prevention is the limited understanding of the biological mechanisms underlying suicide. Recent findings suggest impairments in pain processing in acutely suicidal patients. However, little is known about the biological factors that may drive these discrete physiological abnormalities. In this study, we examined plasma peptides involved in analgesic and inflammatory responses and physical pain threshold in acutely suicidal patients. MethodsThirty-seven depressed patients of both sexes hospitalized for severe suicidal ideation or a recent suicide attempt were characterized clinically including history of suicidal ideation and behavior. Psychological and physical pain, and pressure pain threshold was also measured. Plasma levels of β-endorphin, neurotensin, agouti-related protein (AgRP), C-reactive protein (CRP), adrenocorticotropic hormone (ACTH), and brain-derived neurotrophic factor (BDNF) were run in Milliplex multiplex assays. ResultsThe number of lifetime suicide attempts was positively correlated with β-endorphin (r = 0.702; p = 0.007), and neurotensin (r = 0.728, p = 0.007) plasma levels. Higher pain threshold was measured in the suicide attempt group as compared to the suicidal ideation group. Pain threshold was strongly and negatively associated with CRP plasma levels (r = −0.548; p < 0.001). In patients reporting chronic pain, lower AgRP levels and lower pain threshold were observed (t = 4.472; p = 0.001). ConclusionOur results suggest that abnormalities in the opioid and neurotensin systems may underlie the increase in pain threshold found in suicide attempters, and possibly risk for suicidal behavior. Targeting pain circuits and systems may provide therapeutic mechanisms for suicide prevention.

The Relationship Between β-Endorphin and Experimental Pain Sensitivity in Older Adults With Knee Osteoarthritis.

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 (SD = 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, p = .02) and positively related to punctate mechanical pain (β = 17.13, p = .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.

Odor perception and hedonics in chronic schizophrenia and in first episode psychosis.

Background and purposeThe study evaluated olfactory performance and pleasantness rating of odors in patients with first episode psychosis (FEP) and chronic schizophrenia (SCH) with regard to the severity of psychopathological symptoms and plasma β-endorphin concentration.Patients and methodsTwenty patients with FEP, 27 with SCH and 29 healthy individuals, were recruited to the research . The University of Pennsylvania Smell Identification Test (UPSIT), subjective odor hedonic judgment and plasma levels of β-endorphin (BE) assay were performed in all participants.ResultsIndividuals with SCH revealed higher BE concentration than other study groups (P=0.000). All patients identified pleasant odors poorer than controls, however, SCH made more identification errors (P=0.000) than those with FEP. Moreover, participants with FEP rated pleasant odors as more pleasant than individuals with chronic schizophrenia and healthy controls (P=0.009). Nevertheless, higher β-endorphin level was related with lower scores in pleasant odor identification (Rs=−0.452; P=0.046) and more severe psychotic symptoms in FEP sample. Chronic schizophrenia patients did not demonstrate any relationship between symptom severity, odor identification performance and β-endorphin concentration. No relationship was found between BE concentration and hedonic judgment of the presented odors among all study groups. Chronically ill subjects identified odors significantly more poorly than those with first episode psychosis. Deficits in identifying pleasant odors might not be the only potential risk factor for undergoing chronic, recurrent schizophrenia. All patients subjectively overrated pleasant odors. Those with SCH and more severe negative symptoms made significantly more identification errors.ConclusionThe endogenous morphine system deregulation is observed in first episode psychosis as well as in chronic schizophrenia. In first episode schizophrenia higher beta-endorphin concentration is related to pleasant odor identification deficit.

Prefrontal expectancy and reinforcement-driven antidepressant placebo effects

Placebo responses in depression exemplify how expectancies and appraisals impact mood. Cognitive and neural mechanisms underlying these responses are still poorly understood, partly due to the difficulty of simulating antidepressant effects and manipulating mood experimentally. To address these challenges, we developed an acute antidepressant placebo experiment involving the intravenous administration of a “fast-acting antidepressant” and a trial-by-trial sham fMRI “neurofeedback” manipulation, purporting to reveal mood-relevant neural responses. Twenty volunteers with major depression underwent this experiment while rating their expected and actual mood improvement. Mixed-effects analyses of trial-by-trial ratings revealed that the “drug” infusion cues induced higher expectancies of mood improvement, while both the “drug” infusion cue and the sham neurofeedback induced a reported mood improvement. Neurofeedback of greater magnitude, compared to lower magnitude, recruited the lateral prefrontal cortex (lPFC). Individuals with greater lPFC responses to neurofeedback displayed: (1) greater effect of previous mood improvement on expectancy ratings and (2) greater effect of sham neurofeedback on mood improvement. Behavioral antidepressant placebo effects were additionally moderated by changes in peripheral β-endorphin plasma levels and depressive symptomatology. These data demonstrate the feasibility of trial-by-trial manipulation of antidepressant placebo-associated expectancies and their reinforcement. We provide initial insights into the role of the lPFC in the interplay between placebo-induced expectancies and mood, as well as preliminary evidence for the role of the opioid system in antidepressant placebo effects.

Can Beta-Endorphin Be Used as a Biomarker for Chronic Low Back Pain? A Meta-analysis of Randomized Controlled Trials.

Chronic low back pain (CLBP) is usually quantified using the visual analog scale (VAS). However, the VAS is a subjective measure and prone to reporting bias, therefore making it difficult to differentiate patients with true pain from those seeking to obtain secondary gain. This study aimed to evaluate the feasibility of using plasma β-endorphin as an objective biomarker for CLBP. We searched PubMed, Embase, and the Cochrane Library for randomized trials that compared treatment vs sham procedures for patients with CLBP. Changes in VAS and β-endorphin levels between baseline and final evaluations were assessed for the treatment and control groups. A meta-regression model was developed to evaluate the association between the β-endorphin level and VAS. We included data from seven trials involving 375 patients. There was no significant difference in VAS scores and β-endorphin levels between both groups at baseline. At final evaluation, the treatment group demonstrated significantly greater improvements in VAS scores and an increased β-endorphin level compared with the control group. The change in the plasma β-endorphin level may be a surrogate marker of treatment response for patients with CLBP (explanatory power: 80%). The plasma β-endorphin level might be rarely affected by sham procedures. For patients with CLBP, the baseline β-endorphin level may reflect the intensity of CLBP (explanatory power: 66%). A change in plasma β-endorphin level may be a surrogate marker of the treatment response for patients with CLBP. Advancements in β-endorphin measurements may help us better quantify pain intensity.

Is β-endorphin significant in the control of the male sexual response?

It has been assumed that β-endorphin, belonging to the family of opiodergic neuropeptides, might facilitate the inhibition of the male sexual response; however, its role in the control of the penile erectile tissue remains to be elucidated. This study aimed to evaluate in healthy men the course of β-endorphin in the systemic and cavernous blood through different stages of sexual arousal. Thirty-four (34) men were exposed to erotic stimuli to induce penile tumescence and rigidity. Blood was aspirated from the corpus cavernosum and a cubital vein during the penile conditions flaccidity, tumescence, rigidity and detumescence. Plasma levels of β-endorphin were determined by means of radioimmunometric methods. The effects of β-endorphin on isolated human penile erectile tissue were investigated in vitro. β-endorphin did not induce a contractile response of the cavernous tissue or reverse the contraction induced by noradrenaline. β-endorphin decreased in the systemic blood when the penis became tumescent and rigid and increased during detumescence. In the cavernous blood, no alterations in β-endorphin concentrations were observed. The drop in β-endorphin observed during tumescence and rigidity seems likely to reflect the inhibition of the opioidergic input with the beginning of sexual arousal.

Sex differences in binge-like EtOH drinking, corticotropin-releasing hormone and corticosterone: effects of β-endorphin.

Binge drinking is an increasingly common pattern of risky use associated with numerous health problems, including alcohol use disorders. Because low basal plasma levels of β‐endorphin (β‐E) and an increased β‐E response to alcohol are evident in genetically at‐risk human populations, this peptide is thought to contribute to the susceptibility for disordered drinking. Animal models suggest that the effect of β‐E on consumption may be sex‐dependent. Here, we studied binge‐like EtOH consumption in transgenic mice possessing varying levels of β‐E: wild‐type controls with 100% of the peptide (β‐E +/+), heterozygous mice constitutively modified to possess 50% of wild‐type levels (β‐E +/−) and mice entirely lacking the capacity to synthesize β‐E (−/−). These three genotypes and both sexes were evaluated in a 4‐day, two‐bottle choice, drinking in the dark paradigm with limited access to 20% EtOH. β‐E deficiency determined sexually divergent patterns of drinking in that β‐E −/− female mice drank more than their wild‐type counterparts, an effect not observed in male mice. β‐E −/− female mice also displayed elevated basal anxiety, plasma corticosterone and corticotropin‐releasing hormone mRNA in the extended amygdala, and all of these were normalized by EtOH self‐administration. These data suggest that a heightened risk for excessive EtOH consumption in female mice is related to the drug's ability to ameliorate an overactive anxiety/stress‐like state. Taken together, our study highlights a critical impact of sex on neuropeptide regulation of EtOH consumption.

Puerarin acts on the skeletal muscle to improve insulin sensitivity in diabetic rats involving μ-opioid receptor

Puerarin, a major active isoflavone extracted from the root of Pueraria lobate, significantly increases plasma β-endorphin and insulin levels and improves impaired insulin signaling in diabetic animals. However, the target tissues and underlying mechanisms in and through which puerarin functions to ameliorating insulin resistance remains largely unclear. In this study, we showed that puerarin enhanced μ-opioid receptor expression and phosphorylation, and increased insulin-stimulated glucose transporter 4 translocation to the plasma membrane in the skeletal muscle of diabetic rats, which were recaptured by a direct application of puerarin in the palmitate-induced insulin-resistant L6 myotubes. Naloxone, an antagonist of μ-opioid receptor, blocked these functions of puerarin. No β-endorphin was detected either in the muscle of diabetic rats or in the palmitate-induced insulin-resistant L6 cells. Furthermore, we presented the evidence to show the interaction between μ-opioid receptor and insulin receptor substrate 1 in the muscle tissues and cells. These results suggested that puerarin improved insulin sensitivity in the skeletal muscle at least in part by its local effects involving μ-opioid receptor function.

The effect of laserpuncture at the LI4 Hegu point on the plasma levels of β-endorphin in healthy subjects

Laserpuncture is an acupuncture method for pain management. The goal of this study was to determine the effect of laserpuncture at the LI4 Hegu point on the plasma levels of β-endorphin in healthy subjects. A randomized, double-blind, controlled trial with placebo controls was conducted on 29 healthy subjects. Subjects were allocated into the laserpuncture group (n = 15) and the laserpuncture placebo group (n = 14). The plasma levels of β-endorphin were used to measure the output of the study assessed both before treatment and posttreatment. There are statistically significant differences in the mean plasma levels of β-endorphin before and after treatment in the laserpuncture group: changes in mean value from 0.22±0.06 ng/ml to 0.29±0.07 ng/ml with a p value = 0.005 (p < 0.05). There were no statistically significant differences in the mean plasma levels of β-endorphin before and after treatment in the laserpuncture placebo group: changes in mean value from 0.22±0.06 ng/ml to 0.26±0.09 ng/ml with p value = 0.195 (p > 0.05). Between groups, there was not a statistically significant difference in the baseline mean plasma levels of β-endorphin (p = 0.183, p > 0.05). The conclusion of this study is that laserpuncture can affect the plasma levels of β-endorphin in healthy subjects when there is no statistically significant difference in the mean plasma levels of β-endorphin between groups.

Electroacupuncture effect at the LI 4 Hegu point on the plasma β-endorphin level of healthy subjects

As a therapy modality, acupuncture is becoming popular for treating diseases. Nevertheless, the acupuncture mechanism of action remains unclear until now. Some studies suggest that acupuncture works by stimulating the β-endorphin release, whereas other studies show the opposite. This study aims to determine whether electro acupuncture at the LI 4 Hegu point could increase the plasma β-endorphin level as a basic of acupuncture mechanism of action. Thirty-six healthy subjects were involved and divided randomly into two groups, namely, intervention (n=18) and control (n=18). In the intervention group, electroacupuncture was applied at the LI 4 Hegu point with a low frequency for 30 min. In the control group, sham electroacupuncture was applied at a non-acupoint for 30 min. The plasma β-endorphin was examined before and after intervention using the ELISA method. A significant difference was found between the intervention and control groups in increasing the plasma β-endorphin level (9(50%) vs. 1(5.6%); p = 0.009). A significant difference was also observed in the plasma β-endorphin level after intervention between the two groups (35.1±3.4 vs. 10.3±1.8; p=0.003). Electroacupuncture at the LI 4 Hegu point was found to increase the plasma β-endorphin level in healthy subjects.

Cerebrospinal fluid and plasma β-endorphin levels in children with cerebral malaria.

ObjectivesCerebral malaria (CM) is the most lethal form of malaria, yet its pathogenesis is not fully understood. Cytoadherence, sequestration, alterations in cytokine expression, inflammation, and microvascular obstruction are all hypothesized to be important in the aetio‐pathogenesis of coma which characterizes cerebral malaria and the death which sometimes result. Beta (β)‐endorphin has been postulated to be involved in the pathogenetic processes of inflammation and cytokine expression, although the exact role is unknown. The aim of this study was to determine the levels of β‐endorphin in cerebrospinal fluid (CSF) and plasma of children with CM and compare the levels of β‐endorphin in the plasma of children with CM with that of apparently healthy age‐ and sex‐matched controls at Ile‐Ife, Nigeria.Materials and MethodsAdditional to the standard investigation for CM, CSF and venous blood samples were obtained from the subjects for the determination of β‐endorphin levels.ResultsForty children with CM were studied along with forty age‐ and sex‐matched controls. The mean CSF β‐endorphin (± SD) level for the children with CM was 1.8 ± 0.9 pmol/L. The mean plasma β‐endorphin levels at admission (3.1 ± 2.0 pmol/L) and discharge (4.1 ± 3.3 pmol/L) were higher in children with CM than in the control subjects (2.7 ± 0.7 pmol/L). However, only the mean plasma β‐endorphin levels at discharge was significantly higher than that of controls (p = .012).ConclusionChildren with CM had higher mean plasma β‐endorphin levels compared to the controls and there was increased production of β‐endorphins in children with CM during the course of the illness.

Do Resting Plasma β-Endorphin Levels Predict Responses to Opioid Analgesics?

Clinically feasible predictors of opioid analgesic responses for use in precision pain medicine protocols are needed. This study evaluated whether resting plasma β-endorphin (BE) levels predicted responses to an opioid analgesic, and whether chronic pain status or sex moderated these effects. Participants included 73 individuals with chronic low back pain (CLBP) and 88 pain-free controls, all using no daily opioid analgesics. Participants attended 2 identical laboratory sessions during which they received either intravenous morphine (0.08 mg/kg) or saline placebo, with blood samples obtained before drug administration to assay resting plasma BE levels. Once peak drug activity was achieved in each session, participants engaged in an ischemic forearm pain task (ISC) and a heat pain task. Morphine analgesic effects were derived reflecting the difference in pain outcomes between placebo and morphine conditions. In hierarchical regressions, significant Type (CLBP vs. control)×BE interactions (Ps<0.05) were noted for morphine effects on ISC tolerance, ISC intratask pain ratings, and thermal VAS unpleasantness ratings. These interactions derived primarily from associations between higher BE levels and smaller morphine effects restricted to the CLBP subgroup. All other BE-related effects, including sex interactions, for predicting morphine analgesia failed to reach statistical significance. BE was a predictor of morphine analgesia for only 3 out of 9 outcomes examined, with these effects moderated by chronic pain status but not sex. On the whole, results do not suggest that resting plasma BE levels are likely to be a clinically useful predictor of opioid analgesic responses.