Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our observations that opioid peptides have direct effects on islet insulin secretion and liver glucose production prompted a search for endogenous opiates and their receptors in these peripheral tissues. Mu-, delta- and kappa-receptor-active opiates were demonstrated in brain, pancreas and liver extracts by displacement studies using selective ligands for the three opiate receptor subtypes [( 3H][D-Ala2,MePhe4,Gly5-ol]enkephalin, [3H][D-Ala2,D-Leu5]enkephalin and [3H]dynorphin respectively). Receptor-active opiates in brain extracts exhibited a stronger preference for delta-opiate-receptor sites than for mu and kappa sites. Pancreatic extract opiates demonstrated a similar activity at mu and delta sites, but substantially less at kappa sites. Liver extracts displayed similar selectivity for all three sites. The affinities of the receptor-active opiates for mu-, delta- and kappa-receptor subtypes displayed a rank order of potency: brain much greater than pancreas greater than liver. Total immunoreactive beta-endorphin and [Met5]enkephalin levels in liver and hepatocytes were greater than those in brain. Immunoreactive [Met5]enkephalin levels in pancreas were similar to, but beta-endorphin levels were substantially higher than, those in brain. Delta and kappa opiate-binding sites of high affinity were identified in crude membrane preparations of islets of Langerhans, but no specific opiate-binding sites could be demonstrated in liver membrane preparations. Immunoreactive dynorphin and beta-endorphin were demonstrated by immunogold labelling in rat pancreatic islet cells. No positive staining of liver sections for opioids was observed. These results suggest that the tissue content of opiate-receptor-active compounds in the pancreas and the liver is very significant and could contribute to the regulation of normal blood glucose levels.
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PMID:The occurrence and receptor specificity of endogenous opioid peptides within the pancreas and liver of the rat. Comparison with brain. 197 Feb 40

The responses of plasma glucose, insulin, C-peptide and glucagon to an infusion of human beta-endorphin (0.5 mg/h) were studied in 10 formerly obese subjects who had lost 35 kg by dieting (body mass index less than 25) and compared with those of 10 normal-weight control (body mass index less than 25) and 10 obese (body mass index greater than 30) subjects. The fasting plasma concentrations of beta-endorphin were significantly higher in both the obese and the post-obese group than in the control group. In both obese and post-obese subjects, the infusion of beta-endorphin caused significant increases in peripheral plasma glucose, insulin, C-peptide and glucagon concentrations. In the control group, matched for age, sex and weight with the formerly obese group, there was no appreciable change in plasma insulin and C-peptide concentrations during the infusion of beta-endorphin, but the rise in plasma glucose was more sustained. Thus, 1. the increased plasma beta-endorphin concentrations found in human obesity are not corrected by normalization of body weight; and 2. formerly obese, normal-weight subjects behave as obese subjects in their metabolic and hormonal responses to beta-endorphin infusion. The alteration of the opioid system in human obesity may play some role in the predisposition to weight gain.
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PMID:Persistence of altered metabolic responses to beta-endorphin after normalization of body weight in human obesity. 200 75

Candida albicans is a dimorphic yeast that causes vaginal infections after its transition from a budding yeast to a germinating hyphal form. We report here that physiologic concentrations of beta-endorphin, a neuropeptide with immunomodulating activity produced during stress or physical exercise, stimulates germ tube formation in C. albicans. The percent of germination was proportional to the endorphin concentration, over the 5 x 10(-12) to 5 x 10(-10) mol/L range tested. beta-Endorphin modified by removal of the 4-carboxy-terminal amino acids and (D-Ala2)-beta-endorphin, a peptide with a protease-resistant amino terminal end, were equally effective in stimulating germination. In contrast, N-acetylated beta-endorphin did not stimulate germination. Antisera to beta-endorphin also completely blocked beta-endorphin-stimulated germ tube formation. Two clinical isolates of C. albicans were also responsive to beta-endorphin. Stimulation of germ tube formation by beta-endorphin occurred only in sera from ovulating women. Germination in sera from women using oral contraceptives, in sera from men, or in glucose beef extract broth was not influenced by beta-endorphin. Thus C. albicans may be able to recognize and respond to neuroendocrine signals in ovulating women.
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PMID:Enhancement of germ tube formation in Candida albicans by beta-endorphin. 200 58

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.
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PMID:[Plasma levels of beta-endorphin in obese subjects with normal glucose tolerance test and in diabetics]. 202 70

Seventeen normotensive, premenopausal women were treated with the 5-hydroxytryptamine-reuptake inhibitor dexfenfluramine 30 mg per day, for 4 days in a randomised double-blind, cross-over, placebo controlled trial. Energy intake was held constant during the study as the aim was to study the endocrine and metabolic effects of dexfenfluramine dissociated from its weight-lowering properties. Body weight, blood glucose, plasma insulin, cholesterol triglycerides and C-peptide after an overnight fast and during an oral load of 100 g glucose did not change after dexfenfluramine compared to placebo. Supine and standing systolic and diastolic blood pressures were significantly decreased, while heart rate remained unchanged. Plasma noradrenaline and plasma renin were markedly reduced by dexfenfluramine, and cortisol, beta-endorphin and thyroid hormones were not changed. Thus, dexfenfluramine has a significant hypotensive effect in normotensive, obese women after 4 days of treatment, independent of a negative energy balance. This was associated with decreased circulating plasma noradrenaline, indicating decreased sympathetic nerve activity. Dexfenfluramine may be a candidate drug for longer-term trials in the treatment of primary hypertension associated with obesity.
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PMID:Haemodynamic, metabolic and endocrine effects of short-term dexfenfluramine treatment in young, obese women. 206 May 60

Intraperitoneal administration of beta-endorphin (1 mg/kg) to ob/ob mice doubled fasting plasma insulin concentrations within 30 min, while plasma glucose concentrations were unaltered. In lean mice, beta-endorphin failed to alter plasma insulin or glucose responses. In glucose-loaded ob/ob mice, beta-endorphin (1 mg/kg) reduced insulin levels at 40 min, and delayed glucose disposal. A lower dose of beta-endorphin (0.1 mg/kg) decreased plasma insulin at 90 min, with no effect on plasma glucose disposal. In lean mice, only the higher dose of beta-endorphin suppressed the glucose-stimulated rise in plasma insulin concentrations, without affecting plasma glucose. Beta-endorphin's actions were blocked by naltrexone and could not be mimicked by N-acetyl-beta-endorphin. Beta-endorphin (10(-8)M) enhanced insulin release from isolated ob/ob and lean mouse islets incubated in medium containing 6 mM glucose, but inhibited release when 20 mM glucose was present. These effects were naloxone reversible. The results indicate that 1) ob/ob mice display a greater magnitude of response in vivo to beta-endorphin's actions on insulin release compared with lean mice, 2) high concentrations of beta-endorphin exacerbate glucose disposal in ob/ob mice. 3) the prevailing glucose concentration is an important determinant of whether beta-endorphin's effects on insulin release will be stimulatory or inhibitory and 4) these actions are mediated via opiate receptors.
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PMID:Dual action of beta-endorphin on insulin release in genetically obese and lean mice. 206 74

Several experimental data have documented the ability of both opiates and opioid peptides to stimulate food intake. On the other hand, the plasma beta-endorphin levels found in obese patients are higher than those observed in normal-weight controls, which may have pathogenetic implications. We have investigated the responses of plasma glucose, insulin, C-peptide and glucagon to an infusion of human beta-endorphin in formerly obese subjects who had obtained by dieting the normalization of body weight and in lean controls. The data show that: a) the increased plasma beta-endorphin concentrations found in human obesity are not corrected by normalization of body weight; b) formerly obese subjects behave as obese subjects in their metabolic and hormonal responses to beta-endorphin.
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PMID:[Beta-endorphin and obesity. Possible pathogenetic implications]. 209 58

The effect of general anaesthesia and arthroscopic surgery on blood glucose and lactate, plasma non-esterified fatty acids, insulin, beta-endorphin and cortisol was investigated in seven horses. Animals were premedicated with xylazine and anaesthesia was induced with guaifenesin and sodium thiamylal and maintained with halothane vaporised in oxygen. Blood samples were collected in the pre-, intra- and post operative period. Induction of anaesthesia was associated with a transient hyperglycaemia and a significant rise in plasma insulin levels. Plasma insulin values fell during surgery but showed a significant increase post operatively. Surgery stimulated a small but significant rise in plasma beta-endorphin and cortisol values but these had returned to baseline values in the early post operative period. No changes in blood lactate were recorded.
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PMID:Metabolic and hormonal changes associated with arthroscopic surgery in the horse. 222 92

Plasma concentrations of glucose, insulin, and beta-endorphin/beta-lipotropin were measured in male Sprague-Dawley rats with experimental renal failure after intravenous glucose challenge in the presence and absence of opioid blockade with intravenously administered naloxone. The results were compared with those obtained in sham-operated normal control and pair-fed groups of animals. Baseline glucose concentrations were similar in the three groups of animals. Plasma baseline insulin concentrations were significantly lower in the rats with renal failure and the pair-fed animals compared with the normal controls. After glucose challenge the renal failure group demonstrated glucose intolerance, which was not improved after naloxone treatment given 15 minutes before glucose challenge. Peak insulin levels after glucose challenge in the renal failure and pair-fed groups increased significantly after naloxone administration. Interestingly, circulating concentrations of plasma beta-endorphin/beta-lipotropin were not significantly different in the three groups of animals when measured either in the baseline state or after glucose challenge. The data indicate that the carbohydrate intolerance in experimental renal failure may be partly due to an increase in pancreatic islet opioidergic tone, because an improvement in insulin secretion was demonstrated in the absence of any change in circulating beta-endorphin/beta-lipotropin concentrations after naloxone. The failure to demonstrate any improvement in glucose disposal after naloxone, despite the augmented secretion of insulin after naloxone in the animals with renal failure, points to peripheral resistance to the effects of insulin that is not influenced by opioid blockade.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucose intolerance in renal failure: role of endogenous opioids. 214 12

In young male volunteers, the changes in growth hormone (GH), prolactin (PRL), and adrenocorticotropic hormone (ACTH) release in response to insulin injection combined with the infusion of saline, glucose, and fructose were evaluated. Glucose infusion in a dose which prevented insulin hypoglycemia completely abolished endocrine responses. Infusion of fructose, which is known not to cross the blood-brain barrier (BBB), did not influence the GH release during hypoglycemia; however, it inhibited PRL secretion. The ACTH response was slightly attenuated and delayed, while the hypoglycemia-induced rise in cortisol levels was not modified by fructose infusion. These data indicate that the glucoreceptors mediating the signals for a complete counterregulatory neuroendocrine response are not located in a single brain structure. Stimuli for GH release are produced in areas of the central nervous system protected by the BBB, while those for PRL release are presumably present in structures not protected by the BBB. Glucoreceptors triggering ACTH release are located both inside and outside the BBB.
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PMID:Glucoreceptors located in different areas mediate the hypoglycemia-induced release of growth hormone, prolactin, and adrenocorticotropin in man. 215 98


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