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)

The presence and distribution of regulatory peptides in nerves and endocrine cells of the stomach, intestine and rectum of a urodele amphibian, the mudpuppy, Necturus maculosus, was studied immunohistochemically in sections or whole-mount preparations of the gut wall. The effect of the occurring peptides on gut motility was studied in isolated strip preparations of circular and longitudinal smooth muscle from different parts of the gut. Bombesin-, neurotensin-, substance P- and VIP-like immunoreactivity was present in abundant nerve fibres in the myenteric plexus of both stomach, intestine and rectum. Single fibres or bundles were present in the circular muscle layer and in a well-developed deep muscular plexus in the intestine and rectum. Immunoreactive nerve cells were found in the myenteric plexus of the stomach, intestine (neurotensin only) and rectum. Gastrin/CCK-like immunoreactivity was observed only in a few fibres in stomach and rectum. Endocrine cells containing bombesin-, met-enkephalin-, gastrin/CCK-, neurotensin-, somatostatin- or substance P- like immunoreactivity were present in the mucosa. The effect of bombesin was an inhibition of the rhythmic activity in circular muscle preparations and in longitudinal muscle from the rectum, while longitudinal muscle from the stomach usually responded with a weak increase in tonus. Neurotensin, like-bombesin, was inhibitory on the spontaneous rhythmic activity of circular muscle throughout the gut, while the effect on longitudinal muscle was an increase in tonus. Met-enkephalin and substance P increased the tonus of all types of preparations, and often, in addition, initiated a rhythmic activity superimposed on this maintained tonus. VIP had a general inhibitory effect on the preparations, decreasing tonus and/or abolishing rhythmic activity. It is concluded that bombesin-, neurotensin-, substance P- and VIP-like peptides are present in nerves throughout the urodele gut and may have physiological functions in regulating the motility of the gut. The gastrin/CCK-like peptide present in nerves of the stomach and rectum may affect the function of these parts of the gut. The regulatory peptides present in endocrine cells may, perhaps with the exception of the somatostatin-like peptide, affect the motility humorally.
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PMID:Neuropeptides in the gastrointestinal canal of Necturus maculosus. Distribution and effects on motility. 241 14

Cisapride is a gastrointestinal prokinetic agent reported to be devoid of direct cholinergic effect from the myenteric plexus of the gut. The effect of cisapride (0.125, 0.5, 2mg/kg, i.p.) on the concentration beta-endorphin and substance P in rat gastrointestinal tract was studied. beta-Endorphinlike immunoreactivity contents were significantly increased in both mucosal and muscular layers of the entire gastrointestinal tract (from gastric body to rectum) of the rats treated with 2 mg/kg of cisapride. beta-Endorphinlike immunoreactivity contents were also increased in a part of the gastrointestinal tract of the rats treated with 0.125 or 0.5 mg/kg of cisapride. Substance P like immunoreactivity contents were significantly decreased in muscular layers of the rectosigmoid colon of the rats treated with 2 mg/kg of cisapride. This study suggests that the prokinetic effects of cisapride may relate to the contents of beta-endorphinlike immunoreactivity and substance P like immunoreactivity in gastrointestinal tract.
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PMID:Effect of cisapride on the concentrations of beta-endorphinlike immunoreactivity and substance P-like immunoreactivity in the rat gastrointestinal tract. 244 24

Proximal duodenal mucosal bicarbonate secretion is an important factor in the pathogenesis of duodenal ulcer disease. To examine the central nervous system regulation of duodenal bicarbonate secretion, an animal model was developed that allowed cerebroventricular and intravenous injections as well as collection of duodenal perfusates in awake, freely moving rats. The hypothalamic peptide corticotropin-releasing factor (CRF) and stress (physical restraint) significantly stimulated duodenal bicarbonate secretion. These responses were abolished by pretreatment of the animals with the CRF receptor antagonist alpha-helical CRF-(9-41), hypophysectomy, and naloxone. In contrast, blockade of autonomic efferents by surgical and pharmacological means did not prevent the stimulatory effects of stress and CRF. Intravenous, but not cerebroventricular, administration of beta-endorphin that produced plasma concentrations of beta-endorphin that were similar to those produced by exogenous CRF and stress significantly stimulated duodenal bicarbonate secretion. These results indicate that endogenous CRF released during stress and exogenously administered CRF stimulate duodenal bicarbonate secretion by release of beta-endorphin from the pituitary, thus, demonstrating a functional hypothalamus-pituitary-gut axis.
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PMID:Regulation of duodenal bicarbonate secretion during stress by corticotropin-releasing factor and beta-endorphin. 252 53

Endogenous opioid peptides derive from three precursors: proenkephalin A, maturing into enkephalins, proenkephalin B, maturing into dynorphins, and proopiomelanocortin, maturing into beta-endorphin and non-opioid fragments. All these opioid peptides can be detected by immunocytochemical methods in many neurons intrinsic to the gut and in cerebral and medullary neurons. The involvement of opioid peptides in the control of intestinal motility is demonstrated by experiments using injection of exogenous peptides or analogues, administration of antagonists or inhibition of their in vivo degradation. However, the pattern of action of opioids on intestinal motility is complex, since stimulant and inhibitory effects may occur via the different mu, delta and kappa opioid receptors, on muscle cells or on nerves and at central or peripheral sites. On the whole, opioid peptides should be considered as important neurotransmitters. Their main function on gut motility seems to be the regulation of other stimulant and inhibitory neurons inputting to the muscle cells of the gut.
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PMID:[Role of opioid peptides in intestinal motility]. 253 71

Sexually mature landlocked sea lamprey were captured during their upstream migration. Different tissues, including the brain, pituitary, heart, liver, gut, testis, and ovary, were dissected from the animals and an acetone powder was prepared from each tissue. The tissue acetone powders were subjected to heat treatment and were then extracted with an acidic medium in order to inactivate any proteases present. The resulting acid acetone powders were then tested for their ability to stimulate corticosterone production from isolated rat adrenal cells and to displace the binding of D-Ala2-D-Leu5-[tyrosyl-3,5-3H]-enkephalin to rat brain membranes. It was found that the brain and liver contained steroidogenic activity while opiate activity was detected in the heart, liver, gut, brain, and pituitary. No steroidogenic activity was found in the heart, ovary, testis, gut, and pituitary while ovary and testis did not contain assayable opiate activity. None of the tissues contained beta-endorphin-like immunoreactivity.
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PMID:The presence of corticotropin-like and opiate-like activities in tissues of adult sea lamprey, Petromyzon marinus L. 254 13

Clinical and laboratory evidence indicates that the brain exerts major control on the gastrointestinal tract. Specific brain loci and circuits that send efferent viscerotropic projections to the gut have been described. A variety of aminergic and peptidergic neurotransmitters have been shown to occur along these cerebrogastrointestinal pathways and to influence motor and secretory functions of the gut. Some of the newly identified peptides have been shown to influence the development of gastroduodenal ulcers. Findings with thyrotropin-releasing hormone (TRH) indicate that this endogenous tripeptide induces a full spectrum of gut effects, prominent among which is production of gastric ulcers. By contrast, other peptides including beta-endorphin, neurotensin, and bombesin induce gut effects opposite to those of TRH, namely, inhibition of gastric acid and motility and prevention of experimental ulcers. These laboratory findings suggest that ulcer disease may represent a brain-driven event, which may be the result of a neurochemical imbalance within the brain. Further neurobiological research will generate additional data on brain-gut interactions and will probably disclose new information to explain certain functional and organic disorders of the gut.
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PMID:Neurobiology of brain-gut interactions. Implications for ulcer disease. 257 55

Peripheral neuropathy is a correlate of experimental diabetes induced in rats by means of a single injection of alloxan. The autonomic and enteric innervation of the gut are profoundly affected in the small intestine of such animals. A complex process of denervation and hyperinnervation of the gut wall of diabetic animals is observed. It was previously reported that the cholinergic parasympathetic innervation of the intestine is markedly reduced. We have found that noradrenergic sympathetic axons hyperinnervate the duodenum of diabetic rats, whereas noradrenaline levels are significantly reduced in the jejunum. The putative enteric neurotransmitter dopamine is also present in higher levels in the duodenum. The intrinsic peptidergic neurons of the gut are deeply affected as well in diabetic rats. Substance P and met-enkephalin content are remarkably reduced throughout the small intestine, whereas vasoactive intestinal polypeptide levels (VIP) are significantly increased in the duodenum. Indeed, immunocytochemical staining of the ileum did reveal hypertrophy of VIP-positive axons in diabetic rats. The intrinsic serotoninergic innervation of the gut is apparently unaffected. Our results indicate that the changes of gut innervation observed in experimental diabetes are consistent with increased content and also likely with hyperinnervation by the neuronal systems involved in smooth muscle relaxation and decreased content and with denervation by those systems with smooth muscle contraction properties. Such a perturbed gut innervation may be responsible of the gastrointestinal dysfunctions that are among the most common complications of diabetes.
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PMID:Denervation and hyperinnervation in the nervous system of diabetic animals. I. The autonomic neuronal dystrophy of the gut. 259 79

Stress in humans commonly results in gastrointestinal dysfunction, which is characterized by its symptomatology because the etiology is completely unknown. We developed an animal model in which to study the effects of stress on the gastrointestinal tract, and characterized the model as a stressor by evaluating endocrine and analgesic responses to mild restraint. Mild restraint (wrap restraint) elevated plasma levels of adrenocorticotropic hormone and beta-endorphin, and caused analgesia. The different regions of the gastrointestinal tract responded differently to the stress stimulus. Gastric emptying was not affected, small intestinal transit was inhibited, and large intestinal transit was stimulated by stress, and there was an associated increase in fecal excretion. Wrap-restraint stress did not result in the formation of ulcers. There was a strong correlation between stress-induced adrenocorticotropic hormone release and stress-induced intestinal dysfunction over a 24-h period that suggested a circadian influence. However, neither exogenous adrenocorticotropic hormone nor beta-endorphin had any effect on intestinal transit. Furthermore, neither adrenalectomy nor hypophysectomy prevented the response of the intestine to stress, suggesting that neither adrenal nor pituitary-derived factors are responsible for mediating the effects of stress on the gut. We conclude that wrap-restraint stress produces different effects on different regions of the intestine, suggesting that the small and large intestines are independently regulated and can respond differently to different stimuli. There were similarities between the intestinal effects of wrap-restraint stress in rats and intestinal symptoms associated with stress and irritable bowel syndrome in humans. Therefore, wrap restraint may be an appropriate animal model in which to study stress-related intestinal dysfunction. The mechanisms by which stress affects intestinal transit are still unresolved; however, the intestinal effects of stress are not mediated by either pituitary or adrenally derived factors.
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PMID:Stress-induced changes in intestinal transit in the rat: a model for irritable bowel syndrome. 282 44

The serotonergic modulation of the brain, pituitary and gut beta-endorphin and dynorphin systems in the rat was determined pharmacologically. Acute administration of fenfluramine (20 mg/kg), m-chlorophenylpiperazine (m-CPP 2.5 mg/kg), fluvoxamine (15 mg/kg) and 5-hydroxytryptophan (5-HTP 160 mg/kg) increased immunoreactive (ir)beta-endorphin (beta E) in the hypothalamus and decreased it in the anterior lobe of the pituitary. That effect was antagonized by cyproheptadine (1 mg/kg). None of the treatments altered significantly ir-dynorphin (DYN) level in the hypothalamus and pituitary, however, ir-DYN in the gut was dramatically decreased after fenfluramine, m-CPP, fluvoxamine, femoxetine and 5-HTP, the latter effects being antagonized by cyproheptadine. The obtained results suggest that the serotonin system might stimulate the release of the anterior pituitary beta-endorphin and gut dynorphin pools, while the brain beta-endorphin system appears to be inhibited by activation of serotonin neurons.
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PMID:Differential modulation of the beta-endorphin and dynorphin systems by serotonergic stimulation in the rat. 286 Jun 13

The levels of dynorphin, alpha-neoendorphin and beta-endorphin immunoreactivity (ir-DYN, ir-alpha-NEO, ir-beta-E) were measured in the brain, pituitary and gut of rats subjected to a variety of manipulations. Water deprivation caused an increase in the ir-DYN and ir-alpha-NEO content in the hypothalamus and a decrease in the neurointermediate (NI) lobe of the pituitary. The ir-beta-E level decreased in the hypothalamus and anterior lobe of the pituitary, while it increased in the NI-pituitary. Food deprivation, as well as chronic fenfluramine (10-20 mg/kg) treatment increased, while acute muscimol (0.5 micrograms/10 microliter) treatment decreased the ir-beta-E, but not ir-DYN or ir-alpha-NEO content in the hypothalamus. The anterior pituitary content of ir-beta-E was increased after food deprivation and decreased after chronic fenfluramine treatment. However, the ir-DYN and ir-alpha-NEO contents in the duodenum were markedly increased after food deprivation, while chronic fenfluramine treatment led to a dramatic decrease in the ir-DYN content. These results suggest that the levels of opioid peptides in the brain, pituitary and gut may be differentially and independently affected by alteration of the ingestive behavior.
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PMID:Brain and peripheral opioid peptides after changes in ingestive behavior. 286 26


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