Role of cyclic nucleotides and calcium in the nutrient‐induced release of cholecystokinin‐like immunoreactivity in rats.

Cuber, Jean‐Claude; Aucouturier, Sylvie; Bernard, Christine; Chayvialle, Jean‐Alain

doi:10.1113/jphysiol.1992.sp019073

Cited by 8 publications

(5 citation statements)

References 22 publications

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“…Administration of calcium channel blockers strongly reduced the bombesin-induced release of gastrin in the isolated vascularly perfused stomach preparation (Guo, Thompson & Singh, 1988). Similarly, the cholecystokinin secretion was strongly dependent on calcium in the isolated vascularly perfused rat duodenojejunum preparation since calcium channel blockers of the phenylalkylamine and dihydropyridine families reduced the peptone-induced cholecystokinin secretion (Cuber, Aucouturier, Bernard & Chayvialle, 1992). The same compounds, perfused in the present study at the same concentrations as in that previous report, were unable to reduce the glucose-evoked NTLI secretion.…”

Section: Discussionmentioning

confidence: 93%

Functional coupling between the active transport of glucose and the secretion of intestinal neurotensin in rats.

Dakka

Cuber

Chayvialle

1993

The Journal of Physiology

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SUMMARY1. In this study, the mechanisms involved in the release of neurotensin-like immunoreactivity (NTLI) by glucose were investigated with the isolated, vascularly perfused rat jejunoileum preparation.2. Luminal infusion of glucose (1-250 mM) produced a sharp and sustained release of NTLI in the intestinal venous effluent. The first significant response was observed with 5 mm glucose and the release reached a maximum under 250 mm glucose with a plateau secretion at 500% of basal.3. There was no significant difference in the ability of galactose and 3-0-methylglucose to release NTLI when compared to glucose, but ac-methylglucose, mannose, 2-deoxyglucose and fructose did not stimulate NTLI release.4. Luminal infusion of 5 mm phloridzin reduced the glucose-induced release of NTLI by 90 %. Intra-arterial infusion of glucose (25 mm) or of phloretin (20 jiM) had no significant effect on the glucose-evoked NTLI secretion.5. Intra-arterial infusion of ouabain (1 mM) produced a dramatic increase (at about 1500% of basal) in portal NTLI although it drastically reduced intestinal absorption of glucose.6. Intra-arterial infusion of tetrodotoxin (1 ,sM), atropine (10 /LM), verapamil (50 ,tM) or nifedipine (50 /LM) did not modify the glucose-induced NTLI secretion.7. Intra-arterial infusion of forskolin (2-20 /SM) evoked a prompt and wellsustained secretion of NTLI which was increased to a mean value of 800 % of basal with the highest dose tested. 3-Isobutyl-1-methylxanthine (IBMX, 10-100 ,tM) also stimulated the secretion of NTLI (maximal increase at 725% of basal at 100 pM).In contrast, intra-arterial infusion of 4-,8-phorbol 12-myristate, 13-acetate (PMA, 0 05-0-5 /SM) had no effect on NTLI release.8. IBMX (10-100 /iM) synergistically enhanced NTLI responses induced by 250 mm glucose; the integrated response of NTLI release was 3-to 5-fold higher * To whom correspondence should be addressed. MS 1650T. DAKKA, J.-C. CUBER AND J.-A. CHAYVIALLE than the sum of individual responses produced by the same stimulants given separately. 9. It is concluded that the carbohydrate-induced NTLI release is related to the active, sodium-dependent hexose transport, but not to the carbohydrate catabolic pathway. Furthermore, the intramural nerves and L-type calcium channels are not involved in the glucose-induced NTLI secretion. Finally, the secretory activity of the intestinal N cell seems to be mainly stimulated through a cAMP-dependent pathway.

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Section: Discussionmentioning

confidence: 93%

Functional coupling between the active transport of glucose and the secretion of intestinal neurotensin in rats.

Dakka

Cuber

Chayvialle

1993

The Journal of Physiology

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“…Indeed, vascularly perfused EGTA abolished the CCK response to peptones, whereas complexing luminal calcium by infusing EGTA into the duodenum had no effect (36). Additionally, peptone induced CCK secretion was strongly reduced upon intraarterial infusion of blockers of L-type Ca 2ϩ channels (36). To further test the hypothesis that intracellular Ca 2ϩ is required for CCK secretion, we incubated the STC-1 cells with BAPTA-AM and peptone or CPX.…”

Section: Discussionmentioning

confidence: 98%

Regulation of Cholecystokinin Secretion by Peptones and Peptidomimetic Antibiotics in STC-1 Cells

Némoz-Gaillard¹,

Bernard²,

Abello³

et al. 1998

Endocrinology

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Peptones are potent stimulants of cholecystokinin (CCK) release in rats, both in vivo and ex vivo in a model of isolated vascularly perfused duodeno-jejunum preparation and in vitro in the intestinal CCK-producing cell line STC-1. The underlying mechanisms were here investigated with this cell line. Protein hydrolysates from various origins (meat, casein, soybean, and ovalbumin; 0.5-1%, wt/vol) dose dependently increased CCK release. Cephalosporin antibiotics, which mimic tripeptides, also stimulated the release of CCK over the concentration range 1-20 mM. The study of concentration dependence of cephalosporin uptake indicated a passive diffusion process at either pH 7.4 or pH 6.0, thus arguing against the involvement of a peptide transporter in CCK secretion. After pertussis toxin treatment (200 ng/ml; 5 h), the peptone- and cephalexin-induced CCK secretion was significantly reduced, suggesting the involvement of pertussis toxin-sensitive heterotrimeric G protein(s) in the secretory activity of STC-1 cells. Consistent with this was the identification by Western blot of G(i2)alpha, G(i3)alpha, and G(o)alpha immunoreactivities in STC-1 cell extracts. Additionally, peptones and cephalexin increased the cellular content in inositol phosphates, whereas a mild increase in cAMP content was restricted to peptone-treated cells. Protein kinase A or C inhibition did not modify peptone- or antibiotic drug-evoked CCK release. The extracellular Ca2+ chelator EGTA (500 microM) and the intracellular Ca2+ chelator BAPTA-AM [1,2-bis-(O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetra(acetoxymethyl) ester; 20 microM] abolished the peptone- and antibiotic drug-induced CCK release. Nifedipine and verapamil (10 microM) reduced by about 50% the CCK secretion evoked by these two secretagogues. In conclusion, peptones and some cephalosporins are potent stimulants of CCK release in the STC-1 cell line. The cellular mechanisms involve pertussis toxin-sensitive G protein(s) and are dependent on Ca2+ availability. We suggest that the STC-1 cell line is a useful model to study the molecular basis of peptone-induced CCK secretion.

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“…In addition to these putative effectors, it was recently shown that rab3 interacts in a Ca 2+ ‐dependent manner with calmodulin to regulate exocytosis [35,40]. As bombesin and protein hydrolysates, potent stimulants of CCK release in I‐cells [2] and in STC‐1 cells [23] require intracellular calcium to exert their effect. An attractive hypothesis could be the formation of a rab3A‐Ca 2+ /calmodulin complex, which could contribute to a fine tuning of CKK exocytosis.…”

Section: Discussionmentioning

confidence: 99%

“…Cholecystokinin (CCK) exerts important actions in the digestive tract [1]. Agonist‐induced stimulation of CCK release from intestinal endocrine I‐cells is achieved through activation of protein kinase A and C, and of calcium channels [2,3]. This was observed as well in the enteroendocrine cell line STC‐1 [4,5], in which the role of the extracellular signal‐regulated kinase (ERK)1/ERK2 transduction pathway and of SNARE (soluble N ‐ethylmaleimide‐sensitive factor attachment protein receptor) proteins in the control of CCK release was demonstrated [6,7].…”

Section: Introductionmentioning

confidence: 99%

Rab3a controls exocytosis in cholecystokinin‐secreting cells

et al. 2001

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The expression of rab3A and rab3D isoforms in the enteroendocrine, cholecystokinin-secreting, cell lines STC-1 and GLUTag is here demonstrated. In contrast, rab3B is undetectable in these two cell lines, and rab3C is only slightly expressed in GLUTag cells. Using a transient co-transfection system with human growth hormone as reporter protein, we show that overexpression of the GTPase-deficient mutant rab3AQ81L, but not rab3DQ81L, significantly decreases human growth hormone secretory responses to various agonists in STC-1 cells. These results indicate that endocrine cell lines of intestinal origin express rab3A and rab3D proteins, but the GTP-bound form of rab3A only acts as a negative modulator in the control of cholecystokinin secretion from STC-1 cells. ß

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Role of cyclic nucleotides and calcium in the nutrient‐induced release of cholecystokinin‐like immunoreactivity in rats.

Cited by 8 publications

References 22 publications

Functional coupling between the active transport of glucose and the secretion of intestinal neurotensin in rats.

Functional coupling between the active transport of glucose and the secretion of intestinal neurotensin in rats.

Regulation of Cholecystokinin Secretion by Peptones and Peptidomimetic Antibiotics in STC-1 Cells

Rab3a controls exocytosis in cholecystokinin‐secreting cells

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