beta-endorphin and Weight-Loss

Individual responses to weight loss (WL) medications vary widely and prediction of response remains elusive.. We investigated biomarkers associated with use of lorcaserin (LOR), a 5HT2cR agonist that targets proopiomelanocortin (POMC) neurons that regulate energy and glucose homeostasis, to identify predictors of clinical efficacy.. Thirty individuals with obesity were treated with 7 days of placebo and LOR in a randomized crossover study. Nineteen participants continued on LOR for 6 months. Cerebrospinal fluid (CSF) POMC peptide measurements were used to identify potential biomarkers that predict WL. Insulin, leptin, and food intake during a meal were also studied.. LOR induced a significant decrease in CSF levels of the POMC prohormone and an increase in its processed peptide β-endorphin after 7 days; β-endorphin/POMC increased by 30% (P < .001). This was accompanied by a substantial decrease in insulin, glucose, and homeostasis model assessment of insulin resistance before WL. Changes in CSF POMC peptides persisted after WL (6.9%) at 6 months that were distinct from prior reports after diet alone. Changes in POMC, food intake, or other hormones did not predict WL. However, baseline CSF POMC correlated negatively with WL (P = .07) and a cutoff level of CSF POMC was identified that predicted more than 10% WL.. Our results provide evidence that LOR affects the brain melanocortin system in humans and that effectiveness is increased in individuals with lower melanocortin activity. Furthermore, early changes in CSF POMC parallel WL-independent improvements in glycemic indexes. Thus, assessment of melanocortin activity could provide a way to personalize pharmacotherapy of obesity with 5HT2cR agonists.

Topics: beta-Endorphin; Cross-Over Studies; Glucose; Humans; Insulin; Melanocortins; Obesity; Pro-Opiomelanocortin; Weight Loss

This study aims to investigate the role of changes in leptin and beta endorphin (BE) levels in weight loss following electroacupuncture (EA) application in obesity treatment. EA was applied to 20 females who were 41.45 +/- 4.71 years old and had a body mass index of 36.00 +/- 2.66; and a diet program was applied to 20 females who were 42.30 +/- 4.35 years old and had a body mass index of 34.90 +/- 3.21. There was a 4.5% weight reduction in the patients with EA application, whereas patients on diet restriction had a 3.1% weight reduction. A decrease of loss of body weight was observed in the EA group (p < 0.000) when compared against the diet restricted group. A decrease of serum leptin levels (p < 0.000) and an increase in the serum BE (p < 0.05) levels were observed in the EA group compared to the diet restricted group. In this study, reduced serum leptin levels paralleling to weight loss were observed in the EA group. Furthermore, it is thought that in the EA applied group, increasing serum BE level probably enhanced the lipolitic activity which may have caused weight loss in obese people by mobilizing energy stores. It may be considered that the EA application with diet restriction in obesity treatment is more effective than the diet restriction alone.

Topics: Adult; beta-Endorphin; Body Mass Index; Diet, Reducing; Electroacupuncture; Female; Humans; Leptin; Obesity; Weight Loss

Levels of beta-endorphin, FSH, LH, PRL, cortisol and estradiol in blood serum were measured in 20 girls with weight loss related amenorrhoea. Serum beta-endorphin levels were also measured in a group of 15 young, regularly menstruating healthy girls (control group). Levels of beta-endorphin were significantly lower in examined group than in control one. Serum levels of FSH, LH, estradiol were low. Serum levels of PRL and cortisol were normal. These observations suggest, that beta-endorphin is involved in the pathogenesis of weight loss related amenorrhoea.

Topics: Adolescent; Adult; Amenorrhea; beta-Endorphin; Estradiol; Female; Gonadotropins; Hormones; Humans; Hydrocortisone; Prolactin; Weight Loss

Catch-up weight gain after malnutrition is a risk factor for metabolic syndrome. Here we show that social isolation enhanced fasting-induced weight loss and suppressed weight gain induced by re-feeding for 6 days following a 24-h fast in prepubertal wild-type mice. These effects of social isolation on weight gain were not associated with significant changes in daily average food consumption. Under the same housing condition, genetic deletion of beta-endorphin reduced the fasting-induced weight loss and enhanced the re-feeding-induced weight gain in prepubertal mice. These effects of social isolation or genetic deletion of beta-endorphin on these weight changes were attenuated and reversed in postpubertal mice. Moreover, genetic deletion of beta-endorphin attenuated these effects of social isolation on the catch-up weight gain in prepubertal mice and reversed them in postpubertal mice. Thus, social isolation, endogenous beta-endorphin, and age can be novel modulators for body weight changes induced by fasting and re-feeding in mice.

Topics: Age Factors; Animals; beta-Endorphin; Fasting; Male; Mice; Mice, Mutant Strains; Social Isolation; Weight Loss

The associations between serum beta-endorphin levels and clinical and metabolic variables as well as beta-endorphin changes after surgically induced weight loss were investigated in 43 morbidly obese patients. A significant positive correlation between beta-endorphin and body weight, degree of body weight increase and ACTH was found preoperatively. Only body weight was independently associated with beta-endorphin levels. Twelve months following vertical banded gastroplasty, there was an extensive weight loss in all patients and improvement in their metabolic profile. A significant reduction in beta-endorphin levels which was proportional to the extent of weight loss was also observed.

Topics: Adrenocorticotropic Hormone; Adult; beta-Endorphin; Female; Gastroplasty; Humans; Lipids; Male; Obesity, Morbid; Time Factors; Weight Loss

beta-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 beta-endorphin, insulin, and glucose responsiveness in morbidly obese patients and the effect of surgically induced weight loss.. Thirty-two healthy, nondiabetic, morbidly obese patients (body mass index over 40 kg/m2) and 32 normal-weight controls were studied. Serum levels of beta-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.. Preoperative basal levels of beta-endorphin, insulin, and glucose and their responses during OGTT in obese patients were significantly higher compared with those of controls. After surgery, basal beta-endorphin, insulin, and glucose levels decreased significantly compared with preoperative values. Postoperative basal insulin and glucose levels were similar to those in controls, while beta-endorphin levels remained significantly higher than those of controls. A significant reduction in total responses of beta-endorphin, insulin, and glucose during OGTT was also observed; however, postoperative beta-endorphin and insulin responses remained significantly higher than in controls.. Morbidly obese patients have an increased glucose-stimulated response of beta-endorphin, insulin, and glucose which is partially corrected with weight loss following vertical banded gastroplasty.

Topics: Adult; beta-Endorphin; Blood Glucose; Case-Control Studies; Female; Gastroplasty; Glucose Tolerance Test; Humans; Insulin; Male; Obesity, Morbid; Time Factors; Weight Loss

This study was undertaken to investigate the effects of melanocortins and opioids on rat early postnatal body and organ growth. Among melanocortins tested desacetyl-alpha-melanocyte-stimulating hormone (alpha-MSH) at dosages of 0.3 and 3 micrograms/g/day was effective in stimulating neonatal growth with a weight gain of 7 and 5.6%, respectively, after 2 weeks of treatment. Likewise, a weight rise of 4.2 and 3% was obtained with 3 micrograms/g/day of both alpha-MSH and Nle4-D-Phe7 alpha-MSH. As far as opioids were concerned, while N-acetyl-beta-endorphin (beta-End) was ineffective, the activity of beta-End was dependent on dosage. Indeed, newborns treated with 0.03 microgram/g/day showed a slight, but significant, increase in weight, whereas a marked decrease in growth followed treatment with 0.3 and, mainly, 3 micrograms/g/day, with a final weight loss of 3.4 and 5.5%, respectively. All melanocortins exerted a positive action on muscular and brain trophism and, in addition, desacetyl-alpha-MSH also induced a rise of fat deposits. On the contrary, while the 0.03 microgram/g/day beta-End dose caused an increase in muscular and brain weight, the higher dosages of the opioid were detrimental, not only for muscle and brain, but also for both liver and spleen weight. A slight, although significant (P < 0.05), enhancement of serum dehydroepiandrosterone sulfate (DHEAS) level was found after the injection of 0.3 microgram/g desacetyl-alpha-MSH, whereas both the 0.3 and 3 micrograms/g doses of desacetyl-alpha-MSH and the 3 micrograms/g dose of alpha-MSH determined the rise of plasma androstenedione (P < 0.05). All tested melanocortins and opioids failed to modify the concentrations of corticosterone. Our results suggest that melanocortins and opioids can modulate early postnatal growth in rats either by direct or indirect mechanisms.

Topics: Adipose Tissue; alpha-MSH; Animals; beta-Endorphin; Body Weight; Brain; Dose-Response Relationship, Drug; Growth; Liver; Muscle, Skeletal; Organ Size; Rats; Spleen; Weight Gain; Weight Loss

Abnormalities in plasma concentrations of beta-endorphin-like immunoreactivity (beta-endorphin) have been reported in depressed patients. This study was done to test the hypothesis that specific clinical characteristics of depression are associated with plasma beta-endorphin concentration.. Plasma beta-endorphin was evaluated in 20 depressed patients diagnosed according to DSM-III-R and in 23 age- and sex-matched comparison subjects, and each was evaluated with the structured Schedule for Affective Disorders and Schizophrenia (SADS). Twelve SADS items involving dysphoric mood and related symptoms were chosen for analysis.. Within the group of all 43 subjects and within the depressed group, beta-endorphin level correlated significantly with psychic anxiety and with phobia. In the depressed group only, beta-endorphin also correlated significantly with obsessions/compulsions. Concentration of beta-endorphin was not significantly correlated with score on the Hamilton Rating Scale for Depression or Beck Depression Inventory or with scores on other SADS symptom items, including somatic anxiety, insomnia, subjective anger, overt anger, agitation, psychomotor retardation, panic attacks, appetite loss, or total weight loss. In the group of 23 comparison subjects, beta-endorphin did not correlate with Beck or Hamilton depression score or with any of the SADS clinical variables.. High levels of plasma beta-endorphin may be associated with more severe anxiety, phobia, and obsessions/compulsions in depressed patients.

Topics: Adult; Aged; Anger; Anxiety Disorders; beta-Endorphin; Depressive Disorder; Feeding and Eating Disorders; Humans; Male; Middle Aged; Obsessive-Compulsive Disorder; Phobic Disorders; Psychiatric Status Rating Scales; Psychomotor Disorders; Severity of Illness Index; Sleep Initiation and Maintenance Disorders; Weight Loss

To test the hypothesis that the hyperendorphinaemia in obesity originates from outside the pituitary.. Intravenous administration of corticotrophin-releasing hormone (CRH) after overnight suppression with 2 mg of dexamethasone in normal-weight controls and in obese subjects before and after weight reduction.. Eleven obese females, age (mean +/- SEM) 30 +/- 2.1 years, body mass index (BMI) 41.2 +/- 1.9 kg/m2. Eight normal-weight females served as controls, age 26 +/- 2.1 years, BMI 21.4 +/- 0.5 kg/m2. Five obese subjects were also studied after weight loss of 18.4 +/- 1.0% of original weight.. Plasma beta-endorphin, ACTH and cortisol. Cortisol production rate in 24-hour urine. Basal (without dexamethasone suppression) plasma beta-endorphin levels.. Basal (without dexamethasone suppression) beta-endorphin levels were 7.7 +/- 0.8 pmol/l in the obese and 3.8 +/- 0.5 pmol/l in the control subjects (P less than 0.005). The degree of suppression of beta-endorphin after dexamethasone was similar in the obese (23.2 +/- 3.7%) and in the control subjects (28.2 +/- 0.12%). Administration of CRH following dexamethasone suppression resulted in a small but significant increase of plasma beta-endorphin in both obese (from 1.55 +/- 0.12 to 2.32 +/- 0.28 pmol/l) and control subjects (from 0.98 +/- 0.24 to 1.69 +/- 0.33 pmol/l). The groups did not differ regarding this response, nor regarding the release of ACTH and cortisol after CRH. Cortisol production rate was higher (P less than 0.001) in the obese (68.7 +/- 3.3 mumol/24 h) than in the controls (40.0 +/- 3.0 mumol/24 h). No correlation between cortisol production rate and basal beta-endorphin levels was found. Weight loss appeared to have no influence on cortisol production rate, basal beta-endorphin levels, or on the responses to dexamethasone or CRH.. Plasma beta-endorphin in obese subjects can be affected by manipulations of the hypothalamic-pituitary-adrenocortical axis; the hypothesis that the hyperendorphinaemia of obesity originates from outside the pituitary cannot be confirmed.

Topics: Adult; beta-Endorphin; Corticotropin-Releasing Hormone; Dexamethasone; Female; Humans; Hypothalamo-Hypophyseal System; Obesity; Pituitary-Adrenal System; Weight Loss

Beta-endorphin (beta-Ep) plasma levels are higher in obese patients than in normal subjects. To establish that this finding constitutes hyperendorphinemia, 28 obese patients aged 12-55 years, six males and 22 females, (weighing 61-117 kg) were investigated twice by an overnight 1-mg p.o. dose dexamethasone suppression test (DST) before and after weight loss. beta-Ep was measured by radioimmunoassay (RIA). Before body weight loss, beta-Ep was higher than normal and unresponsive to DST, whereas ACTH and cortisol were suppressible. After weight loss, beta-Ep was slightly reduced but still insensitive to DST. ACTH and cortisol were responsive as usual. Findings suggest a resistance to DST in obesity as far as beta-Ep is concerned. The disorder persists even after weight loss, indicating that hyperendorphinemia is not secondary to body weight excess. Accordingly, one can argue that the unresponsiveness of the endorphinergic system to its physiological feedback is a pathophysiological characteristic of obesity.

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; beta-Endorphin; Body Weight; Dexamethasone; Feedback; Female; Humans; Hydrocortisone; Male; Middle Aged; Obesity; Radioimmunoassay; Weight Loss

It is speculated that endogenous opioid peptides are involved in glucose metabolism and that their homeostasis might be disturbed in obesity. Despite a different response of the pancreatic beta-cells after beta-endorphin and naloxone injections between obese patients and normal weight controls, there is little knowledge concerning the direct influence of a glucose load on beta-endorphin plasma levels, especially with respect to various nutrition states. During exploration of this topic we gained further insight on the difference of basal beta-endorphin plasma levels between normal and overweight persons. We compared beta-endorphin plasma levels during an oral glucose load in 60 obese, non-diabetic patients and in 20 normal weight controls. We also studied 40 of the obese patients after a weight reduction of 2.1 kg/m2. The following results were obtained: (1) Normal weight females have significantly lower (P less than 0.05) basal beta-endorphin levels compared to the male controls. This difference in gender is abolished in obesity where female and male patients do not differ in basal beta-endorphin plasma levels. Therefore, the difference between normal and overweight persons in beta-endorphin plasma levels was restricted to the subgroup of females. We suppose that former neglect of this difference in gender explains most of the so far reported discrepant results. (2) During the oral glucose tolerance test the beta-endorphin plasma values remained constant in the obese group. Despite improved insulin sensitivity after weight reduction there was still no change of beta-endorphin plasma levels both during the OGTT and when compared to the values before weight reduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; beta-Endorphin; Blood Glucose; Female; Glucose; Glucose Tolerance Test; Humans; Insulin; Insulin Resistance; Male; Middle Aged; Obesity; Sex Characteristics; Weight Loss

In order to clarify a possible relationship between opioid peptides and glucose homeostasis in obesity we studied Beta-Endorphin (B-Ep), ACTH, cortisol and insulin plasma levels in response to an oral glucose tolerance test (OGTT) in 8 subjects after a hypocaloric diet for 90 days. We obtained through this treatment a weight loss superior to 30% of the initial weight excess (WE) compared with ideal body weight. Moreover, we compared the obtained results with our preliminary study that was performed with the same protocol but without caloric restriction. B-Ep was measured by RIA after silicic acid extraction and G75 Sephadex column chromatography. ACTH, insulin and cortisol were measured directly on plasma by an RIA method. Basal and during OGTT-induced levels of glucose, insulin, ACTH and cortisol decreased in comparison with the values obtained before diet. Conversely, B-Ep remained higher than normal both in the basal condition and during OGTT, and showed values consistently similar to those before diet. These data show that hyperinsulinemia is corrected by weight loss, while hyperbetaendorphinemia remains unchanged. Accordingly, it can be suggested that no direct relationship occurs between hyper-B-Ep-hyper-IRI in obesity. A further insight into the role of hyper-B-Ep in obesity is, thus, necessary, assuming as hypothesis that the increase in B-Ep may be a cause and not a corollary of the polymorphic aspects of obesity.

Topics: Adrenocorticotropic Hormone; Adult; beta-Endorphin; Blood Glucose; Female; Glucose Tolerance Test; Homeostasis; Humans; Hydrocortisone; Insulin; Middle Aged; Obesity; Radioimmunoassay; Weight Loss