• Korean Journal of Poultry Science
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• v.17 no.2
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• pp.83-91
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• 1990

The effect of dietary components on cholecystokinin (CCK) release into plasma was investigated in chicks by feeding a meal through a stomach tube, followed by the CCK determination with specific CCK-8 antibody. In experimental 1, the results showed that both isolated soya protein and an amino acid mixture simulating the amino acid composition of the soya protein increased the release of CCK, though to a lesser extent with a delayed response in the former, when added to a protein-free diet. Among amino acids added singly to the protein-free diet, phenylalanine was more efficient than arginine and valine, exerting a response almost identical to the complete amino acid mixture. In experimental 2 and 3, by feeding the protein diets supplemented SBTI, piasma CCK level was promptly increased and this response was in a dose dependent fashion during the measurement time, being higher at 1000 than at 100 mg/kg diet. Since the SBTI supplementation did not affect crop emptying rates significantly, it was concluded that SBTI by itself enhanced CCK release into circulation.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.4
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• pp.275-281
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• 2000

Cholecystokinin (CCK) is a gastrointestinal hormone which plays an important role in satiety and gastric motility. It is also widely distributed throughout the central nervous system, where it appears to be involved in the central control of anxiety, feeding behavior and nociception. Two distinct CCK receptor types, $CCK_A$ and $CCK_B,$ have been found in the brain. Both CCK receptors coexist in the rat nucleus tractus solitarius (NTS), which is the primary center for the coordination of peripheral and central activities related to gastrointestinal, cardiovascular and respiratory functions. In order to study ionic actions of CCK on each type of receptor, we investigated the effects of CCK-8S on neurons located in the NTS of the rat using whole-cell patch-clamp recordings in brainstem slices. Application of CCK-8S, under current clamp, produced a membrane depolarization accompanied by action potential firing. This CCK-evoked excitation was dose-dependent $(10\;nM{\sim}10\;{\mu}M)$ and observed in more than 60% of NTS neurons. Under voltage clamp conditions, CCK-8S induced an inward current with a notably increased spontaneous excitatory synaptic activity. However, CCK-8S did not significantly change the amplitude of pharmacologically isolated and evoked EPSP(C)s. Using selective $CCK_A$ and $CCK_B$ receptor antagonists, we observed two different effects of CCK-8S, which suggest $CCK_A$ receptor-mediated inhibitory and $CCK_B$ receptor-mediated excitatory effects in the NTS. These results may help to explain the ability of CCK to modulate gastrointestinal and other reflex systems in the NTS.

• Journal of Acupuncture Research
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• v.24 no.2
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• pp.101-112
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• 2007

목적 : CCK는 현재까지 가장 많이 연구된 식후의 포만신호 전달물질로, 음식섭취를 감소하고, 캡사이신 반응성의 미주신경에 의해 위장운동과 위내의 공복감을 억제시킨다 전침의 진통효과 발현기전에 영향을 미치는 항아편양 단백물질로서, 내인성 CCK와 그 수용체(CCK-A와 CCK-B)의 역할은 기존의 연구에서 이미 보고되어 왔다. 이에 착안하여， 본 연구에서는 포만감의 측면에서 전침자극이 내인성 CCK의 발현에 어떠한 영향을 미치는가를 살펴보고자 한다. 방법 : 48시간 절식 쥐 모델을 이용하여, 전침자극 후 30분과 60분 동안, 먹이 섭취량 변화를 측정하고, 먹이섭취량에 영향을 주는 신경전달경로에서 CCK가 관여하는지를 확인하기 위해 미주신경절제술을 시행한 쥐와 비교하였다. 한편 48시간 절식 쥐 모델을 대상으로하여 침자극 후 시상하부의 CCK mRNA 발현변화를 관찰하였다. 결과 : 전침군에서 30분과 60분 뒤의 먹이 섭취가 대조군에 비해 현저히 낮게 관찰되었는데, 포만감에 관련된 침의 이와 같은 효과는 CCK 수용체에 길항작용이 있는 lorglumide와 미주신경절제술에 의해 차단됨을 알 수 있었다. 시상하부의 CCK mRNA의 발현되는 대조군에 비하여 전침군에서 증가하는 경향이 관찰되었으나, 통계학적인 유의성은 확인 할 수 없었다. 결론 : 위의 결과에서, 전침은 포만감에 영향을 미치는 내인성 CCK 메카니즘을 활성화시키는 것을 알수 있었다.

• The Korean Journal of Physiology
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• v.29 no.2
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• pp.243-250
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• 1995

A possible potentiation between cholecystokinin (CCK) and secretin in amylase secretion from isolated rat pancreatic acini was investigated. Combined treatment of acini with secretin and CCK at low concentrations, which are known to be physiological, resulted in enzyme secretion larger than the arithmetic sum of their separate effects. Such a potentiating effect also occurred between secretin and A23187 (Ca ionophore), between forskolin (adenylate cyclase activator) and CCK, and between forskolin and A23187. Staurosporin (protein kinase C inhibitor) and W7 (calmodulin antagonist) inhibited markedly the potentiated amylase release induced by the agonists, but KT5720 (protein kinase A inhibitor) did not affect the potentiated amylase release. Therefore, we concluded that the action of CCK in a physiological concentration is potentiated by secretin in a physiological concentration range and vice versa, and that the intracellular mechanism necessary for the potentiation is associated with $Ca^{2+}$. However, it is uncertain what mechanisms are involved in potentiation of amylase release after CAMP and $Ca^{2+}$.

• The Korean Journal of Pharmacology
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• v.19 no.1
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• pp.71-76
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• 1983

Aminoglycoside antibiotics are reported to enhance the amylase release from isolated slices of pancreas in vitro and the mode of action of aminoglycosides on amylase release is considered different from those of acetylcholine or cholecystokinin(CCK), i.e., electronmicroscopically intact zymogen granules are appeared in the lumen of pancreatic acini by treatment of aminoglycosides. It is known that atropine blocks the secretagogue effect of acetylcholine, and phenoxybenzamine is reported to block the effects of CCK or its analogue caerulein. Present study was undertaken to investigate the mode of action of aminoglycosides on the amylase release using atropine, phenoxybenzamine and propranolol as a membrane stabilizing agent in slices of chicken pancreas. The results are summarized as follows : 1) Streptomycin and kanamycin increased the amylase release significantly from slices of chicken pancreas. 2) The effect of streptomycin was inhibited by atropine but not by phenoxybenzamine or propranolol. 3) The amylase release by acetylcholine was blocked by atropine tut the effect of cholecystokinin octapeptide(CCK-8) was not influenced by atropine, phenoxybenzamine or propranolol. 4) Pretreatment of streptomycin enhanced the secretagogue effect of acetylcholine or CCK-8. From these results it is suggested that amylase releasing effects of aminoglycosides are mediated in part by cholinergic stimulation and in part by membrane alteration and these effects are enhanced by acetylcholine or cholecystokinin.

• Nutrition Research and Practice
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• v.8 no.2
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• pp.146-150
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• 2014

BACKGROUND/OBJECTIVES: Cholecystokinin (CCK), a hormone or neuropeptide, is secreted in response to intraluminal nutrients by enteroendocrine I-cells of the intestine and has important physiological actions related to appetite regulation and satiety. The stimulation on CCK secretion from the intestine is of potential relevance for body weight management. Naringenin (4',5,7-trihydroxyflavanone) and its glycoside naringin (naringenin 7-rhamnoglucoside) have been reported to have many biological functions. In the current study, we investigated the question of whether naringenin and naringin could stimulate CCK secretion and then examined the mechanisms involved in CCK release. MATERIALS/METHODS: STC-1 cells were used as a model of enteroendocrine cells. CCK release and changes in intracellular $Ca^{2+}$ ($[Ca^{2+}]_i$) were measured after incubation of cells with naringenin and naringin for 1 h. RESULTS: Naringenin caused significant (P < 0.05) stimulation of CCK secretion, but naringin did not. In addition, regarding the secretory mechanisms, naringenin-induced CCK secretion involved increases in $[Ca^{2+}]_i$, influx of extracellular $Ca^{2+}$, at least in part, and activation of TRP channels, including TRPA1. CONCLUSION: Findings of this study suggest that naringenin could have a role in appetite regulation and satiety.

• The Korean Journal of Pharmacology
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• v.31 no.1 s.57
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• pp.11-15
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• 1995

Serotonergic neurons in medulla oblongata play an important role in the endogenous descending pain inhibitory system. To illucidate the factors involved in the regulation of medullary serotonergic neurons, we studied the effects of cholecystokinin (CCK) and agents acting on various second messenger systems on 5-hydroxytryptamine (5-HT) release from cultured neurons of rat fetal (gestational age 14th day) medulla oblongata. Cultured cells maintained for 10 days in vitro were stimulated for 48 hours with CCK or other neuropeptides at 10 micromolar concentration. CCK ($10{\mu}M$) and substance P ($10{\mu}M$) significantly increased. 5-HT release. However, somatostatin, proctolin, thyrotropin releasing hormone, and interleukin-6 did not have any effects on 5-HT release. Nimodipine ($1{\mu}M$), a calcium channel blocker, almost completely, and calmidazolium ($1{\mu}M$), a calmodulin antagonist, significantly inhibited the CCK-induced 5-HT release. The total 5-HT content (intracellular 5-HT plus released 5-HT) was significantly increased by CCK. However, the intracellular 5-HT content was not significantly changed by CCK. Forskolin ($5{\mu}M$), an adenylate cyclase activiator, but not $2{\mu}M$ phorbol myristate acetate (PMA), a protein kinase C activator, significantly enhanced 5-HT release. The total 5-HT content (intracellular 5-HT plus released 5-HT) was significantly increased by forskolin. However, the intracellular 5-HT content was not significantly changed by forskolin. PMA had no effect on intracellular 5-HT levels. These results suggest that CCK regulates serotonergic neurons in the medulla oblongata by enhancing 5-HT secretion through calcium influx and caimodulin, and that cyclic AMP system but not protein kinase C system is involved in 5-HT release.

• International Journal of Oral Biology
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• v.31 no.4
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• pp.127-133
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• 2006

[ $H_2O_2$ ], a member of reactive oxygen species (ROS), is known to be involved in the mediation of physiological functions in a variety of cell types. However, little has been known about the physiological role of $H_2O_2$ in exocrine cells. Therefore, in the present study, the effect of $H_2O_2$ on cholecystokinin (CCK)-evoked $Ca^{2+}$ mobilization and amylase release was investigated in rat pancreatic acinar cells. Stimulation of the acinar cells with sulfated octapeptide form of CCK (CCK-8S) induced biphasic increase in amylase release. Addition of $30\;{\mu}M\;H_2O_2$ enhanced amylase release caused by 10 pM CCK-8S, but inhibited the amylase release induced by CCK-8S at concentrations higher than 100 pM. An ROS scavenger, $10\;{\mu}M$ Mn(III)tetrakis(4-benzoic acid)porphyrin chloride, increased amylase release caused by CCK-8S at concentrations higher than 100 pM, although lower concentrations of CCK-8S-induced amylase release was not affected. To examine whether the effect of $H_2O_2$ on CCK-8S-induced amylase release was exerted via modulation of intracellular $Ca^{2+}$ signaling, we measured the changes in intracellular $Ca^{2+}$ concentration $([Ca^{2+}]_i)$ in fura-2 loaded acinar cells. Although $30\;{\mu}M\;H_2O_2$ did not induce any increase in $[Ca^{2+}]_i$ by itself, it increased the frequency and amplitude of $[Ca^{2+}]_i$ oscillations caused by 10 pM CCK-8S. However, $30\;{\mu}M\;H_2O_2$ had little effect on 1 nM CCK-8S-induced increase in $[Ca^{2+}]_i$. ROS scavenger, 1 mM N-acetylcysteine, did not affect $[Ca^{2+}]_i$ changes induced by 10 pM or 1 nM CCK-8S. Therefore, it was concluded that $30\;{\mu}M\;H_2O_2$ enhanced low concentration of CCK-8S-induced amylase release probably by increasing $[Ca^{2+}]_i$ oscillations while it inhibited high concentration of CCK-8S-induced amylase release.

• Biomolecules & Therapeutics
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• v.21 no.2
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• pp.121-125
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• 2013

Hesperetin (3',5,7-trihydroxy 4'-methoxyflavanone) and its glycoside hesperidin (hesperetin 7-rhamnoglucoside) in oranges have been reported to possess pharmacological effects related to anti-obesity. However, hesperetin and hesperidin have not been studied on suppressive effects on appetite. This study examined that hesperetin and hesperidin can stimulate the release of cholecystokinin (CCK), one of appetite-regulating hormones, from the enteroendocrine STC-1 cells, and then examined the mechanisms involved in the CCK release. Hesperetin significantly and dose-dependently stimulated CCK secretion with an $EC_{50}$ of 0.050 mM and increased the intracellular $Ca^{2+}$ concentrations ($[Ca^{2+}]_i$) compared to the untreated control. The stimulatory effect by hesperetin was mediated via the entry of extracellular $Ca^{2+}$ and the activation of TRP channels including TRPA1. These results suggest that hesperetin can be a candidate biomolecule for the suppression of appetite and eventually for the therapeutics of obesity.

• The Korean Journal of Pharmacology
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• v.30 no.2
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• pp.205-215
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• 1994

It is well known that chronic stimulation with CCK gives rise to growth of exocrine pancreas and to increased content of enzyme proteins in pancreas. However, littls Is known about changes of the secretory function of exocrine pancreas which has been chronically stimulated with CCK, especially about the responsiveness to secretagogues such as CCK, caerulein and carbachol. The present study was performed to investigate the effect of camostat on secretory profiles and the responsiveness to secretagogues of exocrine pancreas by observing in vitro amylase release stimulated by cholecystokinin-octapeptide(CCK-8) and carbachol in dispersed isolated pancreatic acini from camostat-treated rats for 4 or 10 days. The results summarized as follows : 1) The maximal effective concentration of CCK-8 in amylase release in the camostat treated group was greater than control group, but that of carbachol was not different between groups. 2) Analysis of the stimulated amylase release as the percentage of the maximal response revealed that camostat treatment caused right-shift of the dose-response curve of CCK-8. Camostat did not cause significant changes in the dose-response curve of carbachol. 3) There were considerable increases in the amylase release in the camostat-treated group, compared to the control when acini were stimulated with CCK-8 $10^{-9}\;M$ and carbaochol $10^{-6}\;M$, and higher concentrations. 4) There was a reverse correlation between the tissue content and the maximal release(percent of the total content) of amylase. These results suggest that chronic exposure of exocrine pancreas to increased endogenous CCK can enhance the responsiveness of exocrine enzyme secretion to secretagogues, especially at higher concentrations of CCK and carbachol.