Serum Levels Of Β-endorphin Research Articles

Beta-Endorphin and Oxytocin in Patients with Alcohol Use Disorder and Comorbid Depression.

Background: The neuropeptides β-endorphin and oxytocin are released into the bloodstream as hormones from the pituitary gland but also have an important function as neuroregulators in the forebrain. The blood levels of both polypeptides have been shown to reflect depressive symptoms. β-Endorphin, in particular, is also involved in abstinence from alcohol. Methods: The serum levels of β-endorphin and oxytocin were measured during the early withdrawal phase in patients with alcohol use disorder (AUD) with (N = 35) or without (N = 45) depressive comorbidity and compared with those in healthy volunteers (N = 23). In addition to comparing the groups, the study examined whether serum levels correlated with various psychometric measures of dependence, depression and aggression, as well as with clinical characteristics of dependence. Results: Both serum levels of beta-endorphin and oxytocin were significantly lower in patients than those in healthy controls (p = 0.011 for β-endorphin and p = 0.005 for oxytocin, Kruskal–Wallis test). In patients with depressive comorbidity, the significance was greatest (p = 0.005 for β-endorphin and p = 0.004 for oxytocin, U-test). There was no correlation with clinical or psychometric parameters (p > 0.05, Spearman test), but beta-endorphin levels did correlate significantly with physical aggression (p = 0.026, Spearman test). Conclusions: Serum levels of β-endorphin and oxytocin are lower in patients with AUD, particularly in those with depressive comorbidity. β-Endorphin levels correlated with physical aggression according to the Buss–Durkee (BDHI) estimates.

β-endorphin and opioid growth factor as biomarkers of physical ability in multiple sclerosis

BackgroundMultiple sclerosis (MS) is an autoimmune-mediated degenerative disorder with increased peripheral inflammation disrupting the blood brain barrier. With increasing MS-related healthcare costs, the requirement to validate minimally invasive biomarkers has become imperative. MethodsRelapsing-remitting MS patients on disease modifying therapies were consented at the Penn State Health MS Clinic to provide blood samples for analyses of serum cytokines and endogenous opioid peptides, as well as to complete the MSQOL-54 survey. ResultsSerum OGF levels in MS patients on glatiramer acetate (mean = 326 pg/ml), dimethyl fumarate (mean = 193.3 pg/ml) and natalizumab (mean = 393.4 pg/ml) were significantly elevated (p < 0.01) compared to healthy controls (mean = 98.46 pg/ml). Individuals with elevated OGF levels also had increased levels of TNFα (r = 0.78) and IL-17A (r = 0.81). Only patients treated with glatiramer acetate had significant (p < 0.01) elevations in serum β-endorphin levels. Analyses of MS-QoL 54 data showed no significant differences in physical or mental composite scores between treatment groups. However, serum levels of β-endorphin had a direct correlation with physical health composite score (r = 0.70) in all treatments. Serum vitamin D levels had an indirect relationship with 25-foot walk test times (r = 0.47). ConclusionBoth regression and cohort data suggest that serum levels of OGF, β-endorphin, and vitamin D are potential biomarkers for physical disease status in MS.

Clinical signs, diagnosis and complex treatment of temporomandibular joint osteoarthritis

Aim. To improve complex treatment of temporomandibular joint osteoarthritis. Methods. 45 patients with temporomandibular joint osteoarthritis aged 18-75 years were examined. The main group consisted of 25 patients who were treated using transcranial electric stimulation. Comparison group consisted of 20 patients in whom standard treatment was applied. Control group consisted of 10 healthy volunteers and was used to compare blood cytokine and β-endorphin levels. Clinical examination, computed tomography, immunological blood analysis were performed in all patients. Results. After the complex treatment all the symptoms resolved, and the position of mandibular condyles in mandibular fossae of the temporal bone and results of immunological blood analysis normalized. The baseline level of β-endorphin of patients with temporomandibular joint osteoarthritis did not differ from control group. After transcranial electric stimulation β-endorphin serum levels were significantly raised at day 6 and especially at day 9, while in patients with standard treatment the β-endorphin serum levels were only slightly higher compared to baseline levels. Decrease of interleukin-6 serum levels was more significant in the transcranial electric stimulation group. Transcranial electric stimulation has also leaded to elevation of interleukin-10 serum levels up to normal ranges at day 9, compared to low level (5 times below normal range) at all times in the standard treatment group. After 2 years of treatment there was no symptoms of the disease, normal ranges of motion in temporomandibular joints and no relapses registered in 24 out of 25 patients from transcranial electric stimulation group compared to 11 out of 20 patients from standard treatment group. In 1 patient from transcranial electric stimulation group and 9 patients from standard treatment group clicking on the involved side was still present, those patients were re-treated. Conclusion. Usage of transcranial electric stimulation as a component of complex treatment of patients with temporomandibular joint osteoarthritis increases the effectiveness of their treatment.

Neurotensin is increased in serum of young children with autistic disorder

Autism spectrum disorders (ASD) are a group of pervasive neurodevelopmental disorders diagnosed in early childhood. They are associated with a set of "core symptoms" that include disabilities in social interaction skills, verbal and non-verbal communication, as well as repetitive and stereotypic behaviors. There is no definite pathogenetic mechanism or diagnostic tests. Many children with ASD also have "allergic-like" symptoms, but test negative implying mast cell activation by non-allergic triggers. We measured by Milliplex arrays serum levels of 3 neuropeptides that could stimulate mast cells in children with autistic disorder (n = 19; 16 males and 3 females; mean age 3.0 ± 0.4 years) and healthy, unrelated controls (n = 16; 13 males and 3 females; mean age 3 ± 1.2 years). Only neurotensin (NT) was significantly increased from 60.5 ± 6.0 pg/ml in controls to 105.6 ± 12.4 pg/ml in autistic disorder (p = 0.004). There was no statistically significant difference in the serum levels of β-endorphin or substance P (SP). NT could stimulate immune cells, especially mast cells, and/or have direct effects on brain inflammation and ASD.

Naltrexone Protects Against Hypotension, Hyperthermia, and β-Endorphin Overproduction During Heatstroke in the Rat

Heat stroke is characterized by hyperthermia, arterial hypotension, decreased baroreflex sensitivity, and increased serum levels of β-endorphin. Whereas naltrexone may have therapeutic potential in heat stroke, the underlying mechanism remains unclear. We tested the hypothesis that naltrexone may attenuate heat stroke by reducing hyperthermia, hypotension, decreased baroreceptor sensitivity, and/or increased serum levels of β-endorphin. Heat stroke was induced by exposing the anesthetized adult Sprague-Dawley rats in an incubator at 43°C. The moment in which the mean arterial pressure dropped irreversibly from the peak level was taken as the onset of heat stroke. Control rats were exposed to 24°C. Mean arterial pressure, baroreceptor sensitivity, and maximal reflex bradycardia, after the onset of heat stroke, were all significantly lower than in control rats. However, rectal temperature and serum levels of β-endorphin were all greater after the onset of heat stroke. Intravenous delivery of naltrexone (10 mg/kg) 20 min before the initiation of heat stress, but not immediately at the onset of heat stroke, significantly attenuated the above-mentioned reactions. Accordingly, naltrexone improved survival during heat stroke. These results suggest that naltrexone protects against hypotension and decrement of both baroreceptor sensitivity and maximal reflex bradycardia during heat stroke by reducing both hyperthermia and increment of serum β-endorphin and thus improves survival.

Serum β-endorphin level in patients with depression on fluvoxamine

The main interest of the present study was to determine possible alterations in β-endorphin serum levels in healthy volunteers and in patients with depression, as well as changes in β-endorphin serum levels caused by fluvoxamine treatment. Fluvoxamine maleate (Fevarin®) was administered orally at a dose of 200 mg/day for 4 weeks. The serum levels of β-endorphin were lower in patients with ‘nonendogenous’ depression (104.68±5.29 pg/ml) and those with ‘endogenous’ depression (36.34±2.23 pg/ml) than in healthy volunteers (125.19±1.64 pg/ml). The endogenously depressed patients had significantly lower β-endorphin levels than the nonendogenous patients. A 4-week treatment of fluvoxamine (200 mg/day) caused a statistically significant increase in β-endorphin serum levels in all patients (nonendogenous depression 132.10±2.38 pg/ml and endogenous depression 50.09±2.45 pg/ml) in comparison to values found before the onset of the therapy. The efficacy of fluvoxamine was 11.0 (±9.0) evaluated by the Hamilton Rating Scale for Depression (HAMD) in the patients with a diagnosis of depression. These results indicate that determination of β-endorphin serum levels could be a valuable laboratory test in the diagnosis of depression.

The Effect of Vertical Banded Gastroplasty on Glucose-Induced β-Endorphin Response

Background.β-Endorphin is an endogenous opioid involved in the regulation of food intake and obesity as well as in insulin metabolism. In this study, we investigated glucose-induced β-endorphin, insulin, and glucose responsiveness in morbidly obese patients and the effect of surgically induced weight loss.Methods.Thirty-two healthy, nondiabetic, morbidly obese patients (body mass index over 40 kg/m2) and 32 normal-weight controls were studied. Serum levels of β-endorphin, insulin, and glucose were measured under basal conditions and during an oral glucose tolerance test (OGTT) before and 12 months following vertical banded gastroplasty.Results.Preoperative basal levels of β-endorphin, insulin, and glucose and their responses during OGTT in obese patients were significantly higher compared with those of controls. After surgery, basal β-endorphin, insulin, and glucose levels decreased significantly compared with preoperative values. Postoperative basal insulin and glucose levels were similar to those in controls, while β-endorphin levels remained significantly higher than those of controls. A significant reduction in total responses of β-endorphin, insulin, and glucose during OGTT was also observed; however, postoperative β-endorphin and insulin responses remained significantly higher than in controls.Conclusion.Morbidly obese patients have an increased glucose-stimulated response of β-endorphin, insulin, and glucose which is partially corrected with weight loss following vertical banded gastroplasty.

β-Endorphin in Multiple Trauma Victims

In animals and in humans, stress is known to be accompanied by increased beta-endorphin secretion. Blood samples from 47 patients in a state of stress induced by multiple trauma were assessed for beta-endorphin concentration by radioimmunoassays. We show that there is a clearcut correlation (Spearman's R = 0.72, P = 2.1 x 10(-6) between the level of consciousness evaluated with the Glasgow score and levels of circulating beta-endorphin. In addition, beta-endorphin levels are higher than normal in patients with Glasgow coma with scores higher than seven, and lower than normal in those with Glasgow coma scores of seven or less. Finally, in the complete absence of stress (shown by the lack of brain activity in six irreversible coma patients), there is a severe drop in the level of circulating beta-endorphin. beta-endorphin serum levels correlate with the state of consciousness of multiple trauma patients.

Raised β-endorphin serum levels in children with atopic dermatitis and pruritus

Atopic dermatits (AD) is a pruritic cutaneous inflammatory condition. As pruritus and pain are very close symptoms, we determined the β-endorphin serum concentrations in 21 atopic children with pruritus (group A) and 20 children with healed AD without pruritus (group B). Twenty-five healthy school children were the control group. The β-endorphin serum concentrations (14.95 ± 2.75 pmol/l) in group A were statistically ( P < 0.001) elevated in our patients compared to controls (8.85 ± 2.39 pmol/l) whereas these in group B were not elevated (9.4 ± 2.46 pmol/l). We suggest that the elevated β-endorphin concentrations in atopic patients with pruritus confirm the hypothesis that there is an increased activity of their opioid system and that an opioid antagonist might block itching which is their major clinical symptom.

Physiology of β-endorphins. A close-up view and a review of the literature

When an endogenous morphine, β-endorphin was discovered ten years ago, the fact that this morphine is present in the brain and many other tissues suggested to neurobiologists that these peptide opiates play a role which goes beyond that of a simple modulator of the perception of pain. β-endorphin is a neurohormone which is secreted by the pituitary gland and reaches all tissues present in the body by diffusion. Many laboratories have investigated variations in serum levels of β-endorphin under widely varying physiological or pathological conditions. Many references to these studies in the literature have thus demonstrated that β-endorphins play a role in certain behavioural patterns (stress, alcoholism), in obesity, diabetes and psychiatric diseases. In fact, the activity of β-endorphins would appear to have an interesting role to play and are a promising feature in the treatment of cerebral aging; in this field, β-endorphins act not only as neuroregulators of other neurotransmitting substances but also, via calcium channels, exert an effect on the walls of cerebral arterioles. In situ, the role of β-endorphins at the ionic channel level has been studied using the patch-clamp technique. In 1991, E Neher and B Sakmann received the Nobel Medicine and Physiology Prize for this work. β-endorphin, which may be the “missing link” between the neuron and the wall of the arteriole, must be considered as being a fundamental neurotransmitter in the same way as well-known substances such as noradrenaline, acetylcholine, serotonin, dopamine and the GABAergic system are also neurotransmitters.

Increase of beta-endorphin serum levels by human corticotropin-releasing factor does not affect beta-cell function in overweight women.

Numerous studies have shown a rise of blood sugar concentrations and serum levels of pancreatic polypeptides after pharmacological doses of beta-endorphin. We tested the yet unknown influence of physiological fluctuations in beta-endorphin serum levels on glucose homeostasis by stimulating the pituitary secretion with CRF. 100 micrograms of human CRF or saline solution were intravenously injected in ten healthy male subjects at least one week apart. beta-endorphin serum levels rose significantly after the injection of CRF, but there was no change in blood sugar concentrations or serum levels of glucagon or insulin at all. We conclude that only a pharmacological dose of beta-endorphin influences glucose homeostasis.

Increase of β-Endorphin Serum Levels by Human Corticotropin-Releasing Factor does not Affect Beta-Cell Function in Normalweight Men

Numerous studies have shown a rise of blood sugar concentrations and serum levels of pancreatic polypeptides after pharmacological doses of beta-endorphin. We tested the yet unknown influence of physiological fluctuations in beta-endorphin serum levels on glucose homeostasis by stimulating the pituitary secretion with CRF. 100 micrograms of human CRF or saline solution were intravenously injected in ten healthy male subjects at least one week apart. beta-endorphin serum levels rose significantly after the injection of CRF, but there was no change in blood sugar concentrations or serum levels of glucagon or insulin at all. We conclude that only a pharmacological dose of beta-endorphin influences glucose homeostasis.

Endocrine effects of the cold pressor test: Relationships to subjective pain appraisal and coping

Blood was drawn from 14 normal volunteers twice before, immediately after a 1-minute immersion of the nondominant hand in ice water (cold pressor test), and twice during recovery. Serum levels of β-endorphin, cortisol, prolactin, growth hormone, and opioid activity were determined, and measures of subjective pain appraisal and coping styles were obtained. Cortisol was the only variable to show a significant increase as a function of noxious stimulation. Correlational analysis yielded relationships between neuroendocrine variables and subjective pain appraisal as well as coping styles, suggesting complex interactions between neuroendocrine and psychological processes in human pain.