Plasma Β-endorphin Research Articles

Effects of glucose infusion on the endocrine, metabolic and cardiorespiratory responses to halothane anaesthesia of ponies

Glucose was infused intravenously into six ponies during halothane anaesthesia, to evaluate its effect on their endocrine response to anaesthesia. The ponies were premedicated with acepromazine, and anaesthesia was induced...

Effect of TCM on plasma β-endorphin and placental endocrine in threatened abortion

To explore the effect of TCM on plasma beta-endorphin (beta-EP) and placental endocrine function in patients of threatened abortions (TA). Changes of plasma beta-EP, gonadotrophin releasing hormone (GnRH), human chorionic gonadotrophin (HCG), progesterone (P4) levels were measured with RIA in 40 cases of TA with a history of recurrent spontaneous abortion treated with Chinese herbal medicine for reinforcing Kidney and Qi, hemostasis and antiabortion. And the results were compared with those of normal early pregnant women and patients with incomplete abortion as control. The plasma beta-EP level in TA was significantly higher than that in normal pregnant women, P < 0.01. On the contrary, plasma GnRH, HCG and P4 were obviously lower in TA as compared with those of the normal cases, P < 0.01. After treatment, 36 of the 40 patients succeeded in the continuity of pregnancy, their symptoms of TA disappeared, and the above-mentioned four criteria measured at 10-12th week of gestation were similar to those of normal cases, P > 0.05. TCM treatment can regulate plasma beta-EP and placental endocrine function in threatened abortion.

Effects of age and maternal reactivity on the stress response of the pituitary-adrenocortical axis and the sympathetic nervous system in neonatal pigs

AbstractThe study was conducted to investigate the adreno cortical capacity after injection of ACTH and the sensitivity of the pituitary and the adrenal to immobilization in neonatal pigs at different ages. Furthermore, the endocrine reactivity of the offspring was compared with the stress reactivity of their mothers. Four piglets were selected from each of six different litters and subjected to an immobilization test and an adrenal function test using synthetic ACTH1-24 at the ages of 7, 21 and 35 days; the six sows were also subjected to restraint and an ACTH stimulation test. Plasma β-endorphin, norepinephrine and epinephrine concentrations were measured in blood samples taken 2 min after restraint and cortisol concentrations were measured 60 min after ACTH administration. A highly sensitive adrenal response was demonstrated in both sows and piglets and adrenal reactivity showed also a considerable consistency over time within sows. In neonatal pigs, the cortisol response to ACTH was greatest on day 7 and decreased up to day 35. Plasma epinephrine and norepinephrine levels after the 2-min immobilization were also higher at day 7 compared with the other ages (P &lt; 0·01). Piglets from sows, classified as high reacting according to their cortisol or epinephrine response, also showed significantly higher cortisol levels after ACTH challenge at all ages and significantly higher epinephrine levels after restraint at day 7 than piglets from low reacting sows. The results show an age-related change of pituitary-adrenocortical and sympatho-adrenomedullary responses in neonatal pigs and an absence of a stress hyporesponsive period at all ages studied. The results also indicate different levels of excitability in the offspring depending on the maternal stress reactivity.

Effects of handling, shearing and previous exposure to shearing on cortisol and β-endorphin responses in ewes

The objectives of the study were to compare the effects of handling and shearing on plasma cortisol and β-endorphin levels of ewes and to determine if adaptation to annual shearing occurred. Plasma cortisol and β-endorphin concentrations were determined during either handling only or handling plus shearing in 12 ewes previously exposed to annual shearing (1–4 times) and in 12 naïve ewes. The handling process consisted of four steps: 1) moving ewes from their quarters into the shearing room; 2) moving them in groups of four into a holding pen; 3) moving them in pairs to a shearing platform where they were up-ended and restrained as in shearing; and 4) moving them into another holding pen in the shearing room. Half of the ewes were sheared during step 3 of the handling process. Handling and shearing elevated (P &lt; 0.0001) plasma cortisol and β-endorphin concentrations, but the responses to the handling process and to the handling plus shearing process were similar (P &gt; 0.1). Moving the ewes from their quarters to the shearing platform resulted in significantly higher plasma cortisol, which remained elevated for 60 min. Plasma β-endorphin was only transiently elevated after shearing was completed. Previous exposure to shearing enhanced the cortisol (P &lt; 0.001) and β-endorphin (P &lt; 0.05) responses to handling and shearing. Both responses were significantly greater and longer in the ewes sheared previously. The results indicate that the stress response to handling was equivalent to that of handling plus shearing, and that the stress response was much greater in ewes previously exposed to annual shearing. Key words: Cortisol, β-endorphin, negative adaptation, shearing, stress, ewes

The effect of intraventricularly administered GnRH on plasma β-endorphin levels of the rat

This study investigates the effects of intraventricularly administered gonadotropin-releasing hormone (GnRH) on plasma β-endorphin levels in female proestrous rats.Adult female Wistar rats (220-250 g) were implanted with an indwelling cannula in the third ventricle. Approximately 20 days later, the animals which had established a regular 4-day cycle were implanted with two indwelling catheters, one intracarotid and one intra-jugular, on the morning of proestrus. A single injection of 100 ng GnRH dissolved in 5 μl distilled water or 5 μl of saline (control) was infused slowly through the cannula in the third ventricle. Blood was withdrawn via the intracarotid catheter just before the infusion (12.30 h) andat 14.00, 15.30, 16.30 and 17.30 h for the determination of plasma β-endorphin levels.The results indicated that intracerebroventricular infusion of GnRH causes a significant decline of plasma β-endorphin levels at all time points. It is postulated that GnRH possibly causes desensitization of GnRH receptors, due to the continuous GnRH supply to the pituitary via the blood circulation.

Repressive/defensive coping, endogenous opioids and health: how a life so perfect can make you sick

Hyperactivity of endogenous opioid systems has been postulated to mediate the associations between defensive/repressive coping styles, enhanced stress responsivity, and reduced immunocompetence. Study 1 examined whether repressive/defensive coping would be associated with greater sensitivity to opioid antagonism. Judgments of the painfulness of ascending series of electrocutaneous stimulation applied to the forearm were determined before and after the administration of naloxone and placebo in 38 men and 42 women. All subjects were healthy with a mean age of 32.9 years. Naloxone (10 mg i.v.) and placebo were administered in double-blind fashion and counterbalanced. Subjects were classified as High- and Low-defensive and repressive copers on the basis of scores on the Marlowe—Crowne Social Desirability Scale and the Balanced Inventory of Desirable Responding, respectively. High Self-Deception was associated with naloxone-induced hyperalgesia, whereas no effects of naloxone on pain ratings were observed in low-Self-Deceptive subjects. In Study 2, resting plasma β-endorphin levels were found to be positively correlated with defensiveness in men ( n = 26), but not women ( n = 44). Study 3 examined 82 healthy subjects (mean age = 28.7 years). β-Endorphin/defensiveness correlations were found to be greater following, compared to prior to, electrical nociceptive stimulation in men ( n = 49), but unrelated in women ( n = 33). These findings are consistent with the hypothesized endorphinergic dysregulation associated with repressive/defensive coping styles and are discussed in terms of the immuno-regulatory implications of such a dysregulation.

Endocrine ,neuroendocrine and behavioral effects of oral dehydroepiandrosterone sulfate supplementation in postmenopausal women

Aging in women and men is characterized by a progressive decline of circulating dehydroepiandrosterone (DHEA) levels and its sulfate ester (DHEAS). The improvement of wellbeing described in postmenopausal women treated with DHEA suggests that this steroid may exert specific actions on the central nervous system (CNS). The postmenopausal period is associated with several neuroendocrine modifications. The decrease of circulating levels of β-endorphin is considered a hormonal marker of those changes. The aim of the present study was to investigate neuroendocrine and behavioral effects of three months of DHEAS supplementation in postmenopausal women.Postmenopausal women (n = 22) were divided in three groups: the first group was treated with oral DHEAS (n = 8) (50 mg/day) ,the second treated with the same dose of oral DHEAS + transdermal estradiol (n = 8) (DHEAS) 50 mg/day ,estradiol 50 μg/patch) and the third with transdermal estradiol alone (n = 6) (50 μg/day). Before and after 1 ,2 and 3 months of therapy ,the following circulating steroid and protein hormone levels were evaluated: DHEA ,DHEAS ,androstenedione ,testosterone ,estrone ,estradiol ,17-hydroxyprogesterone ,sex hormone-binding globulin (SHBG) ,follicle-stimulating hormone (FSH) ,luteinizing hormone (LH) ,β-endorphin ,growth hormone (GH) and Cortisol ,and a Kupperman score was performed. Before and after treatments ,plasma β-endorphin levels were evaluated in response to three neuroendocrine tests: (a) clonidine ,an a2-presynaptic adrenergic agonist (1.25 mg IV); (b) naloxone ,an opioid receptor antagonist (4 mg IV) and (c) fluoxetine ,a serotonin selective reuptake inhibitor (30 mg PO).In both groups of women treated with DHEAS ,mean basal serum DHEA ,DHEAS ,androstenedione ,and testosterone levels significantly increased after treatment ,while no changes were shown in the group receiving estradiol alone. Serum estradiol ,estrone ,GH and plasma β-endorphin levels significantly increased progressively for the three months of treatment ,with higher levels for estrone and estradiol in subjects receiving estradiol alone or plus DHEAS. Serum SHBG ,Cortisol ,and 17-hydroxyprogesterone did not show significant variations under any treatment. Serum LH and FSH levels showed a significant decrease in groups treated with estradiol alone or plus DHEAS at the second and third months. The Kupperman score showed that all treatments were associated with similar and progressive improvement. Before therapy clonidine ,naloxone and fluoxetine stimuli failed to modify circulating β-endorphin levels. After each of the treatments ,the β-endorphin response was completely restored and was similar ,independent of the kind of therapy.Restoration of the β-endorphin response to specific stimuli suggests that DHEAS and/or its active metabolites modulates the neuroendocrine control of pituitary β-endorphin secretion ,which may support the therapeutic efficacy of the DHEAS on behavioral symptoms.

Role of endogenous opioids in syncope induced by head-up tilt test and its relationship with isoproterenol-dependent and isoproterenol-independent neurally-mediated syncope

This study was designed to evaluate the role of endogenous opioids in neurally-mediated syncope. Head-up tilt test was performed on 35 patients with syncope of unknown origin. Plasma β-endorphin was measured (1) at baseline, (2) at the end of tilt test or at time of syncope, (3) 15 min before isoproterenol-test, (4) at the end of the isoproterenol-test or at time of syncope. Subjects with a positive tilt testing showed a larger rise in plasma β-endorphin concentrations at time of syncope (baseline 13.7±8.0 vs. syncope 41.4±26.4 pmol l −1; P<0.01). On the contrary, patients with a positive isoproterenol-test showed no rise in plasma β-endorphin levels (baseline 7.9±3.6 vs. syncope 7.4±2.7 pmol l −1; P=ns). Patients with a passive negative tilt test (baseline 6.7±2.8 vs. end of test 7.0±3.3 pmol l −1; P=ns) and negative isoproterenol tilt test (baseline 7.4±3.8 vs. end of test 8.1±3.4 pmol l −1; P=ns) showed no changes in β-endorphin concentrations. To further examine the efficacy of i.v. naloxone to prevent syncope, 10 patients were randomized to naloxone (0.02 mg/kg) or placebo. Second head-up tilt testing was negative in 1/5 patients with naloxone and in 2/5 patients with placebo. We conclude that, (1) endogenous opioids seem to be involved in vasovagal syncope induced by baseline head-up tilt test, (2) changes in plasma β-endorphin concentrations show significant differences between patients who have isoproterenol-dependent and isoproterenol-independent syncope, this finding might occur in the setting of different pathophysiologic mechanisms, and (3) intravenous naloxone at a dose of 0.02 mg/kg was not superior to placebo in order to prevent positive responses to baseline tilt test.

Physiological correlates associated with cribbing behaviour in horses: changes in thermal threshold, heart rate, plasma beta-endorphin and serotonin.

The aim of the present study was to obtain information on the possible mechanisms underlying cribbing behaviour in horses. To investigate the horse's responsiveness to an external stimulus, a device for telemetric measurement of thermal threshold, using the forelimb withdrawal reflex, was developed and validated. Measurements of thermal threshold took place in cribbing horses (n = 11) before and during cribbing periods. Heart rate was monitored continuously in the same horses. Blood samples were collected before and during cribbing periods as well and in age- and sex-matched control horses (n = 11). beta-endorphin and cortisol were determined in plasma using radioimmunoassay techniques, serotonin was analysed by high performance liquid chromatography. Compared with basal values, thermal threshold was significantly (P = 0.003) lower during cribbing periods. The mean difference was 4.9 degrees C. Heart rate decreased significantly (P = 0.026) and showed a mean reduction of 2.4 beats/min during cribbing. Given the fact that arousal usually is associated with an increase in nociceptive threshold and in heart rate, the decrease in both during cribbing provide evidence that cribbing may reduce stress. Cribbers showed 3 times higher basal beta-endorphin levels than controls (mean 49.5 vs. 16.2 pmol/l, P = 0.006) and there was a trend for lower basal serotonin levels (mean 201.5 vs. 414.3 nmol/l, P = 0.07). These data indicate differences in cribber's endogenous opioid and serotonergic systems.

Repressive and defensive coping styles predict resting plasma endorphin levels in the elderly

Jamner, L.D., Schwartz, G.E., 1986, Psychosom. Med. 48, 211–223, have proposed that repressive and defensive coping are associated with greater central endogenous opioid activity. They reasoned that high-defensive (HD) participants’ attenuated distress, increased pain tolerances, attenuated somatic symptomatology, and accentuated reports of positive emotions are consistent with actions of centrally active opioid peptides. The present study assessed plasma β-endorphin (END) levels, Marlowe–Crowne Social Desirability Scale (MCSD), and Taylor Manifest Anxiety Scale (TMAS) scores in men ( n=6) and women ( n=20) between the ages of 59 and 79. Contrary to predictions, HD had lower plasma endorphin levels than did low-defensive (LD) participants. Raw MCSD scores correlated negatively with endorphin levels. Findings were significant for women only, which may have been due to the small sample of men. The results are discussed as they related to the hypothesis that defensiveness involves alteration of central opioid systems.

The relationship between plasma β-endorphin levels and severity of depression

Accumulating evidences suggest that Toll-like receptors (TLRs) were involved in the pathophysiology of major depressive disorder. TLR4 was thought to be associated with major depressive disorder in animal model, but the others were still unknown. In order to examine TLR1-9 mRNA expression levels in peripheral blood and their relationships with the psychopathology of major depressive disorder, 30 patients with major depressive disorder were compared with 29 healthy controls. The 17-item Hamilton Depression Rating Scale (HAMD-17) was used to assess the severity of major depression. The mRNA expression levels of TLRs were examined in parallel with a housekeeping gene using real-time polymerase chain reaction (RT-PCR). Analysis of covariance with age and body mass index adjustment revealed a significantly higher expression of TLR3, 4, 5 and 7 mRNA but lower expression of TLR1 and 6 in patients with major depressive disorder as compared with healthy controls. Multiple linear regression analysis revealed that TLR4 was an independent risk factor relating to severity of major depression. These findings suggest that TLRs, especially TLR4, may be involved in the psychopathology of major depression.

Oscillatory effects of repeated morphine on shock‐induced hypoalgesia and β‐endorphin

Recent research indicates that the sensitization that results from repeated drug or non-drug stress exposure may develop into a pattern of alternating increases and decreases (i.e., oscillation) in response to each subsequent stressor exposure. Oscillation, with or without prior sensitization, has been observed for a number of drug and non-drug stressors, and for various neurochemical and endocrine endpoints. The present studies investigated whether oscillation also occurs in the behavioral and endocrine effects of repeated morphine treatment and if a drug that normalizes the mood swings of bipolar disorder in humans will also attenuate drug oscillation in this animal model. In the first experiment, rats were given 1–5 pretreatments with morphine (15 mg/kg, i.p.), separated by 1-week intervals with the last injection occurring 1 hour prior to being tested for stressor-induced (i.e., 5 seconds, 2-mA electric footshock) hypoalgesia, as measured by latency to paw-lift or jump from a hot-plate. Plasma β-endorphin also was measured. The second experiment replicated the behavioral findings of the first study and, in addition, assessed the effect of continuous lithium chloride, in the drinking water, on morphine-induced oscillation. Caffeine was used as a partial control for the lithium. The results were that one injection of morphine enhanced stress-induced hypoalgesia and subsequent morphine administrations resulted in oscillation. β-endorphin exhibited sensitization but not oscillation, suggesting that it did not mediate oscillation of the behavioral response. In addition, lithium, but not caffeine, eliminated oscillations of the behavioral response without affecting its initial enhancement. Synapse 30:30–37, 1998. © 1998 Wiley-Liss, Inc.

Extent of ischemic stimulus and plasma β-endorphin levels in silent myocardial ischemia

Background β-Endorphin has been reported to play a role in the mechanism of silent myocardial ischemia. Objectives Plasma β-endorphin levels during coronary angioplasty–induced silent and symptomatic myocardial ischemia were compared with those during exercise-induced silent ischemia. Methods and Results The study population consisted of 40 nondiabetic patients with angioplasty-indicated coronary artery disease. All patients underwent exercise treadmill testing 2 to 4 days before angioplasty. Patients were divided into three groups: group 1, 10 patients with silent ischemia during exercise and angioplasty; group 2, 15 patients with silent ischemia during exercise and symptomatic ischemia during angioplasty; and group 3, 15 patients with symptomatic ischemia during both exercise and angioplasty. In group 1, plasma β-endorphin levels during balloon inflation were significantly higher than in groups 2 and 3 and also significantly higher than during exercise. In group 2, plasma β-endorphin levels were significantly elevated at exercise-induced silent myocardial ischemia and balloon-induced symptomatic myocardial ischemia, but the levels between exercise and balloon inflation were not significantly different. Conclusions For "silent" myocardial ischemia, it may be necessary for β-endorphin levels to increase to sufficiently high levels to suppress anginal symptoms in response to the degree of ischemic stimuli. (Am Heart J 1998;135:813-8.)

Effects of stress resulting from short-term restraint on in vitro functional capacity of leukocytes obtained from pigs

Abstract Objective To investigate whether the procedure used to snare and restrain pigs during collection of blood samples would alter in vitro functional capacity of leukocytes in the samples. Animals 8 gilts. Procedure Catheters were surgically inserted into the jugular vein of gilts to enable blood sample collection without restraint. After collection of a control sample, gilts were restrained by use of a snare and samples were collected at 0.5, 3.5, and 6.5 minutes after start of restraint (0 minutes). At each time point, plasma β-endorphin and cortisol concentrations as well as WBC counts were recorded, and functional capacity of leukocytes in cultures of whole blood was assessed by means of mitogen-induced proliferation and interleukin-2 activity, virus-induced interferon-α concentration, and phagocytosis of zymosan particles. Results Concentrations of plasma β-endorphin and cortisol were increased at 3.5 and 6.5 minutes after start of restraint. At these times, virus-induced interferon-α concentration was decreased, whereas proliferative response to Concanavalin A and phytohemagglutinin increased in samples collected at 6.5 minutes. Conclusion and Clinical Relevance It was possible to snare pigs for the purpose of collecting blood samples and restrain them without causing excessive stress that would affect immunologic variables, provided that the collection procedure was completed within a few minutes. (Am J Vet Res 1998;59:421–425)

Metabolism of β-endorphin in plasma studied by liquid chromatography–electrospray ionization mass spectrometry

Degradation of synthetic human β-endorphin by a human plasma proteinase was studied with high-performance liquid chromatography in combination with mass spectrometry. The peptide was metabolized at a rate of 25 pmol/min to the major fragments β-endorphin (1–19) and (20–31), the latter reported as a potent inhibitor of morphine- and β-endorphin-induced analgesia in mice. The proteinase responsible for this process was classified as a metal-dependent serine proteinase and was effectively inactivated by phenylmethylsulfonyl fluoride and ethylenediaminetetraacetic acid. Identification of the products formed during the enzymatic reaction was performed by liquid chromatography on-line with electrospray mass spectrometry, using a reversed-phase or a novel size-exclusion column capable of separating molecules between 0.1–7 kilodaltons. Peptide sequences were verified by tandem mass spectrometry experiments. The conversion of β-endorphin may have physiological implications in the mechanism of pain. The obtained data suggest that several precautions should be considered during recovery and measurement of β-endorphin in plasma by immunological techniques. The applied strategy may also be useful for studying metabolism of various peptidergic compounds with potential pharmacological significance.

Characterization of immunoreactive dynorphin B and β-endorphin in human plasma

Dynorphins and β-endorphin in human plasma were characterized and studied quantitatively using radioimmunoassay, high-performance liquid chromatography (HPLC), and mass spectrometry. Most immunoreactive (ir) dynorphin B and β-endorphin in human plasma coeluted with authentic peptides in analysis. Dynorphin A was not detected. Added to human plasma it was rapidly converted into Leu-enkephalin-Arg 6 followed by elimination of the C-terminal arginine after prolonged incubation. The rate of dynorphin A conversion was estimated at 40 pmol/min/μl plasma. This process was inhibited by the thiol protease inhibitor, PHMB and by EDTA. Dynorphin B, α-neoendorphin and big dynorphin were virtually not metabolized by plasma proteases under the same conditions. β-endorphin was processed into β-endorphin(1–19) and the corresponding C-terminal counterpart β-endorphin(20–31) at a rate of about 25 pmol/min/μl of plasma. Based on the above data, a reliable strategy was established to measure dynorphin B- and β-endorphin-ir in human plasma samples. The basal levels in a male control group were 0.99 ± 0.11 ( n = 11) and 16.3 ± 1.5 ( n = 11) fmol/ml plasma, respectively.

Plasma β-Endorphins as an Indicator of Pain in Response to Care of Thermally-Degraded Tissue

Plasma β-Endorphins as an Indicator of Pain in Response to Care of Thermally-Degraded Tissue

Characteristics of the Proopiomelanocortin System in the Outdoor-Bred Domestic Gander: II. Seasonal and Circadian Rhythmicity; Effect of Ether Stress and Lipopolysaccharide Administration

The responsiveness of the POMC system to exogenous stimuli and the diurnal and seasonal rhythmicity of ACTH and β-endorphin (βE) in plasma were studied in outdoor-reared domestic ganders. Plasma levels of ACTH- and βE-like immunoreactivities were determined by direct and specific radioimmunoassays. In the first series of experiments immunoreactive (ir) ACTH and βE were measured in the plasma of male domestic geese after 5 min of ether stress and after administration of 2 μg/kg lipopolysaccharide (LPS). Both ir-ACTH and ir-βE levels increased 5 and 10 min after ether inhalation, but the increase in the ir-βE concentration was only half that of the ir-ACTH. The plasma ir-ACTH levels were elevated after 60 and 120 min but not after 90 min of LPS administration; ir-βE levels were unchanged at all time points. In a second series of experiments blood samples were taken on 30 March, 16 June, 4 August, and 27 October. On these days diurnal samplings were performed at 02:00, 06:00, 10:00, 14:00, 18:00, and 22:00 h. A two-way analysis of variance showed significant diurnal and seasonal changes for both hormones and significant interaction between the diurnal and seasonal levels. The highest daily mean values of the plasma ir-ACTH and ir-βE concentrations were measured in June. The maximum of the ir-ACTH level was at 10:00 h in March and August, but at 22:00 h in June and October. The changes in ir-βE concentrations paralleled those of ir-ACTH, but the changes did not reach statistical significance in every case.

Neuroendocrine effect of a short-term treatment with DHEA in postmenopausal women

Objectives: A progressive decline of plasma dehydroepiandrosterone (DHEA) levels occurs in women during aging related to the reduction of adrenocortical secretion. A specific action of DHEA on the central nervous system (CNS) is suggested by the improvement of psychological and physical well-being in postmenopausal women after DHEA supplementation. The aim of the present study was to investigate the neuroendocrine effects of short-term DHEA supplementation in postmenopausal women, evaluating changes of plasma β-endorphin ( β-EP) and growth hormone (GH) before and after oral DHEA (100 mg/day) for 7 days in postmenopausal women ( n=6). Methods: Before and after 7 days of DHEA supplementation, postmenopausal women underwent a neuroendocrine test with clonidine, an α2 presinaptic agonist for adrenergic system, (1.25 mg i.v.). Basal plasma DHEA, androstenedione (A), testosterone (T), estrone (E 1) and estradiol (E 2) levels were evaluated before and after treatment, while plasma β-EP and GH levels were measured before and 15, 30, 45, 60 and 90 min after clonidine injection. Results: Basal plasma β-EP and GH levels did not show a significant difference before and after short-term DHEA administration, while circulating A, T, E 1 and E 2 significantly increased after treatment. The clonidine test induced a significant increase of plasma β-EP levels in women after receiving DHEA supplementation but not before; conversely, plasma GH levels increased both before and after treatment. Conclusions: The present study indicates that short-term DHEA supplementation in postmenopausal women is able to restore the impaired response of pituitary β-EP to clonidine, an α2 presinaptic agonist. According to these data it is possible to hypothesize that DHEA could play a role in the psychological and physical well-being of postmenopausal women acting via a restoration of neuroendocrine control of antero-pituitary β-EP secretion.

Beta-endorphin response to oral glucose tolerance test in obese and non-obese pre- and postmenopausal women

Beta-endorphin (β-EP) is a neuropeptide involved in several brain functions, regulating the reproductive axis and behavioral changes. Estrogens play a modulatory role on circulating levels of β-EP in women. Previous clinical studies have demonstrated high plasma β-EP levels in obese subjects and increased β-EP release after an oral glucose tolerance test (OGTT) in normal or obese women. The aim of the present study was to evaluate plasma β-endorphin levels in response to an OGTT in pre-and postmenopausal obese and non-obese women, in order to investigate if the decrease in gonadal steroid levels at menopause could modify in a different manner the control of β-endorphin release in response to glucose administration. A group of 24 normal women (age range 45—55 years) were included in the study. The patients were subdivided in four groups of six subjects each: group A, premenopausal women with body mass index (BMI) < 25 (control); group B, premenopausal women with BMI > 25 (obese); group C, postmenopausal women with BMI < 25 (control); group D, postmenopausal women with BMI> 25 (obese). All women were studied between 8.30 and 9.00 am, after overnight fasting, and underwent an OGTT. In obese premenopausal women, basal plasma β-EP levels were significantly higher than in non-obese women (p < 0.01). In postmenopausal women, regardless of body weight, low basal plasma β-EP levels were found. A significant increase in plasma β-EP levels, at 30 and 60 minutes after oral glucose ingestion, was shown in control premenopausal women. No significant modifications to OGTT were shown in plasma β-EP levels in the other three groups of women. In conclusion, while in premenopausal women the response of plasma β-EP levels to OGTT is maintained, in postmenopause there is a lack of response to OGTT. This suggests that β-EP release is dependent upon gonadal steroids, while it is only in part influenced by body weight.