Purification and characterization of a luminal cholecystokinin-releasing factor from rat intestinal secretion.

Spannagel, Alan W.; Green, Gary M.; Guan, Difu; Liddle, Rodger A.; Faull, Kym F.; Reeve, Joseph R.

doi:10.1073/pnas.93.9.4415

Cited by 104 publications

(56 citation statements)

References 34 publications

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“…It has bee n ex plained tha t di eta ry proteins in th e intestin al lum en are recogni zed by th e feedbac k mechanism in the co ntrol of the exocrine pancrea ti c secreti o n. I S -17J In this mechanism, th e endogeno us CCK-releasing peptides (CCK-RP) but no t di etary proteins, ac t directly to intestina l epi thelia l cells. [18][19][20] Ho wever, specific recepto rs fo r the endogeno us CCK-RP have no t been identified yet. 21 -2 l) In contrast, we and other in vesti gators demonstrated th at pro teins were recogni zed in the intestin al lu men independent o f the feed back mechanism, and these repo rts indicate that pro teins could act d irectly to intestina l epi thelial cells incl uding CCK pro ducing enteroendocrin e cells .6.…”

Section: Discussionmentioning

confidence: 99%

Characterization of Binding Between the Rat Small Intestinal Brush-border Membrane and Dietary Proteins in the Sensory Mechanism of Luminal Dietary Proteins

Hira

Hara

Tomita

2001

Bioscience, Biotechnology, and Biochemistry

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Dietary proteins are recognized by the gastrointestinal tract to display physiological functions, however, the sensory mechanism of the intestinal mucosa is not known. We examined binding properties between the rat small intestinal brush-border membrane (BBM) and proteins by using a surface plasmon resonance biosensor. BBM and solubilized BBM prepared from the rat jejunum bound to casein immobilized on the sensor surface, but not to bovine serum albumin. The ileal BBM showed less binding to casein than the jejunal BBM. Solubilized BBM binding to immobilized a-casein was slightly inhibited by aminopeptidase inhibitors, but still more inhibited by addition of casein with the inhibitors. Guanidinated casein inhibited the solubilized BBM binding to a-casein more strongly than casein (casein sodium and a-casein) inhibited. Trypsinization of solubilized BBM abolished its binding activity to a-casein. These results indicate that some membrane protein, but not aminopeptidases, contained in BBM interacts with dietary proteins, and that guanidinated casein has a higher affinity for BBM than intact casein. These binding intensities for proteins were closely correlated to physiological responsiveness, and are possibly involved in a sensory system for dietary protein in the intestine.

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Section: Discussionmentioning

confidence: 99%

Characterization of Binding Between the Rat Small Intestinal Brush-border Membrane and Dietary Proteins in the Sensory Mechanism of Luminal Dietary Proteins

Hira

Hara

Tomita

2001

Bioscience, Biotechnology, and Biochemistry

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“…Substantial evidence has indicated that at least one mechanism causing CCK release involves endogenously produced releasing factors that are secreted into the lumen of the intestine and under the proper conditions to stimulate CCK secretion (Lu et al 1989;Miyasaka et al 1989;Spannagel et al 1996;Wang et al 2002). There is now strong evidence that a feedback mechanism exists in the chicken, pig, rat, dog and man.…”

Section: Factors Regulating Gastrin and Cholecystokinin Releasementioning

confidence: 99%

Gastrin, cholecystokinin and gastrointestinal tract functions in mammals

et al. 2006

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The aim of the present review is to synthesise and summarise our recent knowledge on the involvement of cholecystokinin (CCK) and gastrin peptides and their receptors in the control of digestive functions and more generally their role in the field of nutrition in mammals. First, we examined the release of these peptides from the gut, focusing on their molecular forms, the factors regulating their release and the signalling pathways mediating their effects. Second, general physiological effects of CCK and gastrin peptides are described with regard to their specific receptors and the role of CCK on vagal mucosal afferent nerve activities. Local effects of CCK and gastrin in the gut are also reported, including gut development, gastrointestinal motility and control of pancreatic functions through vagal afferent pathways, including NO. Third, some examples of the intervention of the CCK and gastrin peptides are exposed in diseases, taking into account intervention of the classical receptor subtypes (CCK 1 and CCK 2 receptors) and their heterodimerisation as well as CCK-C receptor subtype. Finally, applications and future challenges are suggested in the nutritional field (performances) and in therapy with regards to the molecular forms or in relation with the type of receptor as well as new techniques to be utilised in detection or in therapy of disease. In conclusion, the present review underlines recent developments in this field: CCK and gastrin peptides and their receptors are the key factor of nutritional aspects; a better understanding of the mechanisms involved may increase the efficiency of the nutritional functions and the treatment of abnormalities under pathological conditions.

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“…The hypothesis postulated that trypsin-sensitive intestinal-releasing factors were present in the small intestine lumen, and, when pancreatic proteases were absent, endogenously produced releasing factors are intact and would interact with the CCK cell to stimulate CCK release (79). This idea led to the discovery of luminal CCK-releasing factor (LCRF), isolated from rat intestinal washings (133), and diazepambinding inhibitor (DBI), isolated from porcine intestine (47). Both LCRF and DBI are involved in the negative feedback regulation of CCK secretion because they are intact and functional in the absence of the pancreatic proteases.…”

Section: Gut Cck-secreting Cellmentioning

confidence: 99%

How does cholecystokinin stimulate exocrine pancreatic secretion? From birds, rodents, to humans

Wang¹,

Cui²

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Wang BJ, Cui ZJ. How does cholecystokinin stimulate exocrine pancreatic secretion? From birds, rodents, to humans. Am J Physiol Regul Integr Comp Physiol 292: R666-R678, 2007. First published October 19, 2006; doi:10.1152/ajpregu.00131.2006.-The field of cholecystokinin (CCK) stimulation of exocrine pancreatic secretion has experienced major changes in the recent past. This review attempts to summarize the present status of the field. CCK production in the intestinal I cells, the molecular forms of CCK produced and subsequently circulated in the blood, the presence or absence of CCK receptors on the isolated pancreatic acinar cells and the associated signaling for acinar cell secretion, and the actual circuits and sites of action for CCK regulation of exocrine pancreatic secretion in vivo are reviewed in different animal species with an emphasis on birds, rodents, and humans. Clear differences in the relative importance of neural and direct modes of CCK action on pancreatic acinar cells were identified. Rodents seem to be endowed with both modes of action, whereas in humans the neural mode may predominate. In birds, such as duck, the direct mode needs further assistance from pituitary adenylate cyclaseactivating peptide/VIP receptors. However, much further work needs to be directed to the neural mode to map out all sites of CCK action and details of the full circuits, and we foresee a major revival for this field of research in the near future. pancreatic acinar cells; vagal afferent nerves; plasma cholecystokinin concentration; species specificity IT IS GENERALLY ACCEPTED THAT cholecystokinin (CCK) as a gut hormone is an important endogenous secretagogue in exocrine pancreatic secretion. CCK also stimulates gallbladder contraction and enhances growth of the exocrine pancreas (63,115,138). CCK is produced and released by the intestinal mucosal I cells (78). This source of CCK may travel through the circulation to target tissues that include the exocrine pancreas and gallbladder (65,78). CCK peptides are also found in large quantities in neurons, but neuronal CCK contributes negligibly to CCK concentration in the circulation (118). This general picture has been changed drastically by the recent findings that CCK can also stimulate exocrine pancreatic secretion by the excitation of sensory nerves and vagovagal and enteropancreatic reflexes, and this may be the only pathway in humans (65, 105). In addition, major differences have been found in the traditional humoral pathway, depending on the animal species (35,149). Therefore, the purpose of this review is to present the current status of CCK regulation of exocrine pancreatic secretion with a particular emphasis on species specificity as shown in birds, rodents, and humans.

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Purification and characterization of a luminal cholecystokinin-releasing factor from rat intestinal secretion.

Cited by 104 publications

References 34 publications

Characterization of Binding Between the Rat Small Intestinal Brush-border Membrane and Dietary Proteins in the Sensory Mechanism of Luminal Dietary Proteins

Characterization of Binding Between the Rat Small Intestinal Brush-border Membrane and Dietary Proteins in the Sensory Mechanism of Luminal Dietary Proteins

Gastrin, cholecystokinin and gastrointestinal tract functions in mammals

How does cholecystokinin stimulate exocrine pancreatic secretion? From birds, rodents, to humans

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