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 present study was done both in vivo by cannulating pancreatic duct of rats and in vitro using pancreatic slices and dissociated acini to determine the mode of action of endogenous opiate peptides on pancreatic acinar cell. Pancreatic slices were incubated with beta-endorphin or (Met)5-enkephalin alone and in combination with CCK8. Dissociated acini were incubated with naloxone, substance P, VIP, (Met)5- and (Leu)5-enkephalin and alpha-, beta-, and gamma-endorphin alone or in combination with CCK8. In vivo, both beta-endorphin and (Met)5-enkephalin did not alter basal secretion but inhibited CCK8-stimulated amylase secretion. This effect was not reversed by administration of naloxone. In the slices, neither beta-endorphin nor (Met)5-enkephalin altered basal or CCK8-stimulated secretion. In the dissociated acini, substance P and VIP significantly increased amylase secretion, whereas naloxone, enkephalins, and endorphins failed to alter amylase secretion. CCK8 increased amylase secretion greater than sixfold. In combination with enkephalins and endorphins, there was neither inhibition nor potentiation of CCK8 effect. These data indicate that the effect of opiate peptides on pancreatic acinar cells in the rat are nonspecific and appear not to be mediated by opiate receptors.
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PMID:Effect of endorphins on amylase secretion from rat pancreas in vivo and in vitro. 257 22

When rats were exposed to immobilization stress for 1-12 h, gastric lesions did not occur at 1-6 h but did at 12 h of immobilization. Exogenous adenosine increased stress-induced gastric lesions, and dipyridamole, a blocker of adenosine uptake, potentiated the action of adenosine. The selective adenosine A1-receptor stimulants N6-cyclohexyl adenosine (CHA) and N6-(L-phenylisopropyl) adenosine (L-PIA) produced gastric lesions even in non-stressed state and markedly potentiated in dose- and time-dependent manner in stressed state. The stimulatory effect of N6-(D-phenylisopropyl) adenosine (D-PIA) on ulceration was weaker than that of CHA or L-PIA. Furthermore, intracerebral ventricular (i.c.v.) injection of adenosine or adenosine analogues produced the most rapid and most potent exacerbation of stress-induced gastric lesions relative to those induced with subcutaneous (s.c.) injection. The stress lesions enhanced by CHA were not affected by phentolamine, yohimbine, prazosin, naloxone and cholecystokinin (CCK8) but were inhibited by caffeine, clonidine, morphine and beta-endorphin. The inhibitory effect of clonidine was not antagonized by yohimbine or prazosin. The inhibition by morphine was selectively antagonized by exogenous CCK8 as well as naloxone. These results suggest that endogenous adenosine is tonically active in stress lesion formation which is modulated by opiate systems. Clonidine as well as caffeine may function as a purinoceptor antagonist, and it seems unlikely that the inhibitory effect of clonidine on stress ulcer is due to activation of alpha-adrenoceptors.
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PMID:Development of stress-induced gastric lesions involves central adenosine A1-receptor stimulation. 299 4

Cholecystokinin-8 (CCK8)-containing cell bodies in the parvocellular region of the rat paraventricular nucleus (PVN) contain vasopressin and corticotropin-releasing factor (CRF). The CCK8 and vasopressin in these cells can readily be visualized in adrenalectomized, but not in shamoperated animals. Furthermore, CCK8 levels as measured by RIA change in the PVN and in the median eminence in response to adrenalectomy. CCK8 has a stimulatory effect on corticotropin (ACTH) release from primary cultures of the anterior pituitary. This stimulation is additive with that produced by vasopressin; CCK8 plus vasopressin have an effect as great as CRF in stimulating ACTH release. Our results suggest that CCK8 may participate in the regulation of ACTH release under certain physiological conditions.
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PMID:Role of cholecystokinin in corticotropin release: coexistence with vasopressin and corticotropin-releasing factor in cells of the rat hypothalamic paraventricular nucleus. 301 Mar 3

There are now about twelve substances, many of them peptides, that are thought to act as neurotransmitters in the enteric nervous system. Most of the studies of peptides have relied on immunochemical methods for their detection. However, difficulties arise in these studies because of the close similarities between peptides. Related peptides can be grouped in several ways according to similarities of origin, function, effects in bioassays and amino acid sequences. Peptides with the same function in different species, and only slight differences in amino acid sequence, have been called isopeptides. Peptide families that have sequences of amino acids in common, but do not necessarily have similar functions are described. In the guinea-pig small intestine, used as a model, the concentrations of fourteen nerve-related peptides and amines are compared. The actual chemical natures of the peptides are discussed. It is concluded that nerves containing authentic leu- and met-enkephelin, somatostatin and substance P are present. VIP in guinea-pig enteric nerves is different from the porcine standard. Peptides similar to authentic CCK8 and amphibian skin bombesin are present. Angiotensin and neurotensin-like peptides shown immunohistochemically are not the authentic peptides. In the longitudinal muscle plus myenteric plexus, most neuropeptide concentrations are in the range of 10-500 pmole/g. The exception is met-enkephalin (1,300 pmole/g). The amine transmitters have considerably higher concentrations, noradrenaline having a concentration of about 3,500 pmole/g and acetylcholine 1-2 x 10(5) pmole/g.
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PMID:Detection and characterisation of neurotransmitters, particularly peptides, in the gastrointestinal tract. 617 12

Peptide, 5-hydroxytryptamine (5-HT)-, tyrosine hydroxylase (TOH)-, and glial fibrillary acidic protein (GFAP)-like immunoreactivity was studied in the optic tectum of Rana pipiens. Peroxidase-antiperoxidase and indirect immunofluorescence single- and double-labeling methods were used to compare differential laminar distribution of each of these substances. Substance P (SP), leucine-enkephalin (LENK), cholecystokinin octapeptide (CCK8), bombesin (BOM), avian pancreatic polypeptide (APP), and possibly neurotensin display unique individual patterns of laminar distribution of processes and cell bodies throughout the tectum. A correlative analysis of the topographical distribution of SP, LENK, BOM, and APP on the basis of double-labeled sections shows a precise laminar segregation of these substances. Vasoactive intestinal peptide-, beta-endorphin-, and ranatensinlike immunoreactivity is consistently absent from our material. 5HT- and TOH-like immunoreactivity discloses a reticular array of fibers without clear evidence of laminar organization. This peptide-like laminar organization is particularly elaborate throughout the superficial neuropil of the optic tectum, the major retinorecipient zone. The pattern of lamination demonstrated in the present study differs in several important features from that previously described on the basis of several histological methods. The cells of origin of processes (axons and/or dendrites) in the superficial tectal neuropil may be either intrinsic or extrinsic to the tectum. Special reference is made to conflicting evidence regarding the possibility of a retinal contribution to peptide-like tectal lamination.
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PMID:Laminar organization of peptide-like immunoreactivity in the anuran optic tectum. 619 80

The pancreatic zymogen granule membrane protein GP-2 was introduced into cells of exocrine or endocrine origin by transfection of its cDNA in order to investigate the mechanisms by which proteins are specifically incorporated into the membranes of secretory granules. Permanent transformants expressing GP-2 were isolated from exocrine pancreatic-derived AR42J cells as well as AtT20 cells of anterior pituitary origin and insulinoma-derived Rin5F cells. In AR42J cells, GP-2 was localized by immunofluorescence and immunoelectron microscopy to the endogenous zymogen-like granules as well as to the plasma membrane. In experiments supporting the localization data, incubation of the AR42J transformants with the secretagogue cholecystokinin (CCK8) resulted in enhanced release of a shed form of GP-2 into the medium in parallel with amylase, suggesting that the two proteins were secreted from the same compartment. By contrast, when expressed in AtT20 cells, the protein was found by immunofluorescence microscopy on the plasma membrane as well as in intracellular vesicles that differed in size and location from the endogenous secretory vesicles. By electron microscopy, large (approximately 0.5 micron) multivesicular structures were observed. Single- and double-label immunoelectron microscopy demonstrated that these large organelles labeled with anti-GP-2 antibodies, whereas the smaller adrenocorticotropic hormone (ACTH)-containing secretory vesicles did not. In permanent transformants of Rin5F cells, GP-2 was also excluded from the insulin-containing granules and found in multivesicular bodies similar to those in the AtT20 cells and containing the endosomal/lysosomal marker endolyn-78. Despite the apparent accumulation of GP-2 in lysosome-like structures, it turned over slowly and did not undergo rapid endocytosis from the cell surface. We conclude that GP-2 is targeted to secretory granule membranes by cell type-specific mechanisms that likely involve its interaction with other membrane or content proteins expressed only in the exocrine cells.
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PMID:Incorporation of the pancreatic membrane protein GP-2 into secretory granules in exocrine but not endocrine cells. 750 84

Previously, we have shown that intracisternal (i.c.) administration of beta-endorphin suppresses brain and liver DNA synthesis in rat pups. This finding is consistent with the view that endogenous CNS beta-endorphin plays an important role in controlling postnatal growth. Recent evidence suggests that brain CCK8, the sulfated carboxyterminal octapeptide fragment of cholecystokinin, may function physiologically as an endogenous opioid antagonist. We now report that CCK8 injected i.c. together with beta-endorphin effectively prevented beta-endorphin from inhibiting brain and liver DNA synthesis in 10-day-old rats. CCK8 blocked the liver DNA effect of beta-endorphin via actions within the brain, as subcutaneous administration of CCK8 was ineffective. In contrast to CCK8, i.c. administration of CCK8U (the unsulfated form of CCK8) together with beta-endorphin did not prevent beta-endorphin from inhibiting liver DNA synthesis, and only slightly reversed the brain DNA effect. The results obtained support a role for endogenous brain CCK8 in the modulation of tissue DNA responses to CNS beta-endorphin and possibly to other endogenous opioids. If so, interference with brain CCK function could disrupt tissue growth. Thus, normal mammalian development may require a close functional interaction between the cholecystokinin and beta-endorphin systems in the brain.
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PMID:Brain cholecystokinin and beta-endorphin systems may antagonistically interact to regulate tissue DNA synthesis in rat pups. 783 70

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.
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PMID:Alterations in plasma and cerebrospinal fluid levels of neuropeptides in idiopathic senile anorexia. 790 1

In the present study, the effects of experimental lead pollution on gut endocrine cells have been determined in the goldfish Carassius carassius (L.) var.auratus by immunocytochemical reactions. In the mucosa and submucosa, only vasoactive intestinal polypeptide- and 5-HT-like immunoreactive nerve fibers were observed. Endocrine cells displaying immunoreactivity against gastrin, CCK8, metenkephalin, bombesin, neuropeptide Y, pancreatic polypeptide, substance P, secretin, somatostatin and vasoactive intestinal polypeptide antibodies were detected. No immunoreactivity against glucagon, insulin and 5-HT antibodies was revealed in the endocrine cells. Some modifications appeared evident in the endocrine cells 48-96 h after lead intoxication, and can be summarized as follows: 1) discharge of secretory granules (secretin- and vasoactive intestinal polypeptide-like peptides), up to the extent that the cells appeared to be depleted of secretory material; 2) increase of immunoreactivity in the endocrine cells (met-enkephalin- and pancreatic polypeptide-like peptides) or in the frequency of positive cells (met-enkephalin-like peptide); 3) no variations (gastrin-, CCK8, bombesin-, somatostatin- and substance P-like peptides). The alterations were not enhanced by long term treatment. Nerve fibers did not show modifications.
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PMID:Immunocytochemical study of endocrine cells in the gut of goldfish Carassius carassius (L.) var. auratus submitted to experimental lead intoxication. 911 38

The central fragment of cholecystokinin, CCK8, plays a critical role in stress-related changes in behavior and memory. Therefore, we investigated whether the endogenous cholecystokininergic system is involved in the impairment of attention and/or memory induced by stressful conditions. Plasma corticosterone concentrations increased three-fold and plasma adrenocorticotropin (ACTH); concentrations increased five-fold when rats were maintained in the open arm of an elevated plus maze for 5 min. The same stress conditions impaired spatial recognition in the two-trial memory task. In addition, this stress led to a significant decrease in the extracellular levels of cholecystokinin-like immunoreactivity in the dorsal subiculum/CA1 of the hippocampus and partially suppressed the increase obtained during the acquisition phase of memory. This suggests that the cholecystokininergic system in the hippocampus is involved in stress-induced impairment of spatial recognition memory.
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PMID:Involvement of brain endogenous cholecystokinin in stress-induced impairment of spatial recognition memory. 1267 33


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