Bioactivity of intraduodenally and intravenously infused fragments of luminal cholecystokinin releasing factor (LCRF)

Spannagel, Alan W.; Reeve, Joseph R.; Greeley, George H.; Yanaihara, N; Liddle, Rodger A.; Green, Gary M.

doi:10.1016/s0167-0115(97)01074-4

Cited by 12 publications

(8 citation statements)

References 8 publications

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“…The synthetic fragments LCRF(1-41) and LCRF(1-35) have similar potency and efficacy for CCK release in conscious rats (134). Tarasova et al (137) reported that endogenous LCRF was present throughout the gut, including in the pancreas, stomach, duodenum, jejunum, ileum, and colon, with the highest concentration in small intestine, supporting the notion that LCRF is secreted into intestinal lumen to stimulate CCK release from mucosal CCK cells.…”

Section: Gut Cck-secreting Cellmentioning

confidence: 92%

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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Section: Gut Cck-secreting Cellmentioning

confidence: 92%

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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“…The amino acid sequence of this peptide was identical to diazepam-binding inhibitor (DBI ) previously purified by Mutt and co-workers [136]. Intraduodenal administration of a fragment of DBI , DBI [33][34][35][36][37][38][39][40][41][42][43][44][45][46][47][48][49][50] , in anesthetized and atropinized rats resulted in a dosedependent increase in pancreatic protein secretion and elevation of plasma CCK concentration, although the fragment was less potent than DBI [134]. DBI was also Chey/Chang [138], with permission.…”

Section: Feedback Regulation Of Pancreatic Exocrine Secretionmentioning

confidence: 96%

“…The CCK-RP activity of the partially purified LCRF was abolished when it was percolated through an affinity column made of an anti-LCRF 1-6 serum but not that which was made of a normal rabbit serum [132]. Synthetic fragments of LCRF, LCRF , LCRF , and LCRF [11][12][13][14][15][16][17][18][19][20][21][22][23][24][25] , but not LCRF [1][2][3][4][5][6] , were also bioactive [133,134]. Interestingly, intravenous administration of LCRF 1-35 also stimulated CCK release and pancreatic secretion [134].…”

Section: Feedback Regulation Of Pancreatic Exocrine Secretionmentioning

confidence: 99%

Neural hormonal regulation of exocrine pancreatic secretion

Chey¹,

Chang²

2001

Pancreatology

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“…LCRF was identified after several studies showing that CCK release and pancreatic secretions were inhibited by trypsin, chymotrypsin, and elastases implying an intraluminal factor, sensitive to proteases, that elicits CCK secretion (28). Early studies tested the bioactivity of different LCRF fragments and highlighted the activity of fragment 11–25 but not 1–6 for instance, in accordance with the susceptibility of LCRF bioactivity to intestinal and pancreatic enzymes degradation (29). Further, it has been shown that LCRF acts directly on CCK-secreting cells also via an increase in intracellular calcium at least involving the L-type calcium channel (25).…”

Section: Cck Secretion and Bioactive Peptidesmentioning

confidence: 99%

Protein Digestion-Derived Peptides and the Peripheral Regulation of Food Intake

et al. 2017

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The gut plays a central role in energy homeostasis. Food intake regulation strongly relies on the gut–brain axis, and numerous studies have pointed out the significant role played by gut hormones released from enteroendocrine cells. It is well known that digestive products of dietary protein possess a high satiating effect compared to carbohydrates and fat. Nevertheless, the processes occurring in the gut during protein digestion involved in the short-term regulation of food intake are still not totally unraveled. This review provides a concise overview of the current data concerning the implication of food-derived peptides in the peripheral regulation of food intake with a focus on the gut hormones cholecystokinin and glucagon-like peptide 1 regulation and the relationship with some aspects of glucose homeostasis.

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Bioactivity of intraduodenally and intravenously infused fragments of luminal cholecystokinin releasing factor (LCRF)

Cited by 12 publications

References 8 publications

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

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

Neural hormonal regulation of exocrine pancreatic secretion

Protein Digestion-Derived Peptides and the Peripheral Regulation of Food Intake

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