beta-endorphin and Diabetes-Mellitus

Topics: Analgesia; Animals; Asthma; beta-Endorphin; Diabetes Mellitus; Endorphins; Enkephalins; Epilepsy; Humans; Mental Disorders; Pituitary Hormones, Anterior; Receptors, Opioid; Tissue Distribution

Chlorpropamide-alcohol flushing may be due to sensitivity to endogenous opiates. To investigate this possibility the plasma met-enkephalin and beta-endorphin responses to sherry with and without chlorpropamide were studied in six patients with non-insulin dependent diabetes and in six normal subjects. After chlorpropamide all patients showed a rise in met-enkephalin concentrations from a basal level of 50 +/- 7.2 ng/l to a peak of 75 +/- 8.1 ng/l (p less than 0.001). In contrast, before chlorpropamide treatment was started met-enkephalin values did not change after alcohol. No significant changes in beta-endorphin values were observed. In six normal subjects pretreated with chlorpropamide the met-enkephalin concentration also rose from a basal level of 72 +/- 15 ng/l to a peak of 103 +/- 9.4 ng/l (p less than 0.002). Again, the met-enkephalin rise was not observed after placebo. Neither beta-endorphin concentrations nor facial temperature changed significantly. These data suggest that endogenous opiates may be implicated in CPAF. Furthermore, this is the first study in which a significant change in circulating met-enkephalin values has occurred.

Topics: beta-Endorphin; Chlorpropamide; Diabetes Mellitus; Double-Blind Method; Drug Interactions; Endorphins; Enkephalin, Methionine; Enkephalins; Erythema; Face; Female; Humans; Male; Wine

It has been reported that neuropeptides may play a role in the control of appetite and in the mechanism of hormone release. Neuropeptides such as beta-endorphin, neuropeptide Y (NPY), galanin and leptin may affect hormones release, on the other hand the hormonal status may modulate neuropeptide activity.. The material consisted of 90 obese women, 30 women with Anorexia Nervosa, and 30 healthy, lean women of control group. Plasma beta-endorphin, NPY, leptin, somatostatin and serum pituitary and gonadal hormones concentrations were measured with RIA methods.. We observed the highest plasma NPY levels in obese hypertensive and diabetic patients. After carbohydrate administration (OGTT) a marked increase of insulin, beta-endorphin and NPY was found. The blunted response of GH to GH-RH may be connected with increased somatostatin activity and hyperinsulinemia. The abnormal response of LH to opioid blockade may be a result of disturbed opioid and NPY activities in obese patients. However in patients with anorexia nervosa, plasma leptin and NPY concentrations were low. The disturbances in beta-endorphin release are also observed.. The neuroendocrine disturbances in obesity and in anorexia nervosa are opposite. The feedback mechanism between leptin and NPY is disturbed in both in obesity and in anorexia nervosa. An abnormal activity of neuropeptides may lead to disturbed control of appetite and hormonal dysregulation in eating disorders.

Topics: Adult; Anorexia Nervosa; Appetite; beta-Endorphin; Diabetes Mellitus; Feedback, Physiological; Female; Glucose Tolerance Test; Human Growth Hormone; Humans; Hypertension; Leptin; Luteinizing Hormone; Neuropeptide Y; Neuropeptides; Obesity; Somatostatin

Specific binding sites for [125I]beta-endorphin and the delta1-opioid [3H][D-pen(2), D-pen(5)]enkephalin (DPDPE) were quantified using autoradiography in soleus and extensor digitorum longus (EDL) muscles of lean and obese-diabetic (ob/ob) mice. The density of binding was significantly higher in obese-diabetic than lean mice. The uptake of 2-deoxy-D-[1-3H]deoxyglucose, a nonmetabolized glucose analogue, into isolated soleus and EDL muscles was stimulated by beta-endorphin, beta-endorphin 1-27, and DPDPE, but not by the delta2-opioid deltorphin II. Both beta-endorphin and DPDPE stimulated deoxyglucose uptake in obese-diabetic mice. Thus, glucose transport in skeletal muscle may be partly mediated via delta1-opioid receptors. The increased receptor density in obese-diabetic mice may be an adaptive response.

Topics: Animals; Autoradiography; beta-Endorphin; Blood Glucose; Deoxyglucose; Diabetes Mellitus; Enkephalin, D-Penicillamine (2,5)-; Fatty Acids, Nonesterified; Female; Glucose; Insulin; Iodine Radioisotopes; Male; Mice; Mice, Inbred C57BL; Mice, Obese; Muscle, Skeletal; Obesity; Receptors, Opioid, delta; Tritium

Topics: Alzheimer Disease; beta-Endorphin; beta-Lipotropin; beta-MSH; Diabetes Mellitus; HIV Infections; Humans; Neuropeptides; Obesity; Pituitary Gland; Pro-Opiomelanocortin; Protein Precursors; Serine Endopeptidases

Autoradiography was used to study the opioid receptors in soleus and extensor digitorum longus (EDL) muscles from normal mice and mice with type II diabetes. Binding sites for [125I]beta-endorphin were present on the surface membranes in muscles from normal mice. The density of receptors was higher in muscles from obese diabetic mice. The specific delta-opioid ligands DPDPE and [D-Ala2]deltorphin-II inhibited the binding of [125I]beta-endorphin whereas mu and kappa agonists did not. Therefore, the opioid receptor present in skeletal muscle fibers of the mouse is of the delta subtype and the number of these receptors is increased in type II diabetes in the mouse.

Topics: Analgesics; Animals; Autoradiography; beta-Endorphin; Binding, Competitive; Cell Membrane; Diabetes Mellitus; Diabetes Mellitus, Type 2; Enkephalin, D-Penicillamine (2,5)-; Enkephalins; Iodine Radioisotopes; Mice; Mice, Obese; Muscle, Skeletal; Obesity; Oligopeptides; Receptors, Opioid, delta; Reference Values

The differences between diabetic and nondiabetic patients with silent myocardial ischemia were investigated. Based on the results of previous exercise testing, a total of 110 patients (15 diabetic and 95 nondiabetic) with exercise-induced myocardial ischemia were divided into the following 3 groups: 15 diabetics with silent myocardial ischemia, 49 nondiabetics with silent myocardial ischemia, and 46 nondiabetics with anginal symptoms. All patients underwent treadmill exercise testing and 24-hour ambulatory electrocardiographic recording. Before and during exercise, blood samples from the antecubital vein were obtained to determine the plasma beta-endorphin levels, and the pain threshold of each patient was measured with the electrical skin stimulation test. Furthermore, with regard to the ambulatory electrocardiographic recording, the mean of the SDs of all normal sinus RR intervals during successive 5-minute recording periods over 24 hours was analyzed and considered as an index of the autonomic function. The plasma beta-endorphin level during exercise was significantly greater in nondiabetic patients with silent ischemia than in diabetic ones. The SD mean was significantly less in the diabetic group than in the 2 nondiabetic ones. The findings suggest that the role of beta endorphin in diabetic patients with silent myocardial ischemia may be less significant than in nondiabetic ones; therefore, a diabetic neuropathy that affects the autonomic pain fibers that innervate the heart may be involved in the mechanism of silent myocardial ischemia in diabetics.

Topics: Aged; Analysis of Variance; Autonomic Nervous System; beta-Endorphin; Chi-Square Distribution; Diabetes Complications; Diabetes Mellitus; Electric Stimulation; Electrocardiography, Ambulatory; Exercise Test; Female; Humans; Male; Middle Aged; Myocardial Ischemia; Pain Threshold; Skin

Topics: alpha-MSH; Animals; beta-Endorphin; Diabetes Mellitus; Diabetes Mellitus, Experimental; Gene Expression; Immunohistochemistry; Male; Mice; Mice, Inbred C57BL; Mice, Inbred Strains; Mice, Obese; Motor Neurons; Muscles; Obesity; Pro-Opiomelanocortin

Topics: Adrenocorticotropic Hormone; Animals; beta-Endorphin; Binding Sites; Diabetes Mellitus; Diabetes Mellitus, Experimental; Male; Mice; Mice, Inbred Strains; Mice, Obese; Muscles; Obesity; Receptors, Corticotropin; Receptors, Opioid; Receptors, Pituitary Hormone; Reference Values

Immunoreactivity for two derivatives of pro-opiomelanocortin, beta-endorphin and alpha-melanocortin (or corticotropin), was demonstrated, using a conventional immunoperoxidase method, in some of the intramuscular nerves in muscle sections from obese diabetic (ob/ob) mice and homozygous lean (+/+) mice. The endplate regions were visualized in the sections by staining for acetylcholinesterase reaction product. The proportion of muscle endplates with beta-endorphin-immunoreactive motor nerves was approximately 2.5-fold higher in soleus and extensor digitorum longus muscles and approximately 1.5-fold higher in the diaphragm of the obese (ob/ob) mice compared to the normal lean mice. The proportion of muscle endplates with alpha-melanotropin-immunoreactive motor nerves was between 30 and 53% lower, depending on the muscle type, in the ob/ob mice compared to the lean mice. The muscles of ob/ob and lean mice were investigated for the presence of specific binding sites for [125I]beta-endorphin and for [125I]corticotropin, using autoradiography. Some muscle fibres in soleus, extensor digitorum longus and diaphragm in both the ob/ob and the lean mice exhibited specific binding sites for the radioactive ligands. The binding sites were distributed over the entire surface in these muscle fibres. In the ob/ob mice the number of muscle fibres with specific [125I]beta-endorphin binding sites was six-fold higher in soleus and approximately 10-fold higher in extensor digitorum longus and diaphragm, than in the corresponding muscles of the lean mice. In contrast, the number of muscle fibres with specific [125I]corticotropin binding sites was similar in obese (ob/ob) and lean mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adrenocorticotropic Hormone; alpha-MSH; Animals; Autoradiography; beta-Endorphin; Binding Sites; Diabetes Mellitus; Diabetes Mellitus, Experimental; Immunoenzyme Techniques; Iodine Radioisotopes; Mice; Mice, Inbred C57BL; Mice, Obese; Motor Endplate; Muscles; Obesity; Receptors, Corticotropin; Receptors, Opioid; Receptors, Pituitary Hormone; Reference Values

Forty obese subjects with normal glucose tolerance test (NGTT) thirteen diabetic obese subjects and sixteen normal subjects were studied to evaluate the possible interactions between beta-endorphin (B-Ep) and glucose homeostasis. On the basis of baseline B-Ep levels, two subgroups were selected: one group with normal mean values of B-Ep (7.02 +/- 0.59 pmol/l); another group with elevated mean values of B-Ep (18.95 +/- 1.52 pmol/l). No differences between these subgroups were found as regards body mass index (BMI), insulin and glucagon levels. Normal B-Ep values were found in diabetic obese subjects. No significant correlation was found between B-Ep and BMI, insulin or glucagon. Considering that B-Ep is involved in eating behavior and on the basis of our results, we suggest that elevated B-Ep levels can be found only in those obese NGTT subjects whose obesity is probably related to an abnormal modulation of food intake, such as hyperphagia.

Topics: Adult; beta-Endorphin; Blood Glucose; Diabetes Mellitus; Female; Glucagon; Glucose Tolerance Test; Humans; Insulin; Male; Obesity

Plasma opioid levels were determined in 9 obese non-diabetic subjects, their 8 age matched controls, and in 29 diabetic patients; 10 maintained on diet alone, 6 on an oral hypoglycemic agent (chlorpropamide) and 13 treated with insulin. Five age matched controls for the diabetic groups were also studied for comparison. beta-endorphin and met-enkephalin levels were measured by radioimmunoassay. Enkephalin-like activity was measured by a receptor assay. Among the study groups, diabetic patients receiving insulin showed a 64% elevation of plasma beta-endorphins and diabetic patients on chlorpropamide showed a 121% increase in enkephalin-like activity. There were no statistically significant differences in the plasma met-enkephalin values in the treatment groups though levels were decreased (p less than 0.05) in diabetics vs non-diabetics. The pathophysiological importance of these alterations remains to be elucidated.

Topics: beta-Endorphin; Chlorpropamide; Diabetes Mellitus; Diet, Diabetic; Endorphins; Enkephalin, Leucine; Enkephalin, Methionine; Enkephalins; Humans; Insulin; Obesity; Radioimmunoassay; Radioligand Assay; Reference Values

Beta-endorphin is present in the endocrine pancreas, suggesting that endorphins may have a role in islet-cell function. To evaluate this possibility, we infused synthetic human beta-endorphin intravenously in healthy volunteers and in insulin-dependent diabetic patients. In both groups, beta-endorphin increased plasma glucagon concentrations, and this rise was accompanied by a significant increase in plasma glucose concentrations. In nondiabetic subjects, beta-endorphin also increased plasma insulin concentrations. The threshold dose of beta-endorphin for producing increased plasma concentrations of glucose and glucagon was 0.005 mg--a dose that acutely increased plasma concentrations of beta-endorphin by approximately 40-fold. Glucose, glucagon, and insulin responses to beta-endorphin could not be blocked by intravenous naloxone. These studies suggest that endorphins may be involved in gluco-regulation, that their hyperglycemic action is mediated at least in part by glucagon, and that the effect of beta-endorphin on islet-cell function is relatively resistant to naloxone.

Topics: Adult; beta-Endorphin; Blood Glucose; Diabetes Mellitus; Endorphins; Female; Glucagon; Humans; Insulin; Islets of Langerhans; Male; Middle Aged; Naloxone; Sodium Chloride

This study examines the effect of experimentally induced diabetes mellitus in rats on tissue concentrations of opioid peptides in the neurointermediate lobe (NIL), anterior pituitary (AP) and hypothalamus. Diabetic animals were found to have a marked increase in endorphin equivalents, measured by opiate receptor binding assay, in the NIL whereas no change was observed in beta endorphin-like immunoreactivity (beta ELI) or ACTH measured by RIA. These results may indicate the presence of a feedback mechanism and suggest the possibility that opioid peptides may be physiologically important in the maintenance of glucose homeostasis.

Topics: Adrenocorticotropic Hormone; Animals; beta-Endorphin; Diabetes Mellitus; Endorphins; Hypothalamus; Male; Pituitary Gland; Rats; Rats, Inbred Strains