beta-endorphin and Anorexia

This review summarizes recent work that focuses on the role of endogenous opioids (EOs) and opiate receptors in the control of food intake. Although the anorexic effect of opiate antagonists are now well accepted, the exact EO, site(s), and mechanism(s) of action remain to be established. However, accumulating evidence suggests that dynorphin, an endogenous ligand for kappa-type opiate receptors, is an important regulator (stimulant) of appetite. The roles of other EOs, such as beta-endorphin, are less clear. EOs appear to be involved in maintaining normal feeding behavior and are likely responsible for the overconsumption of fat in genetically obese and stressed subjects. Opiate antagonists block overconsumption of palatable foods, thus offering a promising approach to weight reduction for some overweight individuals. Anorexias may follow from a deficiency of kappa-type opioid activity, and surprisingly, can also result from excess opioid activity. Indeed, opiate antagonists of the mu type (naloxone) can enhance eating and weight gain in certain anorexic conditions. Therefore, it appears that excess opioid agonist activity may result in hyperphagia or anorexia (depending on the opiate receptor type). Finally, opiate antagonists may help normalize both types of pathological feeding states.

Topics: Animals; Anorexia; Appetite Regulation; beta-Endorphin; Dynorphins; Endorphins; Feeding and Eating Disorders; Food Preferences; Humans; Models, Biological; Narcotic Antagonists; Receptors, Opioid; Stress, Physiological

The purpose of this study was to investigate whether serum β-endorpin and neuropeptide Y were associated with changes in levels of thyroid hormones in children suffering from anorexia. One hundred and five anorexic children admitted to Xianning City Central Hospital, China, from August 2019 to July 2021, were selected as case group, while 105 normal children were selected as normal control group. Serum β-endorpin and neuropeptide Y levels in the case group were lower than those in the normal control group (both p<0.001), and serum triiodothyronine and thyroxine levels were also lower (both p<0.001). Serum β-endorpin and neuropeptide Y levels in the case group were positively correlated with triiodothyronine and thyroxine. There is a reduced level of serum β-endorpin, neuropeptide Y, and thyroid hormones in anorexic children, and it is possible that they are connected and work together in regulating ingestion.

Topics: Anorexia; beta-Endorphin; Child; Humans; Neuropeptide Y; Thyroid Hormones; Thyrotropin; Thyroxine; Triiodothyronine

Anorexia nervosa (AN) is a debilitating eating disorder characterized by severely restricted eating and significant body weight loss. In addition, many individuals also report engaging in excessive exercise. Previous research using the activity-based anorexia (ABA) model has implicated the hypothalamic proopiomelanocortin (POMC) system. Using the ABA model,

Topics: Animals; Anorexia; Arcuate Nucleus of Hypothalamus; beta-Endorphin; Body Weight; Food; Hypothalamus; Mice; Neurons; Pro-Opiomelanocortin

Anorexia nervosa (AN) has a lifetime prevalence of up to 4% and a high mortality rate (~5-10%), yet little is known regarding the etiology of this disease. In an attempt to fill the gaps in knowledge, activity-based anorexia (ABA) in rodents has been a widely used model as it mimics several key features of AN including severely restricted food intake and excessive exercise. Using this model, a role for the hypothalamic proopiomelanocortin (POMC) system has been implicated in the development of ABA as Pomc mRNA is elevated in female rats undergoing the ABA paradigm. Since the Pomc gene product α-MSH potently inhibits food intake, it could be that elevated α-MSH might promote ABA. However, the α-MSH receptor antagonist SHU9119 does not protect against the development of ABA. Interestingly, it has also been shown that female mice lacking the mu opioid receptor (MOR), the primary receptor activated by the Pomc-gene-derived opioid β-endorphin, display blunted food anticipatory behavior (FAA), a key feature of ABA. Thus, we hypothesized that the elevation in Pomc mRNA observed during ABA may lead to increased β-endorphin concentrations and MOR activation to promote ABA. Further, given the known sex differences in AN and ABA, we hypothesized that MORs may contribute differentially in male and female mice. Using wild-type and MOR knockout mice of both sexes, a MOR antagonist and careful analysis of food anticipatory behavior and β-endorphin levels, we found 1) increased Pomc mRNA levels in both female and male mice that underwent ABA, 2) increased β-endorphin in female mice that underwent ABA, and 3) blunted FAA in both sexes in response to MOR genetic deletion yet blunted FAA only in males in response to MOR antagonism. The results presented provide support for both hypotheses and suggest that it may be the β-endorphin resulting from increased Pomc transcription that supports the development of some features of ABA.

Topics: Animals; Anorexia; beta-Endorphin; Female; Hypothalamus; Male; Mice; Physical Conditioning, Animal; Pro-Opiomelanocortin; Receptors, Opioid, mu

Pro-opiomelanocortin (POMC) neurons in the hypothalamus are direct targets of peripheral satiety signals, such as leptin and insulin in mammals. The stimulation of these signals activates hypothalamic POMC neurons and elevates POMC-derived melanocortin peptides that inhibit food intake in mammals. On the other hand, it has been recognized that beta-endorphin, a post-translational processing of POMC, acts in an autoreceptor manner to the micro-opioid receptor (MOR) on POMC neurons, diminishing POMC neuronal activity in mammals. Recently, we found that central insulin functions as an anorexic peptide in chicks. Thus, the present study was done to elucidate whether beta-endorphin affects the activation of POMC neurons by insulin in neonatal chicks. Consequently, quantitative real-time PCR analysis shows that intracerebroventricular (ICV) injection of insulin with beta-endorphin significantly decreases brain POMC mRNA expression when compared with insulin alone. In addition, co-injection of MOR agonist (beta-endorphin or [d-Ala2, N-MePhe4, Gly5-ol]-enkephalin (DAMGO)) significantly attenuates insulin-induced hypophagia in chicks. These data suggest that beta-endorphin regulates the activity of the central melanocortin system, and its activation may provide an inhibitory feedback mechanism in the brain of neonatal chicks.

Topics: Animals; Animals, Newborn; Anorexia; beta-Endorphin; Chickens; Dose-Response Relationship, Drug; Drug Interactions; Eating; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; Gene Expression Regulation; Hypoglycemic Agents; Injections, Intraventricular; Insulin; Neurotransmitter Agents; Pro-Opiomelanocortin; Time Factors

Fasting attenuates disease-associated anorexia, but the mechanisms underlying this effect are not well understood. In the present study, we investigated the extent to which a 48 h fast alters hypothalamic neuronal activity in response to the anorectic effects of lipopolysaccharide in rats. Male rats were fed ad libitum or fasted, and were injected with i.p. saline or lipopolysaccharide (250 microg/kg). Immunohistochemistry for Fos protein was used to visualize neuronal activity in response to lipopolysaccharide within selected hypothalamic feeding regulatory nuclei. Additionally, food intake, body weight, plasma interleukin-1 and leptin levels, and the expression of mRNA for appetite-related neuropeptides (neuropeptide Y, proopiomelanocortin and cocaine-amphetamine-regulated transcript) were measured in a time-related manner. Our data show that the pattern of lipopolysaccharide-induced Fos expression was similar in most hypothalamic nuclei whatever the feeding status. However, we observed that fasting significantly reduced lipopolysaccharide-induced Fos expression in the paraventricular nucleus, in association with an attenuated lipopolysaccharide-induced anorexia and body weight loss. Moreover, lipopolysaccharide reduced fasting-induced Fos expression in the perifornical area of the lateral hypothalamus. Lipopolysaccharide-induced circulating levels of interleukin-1 were similar across feeding status. Finally, fasting, but not lipopolysaccharide, affected circulating level of leptin and appetite-related neuropeptides expression in the arcuate nucleus. Together, our data show that fasting modulates lipopolysaccharide-induced anorexia and body weight loss in association with neural changes in specific hypothalamic nuclei.

Topics: Animals; Anorexia; Behavior, Animal; beta-Endorphin; Body Weight; Cell Count; DNA-Binding Proteins; Eating; Enzyme-Linked Immunosorbent Assay; Feeding Behavior; Food Deprivation; Gene Expression Regulation; Hypothalamus; Immunohistochemistry; In Situ Hybridization; Interleukin-1; Interleukin-1beta; Leptin; Lipopolysaccharides; Male; Nerve Tissue Proteins; Neurons; Neuropeptide Y; Oncogene Proteins v-fos; Peptide Fragments; Pro-Opiomelanocortin; Rats; Rats, Wistar; STAT3 Transcription Factor; Time Factors; Trans-Activators

To study the role of cholecystokinin octapeptide (CCK-8),beta endorphin (beta EP), and gastrin in an anorexic infantile rat model and no subsequent regulation of nose peptides by the Yunpi complex prescription ErBao Granule.. We fed infantile rats with special prepared forage. A liquid extract of ErBao Granule was administered to the rats daily for 3 weeks, CCK-8, beta-EP, and gastrin concentrations in hypothalamus, gastric antrum, and plasma of the rats were measured by radioimmunoassay, and were compared with controls.. Treatment of rats with ErBao Granule inhibited CCK-8 secretion and increased beta-EP and gastrin secretion. CCK-8 concentration in hypothalamus and plasma of model control group increased significantly and correlated negatively with food intake of models, respectively. beta-EP concentration in gastric antrum and plasma of model control group decreased significantly and showed a positive correlation with food intake of models, respectively. Hypothalamus concentration of beta-EP was similar in models and controls. Gastrin concentration in gastric antrum of models was lower than in the blank control group, and correlated positively to food intake of models. Finally, CCK-8 concentrations in plasma of rats showed a positive correlation with plasma beta-EP (r=-0.68, P<0.05).. The increased plasma and hypothalamus concentration of CCK-8, decreased gastric antrum and plasma level of beta-EP, and decreased gastric antrum concentration of gastrin are associated significantly with the anorexia of infantile anorexic rat models produced by special for-age. ErBao Granule can reverse these changes, which may be the major mechanisms of ErBao Granule simulating feeding.

Topics: Animals; Anorexia; beta-Endorphin; Diet; Female; Gastrins; Hypothalamus; Male; Models, Animal; Pyloric Antrum; Rats; Rats, Sprague-Dawley; Sincalide

To study the regulatory effect of Erbao granules (EBG) on central and peripheral brain-gut peptide in juvenile animal model of anorexia.. Juvenile rat model of anorexia was established by imitating the major cause of infantile anorexia and treated with EBG. The cholocystokinin-octapeptide (CCK-8) and beta-endorphin (beta-EP) concentration in hypothalamus, antrum pyloricum and peripheral blood were examined by radioimmunoassay.. CCK-8 concentration in hypothalamus and plasma in the model rats increased (P < 0.05), while blood beta-EP concentration decreased (P < 0.05). After EBG treatment, the CCK-8 concentration normalized and beta-EP increased significantly.. EBG could reduce the central and peripheral CCK-8 and increase beta-EP secretion significantly in the juvenile anorexia model.

Topics: Animals; Anorexia; beta-Endorphin; Disease Models, Animal; Drugs, Chinese Herbal; Female; Gastric Mucosa; Hypothalamus; Male; Rats; Rats, Sprague-Dawley; Sincalide

Plasma and cerebrospinal fluid (CSF) concentrations of three well-known satiety neuropeptides, cholecystokinin (CCK), somatostatin and calcitonin gene-related peptide (CGRP), along with two powerful orexigenic neuropeptides, neuropeptide Y (NPY) and beta-endorphin have been measured in elderly persons with idiopathic anorexia and normal weight healthy subjects in a similar age range. Plasma and CSF immunoreactivity levels of the two main fractions of CCK (CCK8s and CCK33) after being separated by HPLC were measured by a radioimmunoassay (RIA) developed in our laboratory, whereas the other neuropeptides were assayed by commercially available RIA kits. Elderly underweight anorectic patients had significantly lower levels of beta-endorphin but increased concentrations of NPY in both plasma and CSF when compared to controls. In addition to significantly higher levels of CCK8s but not CCK33 in plasma, we found a trend to higher CSF concentrations of CCK8s and a positive correlation between the body mass index and either beta-endorphin (r = 0.58, P < 0.05) or CCK8s (r = 0.69, P < 0.01) concentrations in CSF in the anorectic group. CSF somatostatin concentrations were decreased significantly, but plasma somatostatin levels and plasma and CSF concentrations of CGRP were similar in senile anorectics and controls. Treatment of five anorectic patients with megestrol acetate, 480 mg daily for 6 months, reversed only the decrease in CSF beta-endorphin levels but did not normalize the body weight or the fat body mass. On the basis of our findings, we hypothesize that a decrease in CSF beta-endorphin concentration along with a rise in plasma levels of CCK8s might be accounted for the primary anorexia of aging.

Topics: Aged; Aged, 80 and over; Aging; Anorexia; beta-Endorphin; Calcitonin Gene-Related Peptide; Cholecystokinin; Female; Humans; Male; Middle Aged; Neuropeptide Y; Neuropeptides; Somatostatin